Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_37_библиотеки_им_акад_М_И_Перельмана
.pdf
a significant source of aluminum toxicity.56 Thirty
https://t.me/medicina_free
samples of TPN in the same hospital showed that
although the FDA advises the maximum exposure
to aluminum be under 5 mcg/kg/day, aluminum
contamination in TPN for infants younger than 30
days of age was three times higher than the FDA
advisory.56 Clinicians should attempt to reduce
aluminum intake and should monitor levels for
infants at highest risk.
6
Table 16.3 outlines a suggested composition
for a TPN solution (guideline only). Even in the
most knowledgeable hands, accurate calculation
and ordering of parenteral nutrition for preterm or
ill infants is a complex task. Online TPN ordering
programs are available in many units to assist
the clinician with this task. Use of such programs has been shown to decrease order entry
errors and are cost effective.
76,80
The Case Study
illustrates considerations in writing orders for TPN
solutions.
Preparing the Solution
Solutions should be prepared in the hospital
pharmacy under a laminar flow hood in a work
area isolated from traffic and contaminated
supplies. There should be quality control checks to
monitor for sterility breaks in equipment, personnel,
environment, and solutions.
Because many additives potentially can be
insoluble in combination, a mixing sequence
should be established that separates the most
incompatible ingredients. Storage increases the
risk for microbial contamination; therefore TPN
solutions should be prepared on the day
they are needed.82 However, to be able to
provide an amino acid infusion to preterm
infants immediately after admission, some
units maintain a “stock” amino acid solution
(10% dextrose with 2 to 3 g of amino acids
per 100 mL).
119
Administering the Total Parenteral
Nutrition Solution
CHAPTER 16 Total Parenteral Nutrition
TABLE
16.3
COMPONENT DAILY AMOUNT
SUGGESTED COMPOSITION FOR DAILY
INTRAVENOUS NUTRITION REGIMEN
Calories
Dextrose 3.4 kcal/g 10–15 g/kg
Lipids 2.0 kcal/mL (20%) solution 1–3 g/kg
Protein (6.25 g protein = 1 g N2) 3.5–4 g/kg
Electrolytes
Sodium 3 mEq/kg
Potassium 2–3 mEq/kg
Chloride
Acetate 3 mEq/kg
Phosphate 2 mM/kg
Calcium 3 mEq/kg
Magnesium 0.3 mEq (range 0.25–0.5
3–4 mEq/kg
mEq/kg) or 20 mg/kg
(range 10–40 mg/kg) of
elemental magnesium
Vitamins
MVI-Ped
<1 kg 1.5 mL/day
1–3 kg 3.25 mL/day
>3 kg 5 mL/day
Trace Elements
Zinc (zinc sulfate)
<3 kg 400 mcg/kg/day
≥3 kg 250 mcg/kg/day (Max of
4 mg/day)
Copper (cupric sulfate) 20 mcg/kg
Manganese sulfate 5 mcg/kg
Chromium chloride 0.2 mcg/kg
Selenium 2 mcg/kg
469
Proper administration of the TPN solution is
as important as its preparation in preventing
complications. The label on the solution always
should be checked to correctly identify the
patient, using at least two identifiers, and to
verify current formulation order.
Standardized procedures must be established to
avoid infectious complications from solution contamination. Solutions on the nursing units may
be returned to the pharmacy for additives before
hanging, but no additives should be placed in the
solution once it is hanging. The bag or bottle
UNIT THREE Metabolic and Nutritional Care of the Neonate470
12.5g/dl 140ml/kg=17.5g glucose/kg
17.5g glucose/kg 3.4kcal/g glucose=60kcal/kg
()
+ +
(3 mM PO4/4mEqNa )=(3 mEq Na )
/kg
https://t.me/medicina_free
CASE STUDY
The following case example illustrates considerations in writing orders for
total parenteral nutrition (TPN).
History
A male infant born at 26 weeks of gestation at 900 g is now 10 days old
and unable to be fed because he has developed necrotizing enterocolitis
(NEC). Because there will be a prolonged delay in enteral alimentation,
a central vein catheter is placed for TPN. He is currently receiving D10W at
140 mL/kg with maintenance electrolytes. His current weight is 850 g.
Serum electrolytes and blood glucose are normal. He is receiving continuous
infusion pain medications and vasopressors that are equal to 21 mL/kg/
day of fluid. The approach to calculating TPN requirements is as follows.
Caloric Requirement
Because the patient has already had a significant postpartum period without
adequate nutrition, achieving caloric intake necessary for growth is a very
important part of his care. The infant will probably require 100 kcal/kg or
more for tissue repair and growth. We will begin with approximately 60 to
70 kcal/kg (the birth weight is used until weight gain is established) and
advance the intake daily to reach this level.
Carbohydrate
Initially, a dextrose load just above what has been previously tolerated
should be used. Thus the patient may receive D
mL/kg/day; the volume could vary depending on the infant’s fluid requirements. When TPN is ordered, carbohydrate amount should be ordered as glucose infusion rate (GIR) rather than percent dextrose to minimize errors.
This represents:
W at approximately 140
12.5
85
Electrolytes
The patient should receive maintenance sodium ion (approximately 3 mEq/
kg) and potassium ion (2 to 3 mEq/kg) unless there are excessive renal or
gastrointestinal losses.
Anions
Balancing anions is the next consideration. The 3 g/kg of amino acids, if given
as TrophAmine, adds approximately 3 mEq/kg of acetate to the solution (1 mEq
acetate/1 g amino acids). If 3 mEq/kg of potassium is provided as potassium
chloride, the solution has balanced anions. Giving 3 mEq/kg of sodium as sodium
phosphate provides approximately 2.2 mM/kg of elemental phosphorus:
=2.25 mM PO
4
Minerals, Vitamins, and Trace Elements
Calcium, magnesium, phosphorus, vitamins, and trace elements should be
ordered at this point. Calcium initially should be started at 2 to 3 mEq/kg/
day but may be increased as tolerated with growth to 4 to 5 mEq/kg/day.
Use of an online TPN ordering program may assist the clinician by auto-
mating many of these calculations.
76
TPN Orders
Thus the TPN orders would be written for this patient as follows:
Total Fluids = 140 mL/kg/day
Nutritional Volume = 140 mL/kg/day
Fat Emulsion Order: 1 g/kg/day to run at 0.19 mL/hr for 24 hours
TPN Order: 135 mL/kg/day = 5.1 mL/hr
Fat
Lipid emulsion should be added to increase the caloric intake, starting with
1 g/kg/day.
5mL/kg20% lipid emulsion 1.0g
2kcal / mL=10kcal/kg/day
Thus the total nonnitrogen calories on the first day of TPN is 70
(60 + 10).
Protein
Provision of protein nutrition is critical to this preterm infant for growth and
to repair damaged tissues. The initial amino acid replacement is 2.5 to 3
g/kg/day.
TPN Order Ordered Components
Glucose infusion
rate (GIR)
Amino acids 3 gm/kg/day
Cysteine 40 mg/gram of amino acids
Potassium chloride 2.8 mEq/kg/day (2.8 mEq/kg/day K+; 2.8
Sodium phosphate 2.8 mmol/kg/day (3.7 mEq/kg/day Na+; 2.8
Calcium gluconate 2.8 mEq/kg/day
Magnesium sulfate 0.3 mEq/kg/day
Multivitamin 1.5 mL/day
Zinc 400 mcg/kg/day
Copper 20 mcg/kg/day
Manganese 5 mcg/kg/day (some would not add manganese
4 mg/kg/min
mEq/kg/day Cl−)
mmol/kg/day phosphate)
due to cross contamination of other TPN products)
CASE STUDY
https://t.me/medicina_free
CHAPTER 16 Total Parenteral Nutrition
471
TPN Order Ordered Components
Chromium 0.2 mcg/kg/day (some would not add
manganese due to cross contamination of other
TPN products)
Selenium 2 mcg/kg/day
of TPN solution should be changed every 24
hours, and the tubing administration sets should
be changed no more frequently than every 72
to 96 hours. Lipid emulsions and tubing should
be changed every 12 to 24 hours.
13,15,53,72,81,85
Tubing for lipid administration should include
a 1.2 micron filter. Polyvinyl chloride tubing and IV bags containing phthalates should
be avoided to reduce potential toxicity from
plasticizers.
48,120
Exposure of TPN to light generates peroxides, which induce vasoconstriction and oxidant stress associated with bronchopulmonary
dysplasia. Photoprotection of bags, syringes,
and tubing used to deliver TPN and lipids may
reduce the oxidant effect on the lungs and mesenteric blood flow. Light shielding also appears
to diminish oxidative stress and alterations
of lipid metabolism, resulting in lower levels
of triglyceride and better substrate delivery.
Amber-colored tubing may be used for this
purpose.
32,52,66,67
Changes in TPN infusion rates result in changes
in glucose delivery to the newborn and may lead
to hypoglycemia or hyperglycemia if the glucose
homeostatic mechanisms do not adjust fast enough.
Reactive hypoglycemia may occur if the glucose
load is abruptly reduced or discontinued, such as
from loss of vascular access or rapid decrease in dextrose concentration or infusion rate.10 Parenteral
nutrition solutions must infuse at a constant rate
via an infusion pump. Infusion rates should not
be rapidly increased or decreased. If the parenteral nutrition infusion is suddenly discontinued because of a clotted catheter or accidental
removal, an appropriate solution with dextrose
should be infused via a peripheral vein and
blood glucose should be monitored closely.
Progression
On subsequent days, the dextrose concentration and lipids would be
advanced slowly to increase the caloric intake to requirement as tolerated.
The quantity of protein would also be increased to about 4 g/kg/day.
Use of parenteral nutrition may increase an
infant’s risk for hyperglycemia during surgery.
Because rapid fluid infusions may be necessary
during operative procedures, the TPN solution
should be discontinued and replaced with a physiologic infusate during the perioperative period. After
surgery, TPN should be as when the patient is euglycemic, with recent evidence of early postoperative
protein tolerance and improved protein balance.
100
Tapering of the TPN solution occurs as the
infant begins to tolerate enteral feedings. When
the patient is taking approximately two thirds of
the necessary calories enterally, the central line
may be removed.
Administering Fat Solution
Rapid infusion of the fat emulsion may exceed
its clearance rate from the body and accentuate
complications; therefore fat emulsions should not
be infused faster than 0.2 g/kg/hr.
erally are given through a Y-site connection to bypass
the filter in the TPN line or may be given through
a separate venous site. However, some hospitals use
a combined dextrose, amino acid, and lipid solution
known as three-in-one or total nutrient admixture
19,110
(TNA).
A 1.2 micron filter is used with
this solution to remove certain drug precipitates
(Ca/PO4), air, and Candida species but is not
effective in removing bacteria. The decision to use
TNA should be approached with caution in infants.
Lipid emulsions increase the pH of the TPN solution,
limiting the amount of calcium and phosphorus that
can be delivered because of the risk for precipitation.
Precipitates are particularly difficult to detect in
TNA, which is a milky solution. High concentration of calcium and low pH of the solution also can
disrupt TNA, causing it to “crack” and leading to
7,96
Lipids gen-
UNIT THREE Metabolic and Nutritional Care of the Neonate472
S
(Glucose/18)
+
https://t.me/medicina_free
separation of oil from the rest of the solution. One
must store the admixture emulsion at an ambient
temperature below 28° C to prevent coalescence.
74
When administering lipids to ill infants receiving other infusions, care must be taken to
ensure that medications are compatible with
lipids or medications must be provided by a separate IV route to prevent precipitation. It should
also be noted that IV compatibility is different
between lipid products, with mixed oil based
lipid emulsions having limited data regarding
compatibility with other medications or fluids.
COMPLICATIONS
Metabolic Complications
GLUCOSE METABOLISM
Hyperglycemia may occur with increased carbohydrate load, especially in ELBW
138
infants who
may have inadequate endogenous insulin production
or decreased sensitivity to insulin. Hyperglycemia is
arbitrarily defined as a blood glucose concentration
greater than 125 mg/dL (6.9 mmol/L) or a plasma
or serum blood glucose concentration greater than
150 mg/dL (8.3 mmol/L).
59,103
Elevated blood
sugar may lead to hyperosmolality and osmotic diuresis, resulting in dehydration. Manifestations include
polyuria, glucosuria, and excessive weight loss. Serum
sodium is not a reliable measure of serum osmolality
if there is hyperglycemia. Direct measurement or
estimate by use of the following formula is necessary:
erum osmolality = (1.86) Na + (BUN/2.8) +
Transient glucose intolerance may be seen
with stress. If hyperglycemia occurs without appar-
ent change in glucose infusion, the possibility of sepsis,
pain, hypoxemia, intraventricular hemorrhage (especially if the infant is less than 34 weeks’ gestation), glucocorticoid administration, or inadvertent increase in
carbohydrate administration (mistake in preparation
or rate of infusion) should be considered. Glucose
intolerance also may be accentuated during infusions of lipid emulsion, especially in an ELBW
infant. Discontinuation of the lipid infusion without
alteration of the carbohydrate load will often eliminate hyperglycemia in this situation. Some ELBW
infants remain hyperglycemic even on reduced carbohydrate intakes. Controversy still remains over the
use of a continuous insulin infusion to attain adequate
caloric intake. A recent Cochrane review of neonatal
hyperglycemia and insulin treatment showed no
improvement in outcomes with continuous insulin
infusion compared with reduced glucose infusion
rates.23 Treatment with insulin varies, but the
usual infant dose is 0.05 to 0.1 unit/kg/hour and
should be reserved for severe hyperglycemia,
with clinical symptoms and resistance to other medical management changes.6 Routine use of insulin
to promote growth in the preterm infant is not
advised because of side effects.
14
Hypoglycemia may result from an abrupt
interruption of glucose infusion or excessive
exogenous insulin administration. Manifestations
of hypoglycemia include apnea, lethargy, jitteriness, and seizures. If these signs occur
immediately after an interruption of the TPN
infusion, an IV glucose infusion must be initiated at once, followed by close monitoring of
the blood glucose to allow appropriate glucose
administration. The glucose concentration of
the infusate may usually be safely decreased by
a glucose infusion rate (GIR) of 2 mg/kg/min
every 12 hours. Blood glucose values should be
monitored hourly until stable after each change.
AMINO ACID METABOLISM
Hyperammonemia may be seen in preterm infants
given excessive protein loads. Hyperammonemia
will occur also in an infant with a congenital metabolic disturbance, such as a urea cycle
defect, when challenged with an amino acid load.
Hyperammonemia may manifest as somnolence,
lethargy, seizures, and coma. Biochemical screen-
ing is necessary to identify this complication before
symptoms appear.
Azotemia may occur before hyperammonemia,
but blood urea nitrogen (BUN) elevation in the first
week of life of a preterm infant is usually associated
with dehydration and has not been a reliable marker
of protein excess.41 Therefore, although daily
monitoring is common in the first week, rising
BUN is not an indication by itself to decrease
the protein load.
CHOLESTASIS
Infants receiving TPN for more than 2 weeks
frequently develop cholestatic jaundice (direct
CHAPTER 16 Total Parenteral Nutrition
https://t.me/medicina_free
473
bilirubin greater than 2 mg/dL).
34,99,117
The risk
appears to be greatest for the least mature
infants and those receiving the longest period
of TPN without enteral feeding. The cause
appears to be multifactorial, including lack of bile
flow stimulation, delayed enteral feedings, malnutrition, or inflammation after localized or generalized
infection.
135
More recently, IV fat emulsions, particularly polyunsaturated fatty acid, are thought to
contribute to cholestasis.
124
Serum amino transferases
often are normal early in the clinical course. Serum
albumin and prealbumin levels usually remain normal. An abnormality in hepatic synthetic function or
early rise in isoenzyme levels should lead the clinician
to investigate other forms of liver disease.
The differential diagnosis of cholestatic jaun-
dice includes the following:
• Bacterial sepsis
• Congenital viral infection
• Postpartum acquisition of cytomegalovirus
• Neonatal hepatitis
• Bile duct obstruction, such as biliary atresia
or choledochal cyst
• Galactosemia
• Cystic fibrosis
• Alpha1-antitrypsin deficiency
Management of cholestatic jaundice should
include the following (when possible):
• Increase enteral feedings as tolerated and
decrease proportionately the parenteral nutrition
• Dose reduction of soybean-based IV fat
emulsion
129,132
• Reducing copper by 50% or eliminating copper
• Eliminating manganese from trace minerals in
TPN
• Protecting solutions from light by covering the
bag and IV tubing to reduce levels of light-induced toxic peroxides
• Trial of an agent that induces bile flow
33,66
30,111
• For infants with short bowel syndrome, con-
trolling intestinal bacterial overgrowth
64
• Considering an alternative type of fat
emulsion
LIPID METABOLISM
55,75
High-risk infants, including preterm and
SGA low-birth-weight infants, may demonstrate intolerance to fat emulsion infusions.
Hyperlipidemia may result, causing elevation
of triglyceride, FFA, and lipoprotein levels. In
extreme cases, lactescence may be visible in serum
on a spun blood specimen (increased plasma turbidity). For screening, a triglyceride level should
be checked after initiation of therapy and then
weekly and doses adjusted based on results.
Steroid therapy may elevate the triglyceride level.
104
Transient hyperglycemia may result from lipid infusion. This complication is usually dose related and
rarely requires treatment.
43
Competitive displacement of bilirubin by FFA
theoretically may increase the risk for kernicterus in
preterm infants with hyperbilirubinemia. However,
studies of preterm infants have indicated that lipid
infusions may be used in jaundiced infants, but
attention to the infusion rate and monitoring of
FFAs are necessary.
96
Mechanical Complications
Pneumothorax, hemothorax, hydrothorax, air
embolism, thromboembolism, catheter misplacement, cardiac perforation, and tamponade are all
recognized complications of Broviac, subclavian,
or jugular catheter insertions. Potential mechanical complications of percutaneous central lines
include catheter occlusion, accidental dislodgement, erythematous tracking, phlebitis, thrombosis, superior vena cava syndrome, catheter
migration, perforation, and catheter entrapment
or breakage.
pericardial effusion may be blood or chyle or may be
a signal that the catheter has eroded into the pleural
or pericardial space. The effusion may be the infusate.
Therefore chest x-ray examination is necessary
to document correct catheter placement before a
hypertonic solution is instilled, with the superior
vena cava the preferred catheter tip location.
The preceding complications may occur
at any time while the catheter is present.
Documentation of catheter position should be
repeated if there is any history of pulling or tension on the catheter or any apparent change in its
external position or change in the clinical condition
associated with the preceding complications.
Any signs of catheter malfunction require
troubleshooting and assessment for potential
interventions to salvage the line. Some clinicians will flush a partially occluded line with
a thrombolytic agent, such as recombinant
tissue plasminogen activator (rt-PA).
risk of this practice must be weighed against
the benefits of maintaining the central line.
5,20,105,136
(See Box 7.1.) A pleural or
65,115
The
UNIT THREE Metabolic and Nutritional Care of the Neonate474
https://t.me/medicina_free
In most cases, if the catheter is a temporary line,
it may be better to remove it and place a new line
in another site.
Infectious Complications
Infections associated with the central line may
occur from contamination of the solution, tubing
connections, or hubs. Although organisms may contaminate the solution during preparation, usually
colonization occurs with entry into the line or
bag. Intermittent administration of medications,
removal of blood samples through the line, or
multiple tubing changes provide opportunity for
organisms to contaminate the solution.
Rigid criteria for sterile preparation of the solutions are mandatory (see Preparing the Solution
earlier in this chapter).
An in-line 0.22 mcm membrane filter, which
is incorporated into the IV tubing for TPN
administration, is capable of trapping bacteria
and fungi (although not endotoxin) and should
help minimize the risk for septicemia from a contaminated IV bag. In addition, filters lessen the risk
for an air embolism. An in-line filter setup is available that decreases the number of connections.
Nothing should be added to the TPN solution after it leaves the pharmacy.
AVOIDING LINE COLONIZATION
Use of a dedicated central line team for placement, monitoring, maintenance, and troubleshooting has been found to improve line
outcomes and reduce the incidence of neonatal
catheter-related bloodstream infections. Line
insertion and maintenance bundles, which include
hand hygiene, skin antisepsis, maximal barrier precautions, strict adherence to proper hub care, and
daily review of line necessity, are also important for
avoiding line complications.
In addition, pay attention to the following to
avoid line colonization
• When changing IV fluids, one should avoid
bleed-back into the catheter.
• Line setups should be designed to minimize
number of ports and connections.
• Generally, medications should not be given
into injection ports in the IV tubing but
should be given into a dedicated hepa-
rin-locked Y-site entry port instead. Stopcocks
are not recommended.
15,53
:
69
• The source of an infection is usually contam-
ination with an organism that has colonized
the hub or surrounding skin. Scrupulous
attention to hand hygiene and disinfection of
catheter tubing, hubs, ports, and connections by
vigorous rubbing with 70% alcohol before tubing changes or entry are critical infection-prevention strategies.
15,68,69
Dressings are not routinely changed on
PICC lines. If the dressing becomes nonocclusive or moistened, the site should be cleaned
according to hospital protocol and redressed
with a sterile transparent dressing.53 This should
be performed using sterile gloves. The exposed
catheter should be remeasured to ensure that it
was not inadvertently moved during this process.
Dressings are changed routinely on Broviac,
subclavian, jugular, and femoral catheters.
Dressing changes are recommended at least weekly
or more frequently if drainage is noted or the
dressing is no longer occlusive.
EVALUATING INFANTS FOR INFECTIOUS
DISEASE COMPLICATIONS
Central line–associated bacteremia represents
an important source of nosocomial infections
in the intensive care nursery. The prevalence of
this complication varies by unit based on patient
demographics including birth weight, gestational
age, diagnoses (proportion of surgery and medicine),
and care practices.
Bacteremia must be considered in a newborn
with a central line in place who exhibits signs
of sepsis (e.g., temperature instability, lethargy, poor
skin perfusion, increased cardiopulmonary distress,
apnea). Some neonatal infections may be treated
successfully with the line in place. However, if the
infant remains systemically ill, even if the blood
culture result is negative, the central line should
be removed.
22
Altered immune function by lipid deposition
in macrophages and the reticuloendothelial system must be considered in infants with sepsis.
Malassezia furfur is a lipophilic, opportunistic
fungal organism that may cause sepsis in infants
receiving long-term lipid infusions.
112
Although
this organism is infrequently seen, it may contaminate the line and appear as a white film. This organism often will not grow in routine blood culture
media. Specific culture techniques are necessary
when Malassezia is suspected.
35
CHAPTER 16 Total Parenteral Nutrition
https://t.me/medicina_free
475
Guidelines for management of an infant with
a central line in place with suspected sepsis are
as follows:
• The infant should be evaluated for potential
sources of infection, including a general phys-
ical examination looking for non–TPN-related
sources and inspection of peripheral and central
venous sites for erythema.
• Laboratory assessment should include (1) com-
plete blood cell count with platelet count and (2)
aerobic blood cultures. Other cultures, including
urine, tracheal aspirate, and cerebrospinal fluid,
may be indicated, based on clinical findings. A
blood fungal culture should be considered if the
infant has had preceding antibiotic treatment or
signs of fungal infection.
16,17,63
• A chest x-ray evaluation should be performed if
the infant demonstrates signs of respiratory distress
or there is a need to reassess catheter position.
• Consider decreasing or discontinuing lipid
infusion until the infection has been treated for
24 to 48 hours.
11,108
• If the infant is critically ill, the central line should
be removed immediately. If the infant is stable,
treatment may be considered through the line.
• A positive blood culture generally is con-
sidered to indicate bacteremia or sepsis in
a newborn with a central line in place.
However, the coagulase-negative Staphylococcus,
an opportunistic organism that is a common
cause of catheter-related sepsis, also is normal
skin flora and frequently contaminates blood
cultures. Use of ancillary diagnostic tools, such as
the C-reactive protein levels and complete blood
counts, are helpful to distinguish false-positive
results from true infections. Some clinicians also
recommend obtaining two cultures (two periph-
eral, or one peripheral and one from the line)
before starting antibiotics. If both yield positive
results, catheter-related sepsis is confirmed.
83
• If bacteremia is documented but the signs
of sepsis are improved, the catheter may
remain in place while being used for anti-
biotic treatment. One should be sure that the
antibiotics are compatible with the TPN solution
(to avoid stopping the TPN during the antibiotic
infusion). A follow-up blood culture and close
clinical monitoring are necessary to document
that the infection has been treated adequately.
If a central line is pulled because of sepsis, a new
central line should not be placed for 48 to 72 hours.
PARENT TEACHING
In-Hospital Total Parenteral Nutrition
Clinicians caring for an ill newborn must be attentive to the involvement and emotional state of the
parents. There remain a number of concerns for
child abuse, foster placement, and relinquishment
among infants who have been cared for in the
NICU compared with healthy term newborns,
especially when care has been prolonged and
complex.
Clinical conditions or policies that promote
separation of parents from their infant increase the
risk for bonding problems. When a newborn infant
cannot be fed orally, an important, normal part of
the infant’s care is no longer available for the parents.
The placement of a central line may be frightening
to parents and result in less handling and caregiving.
Infants requiring continuous care, including
TPN, should have primary nursing (one regularly scheduled nurse), and the parents should
have regular and consistent communication
with a primary physician. Care providers should
attempt to keep the parents involved in other
parts of the infant’s care because the parents
are unable to feed the infant. Parents should be
fully informed about the purpose and appropriate care of the infant’s central line so they will
feel comfortable handling their infant with the
line in place.
53
Home Total Parenteral Nutrition
Home parenteral nutrition has been used in
infants with congenital intestinal anomalies or
after massive bowel resection for NEC. TPN
is initiated in the hospital. If growing and otherwise well, the infant may be a candidate for TPN
at home. Issues to be addressed include ability and
willingness of parents to care for the infant at home,
available financial support, adequate home setting,
pharmacy support services, and additional skilled
nursing care needed. The infant should have a more
permanent central line placed as early in the discharge process as possible. Parent teaching should
begin early, including verbal and written instruction
and hands-on practice and return demonstrations
(Box 16.1).
Administration of TPN at home is different from
hospital administration of TPN and is typically
UNIT THREE Metabolic and Nutritional Care of the Neonate476
https://t.me/medicina_free
BOX
16.1
PARENT/CAREGIVER TEACHING
HOME ADMINISTRATION OF
PARENTERAL NUTRITION
• Strict handwashing and aseptic handling of tubing connections and
hubs
• Use of infusion pump
• Monitoring of site for signs of infection, phlebitis, or leaking
• Troubleshooting for occlusion, leaking, extravasation
• Evaluation for signs of systemic infection
• Emergency response to broken or dislodged catheter, loss of electrical power
• Developmental care: oral stimulation, holding, appropriate play
activities
• Dressing care and changes
• Monitoring for signs and symptoms of hypoglycemia
• Securing or taping of line to avoid dislodgement with positioning and
handling
managed by a pediatric gastroenterology service
in conjunction with a home infusion therapy or
pharmacy service. Infants often go home on a
cyclic TPN regimen (12 hours/day). An ambulatory
pump improves the mobility and flexibility of the
parent and infant and allows a more normal life.
Compliance and success with home TPN are
greatly increased when the parents understand
the need for and the appropriate way to administer TPN and how to troubleshoot and care for
the catheter.
54
REFERENCES
1. Adamkin DD, Radmacher P, Rosen P. Comparison of a
neonatal versus general-purpose amino acid formulation in
preterm neonates. J Perinatol. 1995;15(2):108.
2. Adamkin DH. Early total parenteral nutrition in very
low birth weight infants: is it safe? Is it worth it? J Pediatr.
2013;163(3):622.
3. Aggarwal R, Gathwala G, Yadav S, Kumar P. Selenium supple-
mentation for prevention of late-onset sepsis in very low birth
weight preterm neonates. J Trop Pediatr. 2016;62(3):185.
4. Ainsworth SB, McGuire W. Percutaneous central venous
catheters versus peripheral cannulae for delivery of parenteral nutrition in neonates. Cochrane Database Syst Rev.
2015;10:CD004219.
5. Ainsworth SB, McGuire W. Peripherally inserted central cathe-
ters vs peripheral cannulas for delivering parenteral nutrition in
neonates. J Am Med Assoc. 2016;315(23):2612.
6. American Academy of Pediatrics. Committee on Nutrition:
aluminum toxicity in infants and children. Pediatrics.
1996;97:413. Reaffirmed in Pediatrics. 2004;114(4):1126.
7. American Academy of Pediatrics. Committee on nutrition:
parenteral nutrition. In: Kleinman RE, ed . Pediatric Nutrition
Handbook. 7th ed. Elk Grove Village, IL: American Academy of
Pediatrics; 2013.
8. American Academy of Pediatrics. Committee on nutrition:
protein. In: Kleinman RE, ed . Pediatric Nutrition Handbook. 7th
ed. Elk Grove Village, IL; 2013.
9. The Academy American Society of Health-System Pharmacists.
The Handbook of Injectable Drugs. 20th ed. Bethesda, MD: ASHP;
2018.
10. Arsenault D, Brenn M, Kim S, et al. And the American Society
for Parenteral and Enteral Nutrition (ASPEN). Clinical
guidelines: hyperglycemia and hypoglycemia in the neonate
receiving parenteral nutrition. J Parenteral Enteral Nutrition.
2012;36(1):81.
11. Avila-Figueroa C, Goldmann DA, Richardson DC, et al.
Intravenous lipid emulsions are the major determinant of
coagulase-negative staphylococcal bacteremia in very low birth
weight newborns. Pediatr Infect Dis J. 1998;17(1):10.
12. Baker RD, Greer FR, Committee on Nutrition. Clinical
report-diagnosis and prevention of iron deficiency and iron-deficiency anemia in infants and young children (0-3 years of
age). Pediatrics. 2010;126(5):1040.
13. Balegar VKK, Azeem MI, Spence K, et al. Extending total parenteral nutrition hang time in the neonatal intensive care unit:
is it safe and cost effective? J Paediatr Child Health. 2013;
49(1):E57.
14. Beardsall K, Vanhaesebrouck S, Ogilvy-Stuart AL, et al. Early
insulin therapy in very-low-birth-weight infants. N Engl J Med.
2008;359(18):1873.
15. Bell T, O’Grady NP. Prevention of central line-associated blood stream infections. Infect Dis Clin North Amer.
2017;31(3):551.
16. Benjamin DK Jr, Miller W, Garges H, et al. Bacteremia, central
catheters, and neonates: when to pull the line. Pediatrics.
2001;107(6):1272.
17. Benjamin DK Jr, Ross K, McKinney RE Jr, et al. When to suspect
fungal infection in neonates: a clinical comparison of Candida
albicans and Candida parapsilosis fungemia with coagulase-negative staphylococcal bacteremia. Pediatrics. 2000;106(4):712.
18. Bishop NJ, Morley R, Day JP, et al. Aluminum neurotoxicity in
preterm infants receiving intravenous feeding solutions. N Engl
J Med. 1997;336(22):1557.
19. Blackmer AB, Partipilo ML. Three-in-one parenteral nutrition
for neonates and pediatric patients: risks and benefits. Nutr Clin
Pract. 2015;30(3):337.
20. Blackwood BP, Farrow KN, Kim S, Hunter CJ. Peripherally
inserted central catheters complicated by vascular erosion in
neonates. J Parenter Enteral Nutr. 2016;40(6):890.
21. Bonsante F, Iacobelli S, Chantegret C, et al. The effect of parenteral nitrogen and energy intake on electrolyte balance in the
preterm infant. Eur J Clin Nutr. 2011;65(10):1088.
22. Borghesi A, Stronati M. Strategies for the prevention of hospital-acquired infections in the neonatal intensive care unit. J
Hosp Infect. 2008;68(4):293.
23. Bottino M, Cowett RM, Sinclair JC. Interventions for treatment of neonatal hyperglycemia in very low birth weight
infants. Cochrane Database Syst Rev. 2011;10:CD007453.
24. Boullata JI, Gilbert K, Sacks G, et al. A.SPEN Clinical guidelines: parenteral nutrition ordering, order review, compounding, labeling, and dispensing. JPEN (J Parenter Enteral Nutr).
2014;38(3):334.
CHAPTER 16 Total Parenteral Nutrition
https://t.me/medicina_free
477
25. Brion LP, Bell EF, Raghuveer TS. Vitamin E supplementation
for prevention of morbidity and mortality in preterm infants.
Cochrane Database Syst Rev. 2003;3:CD003665.
26. Bruzoni M, Slater BJ, Wall J, et al. A prospective randomized
trial of ultrasound vs landmark-guided central venous access in
the pediatric population. J Am Coll Surg. 2013;216(5):939.
27. Burattini I, Bellagamba MP, Spagnoli C, et al. Targeting
2.5 versus 4 g/kg/day of amino acids for extremely low
birth weight infants: a randomized clinical trial. J Pediatr.
2013;163(5):1278.
28. Cairns PA, Stalker DJ. Carnitine supplementation of
parenterally fed neonates. Cochrane Database Syst Rev.
2000;4:CD000950.
29. Chang HY, Hsu CH, Tsai JD, et al. Renal calcification in very
low birth weight infants. Pediatr Neonatol. 2011;52(3):148.
30. Chen CY, Tsao PN, Chen HL, et al. Ursodeoxycholic acid
(UDCA) therapy in very-low-birth-weight infants with parenteral nutrition associated cholestasis. J Pediatr. 2004;145(3):317.
31. Cheong JL, Burnett AC, Kee KJ, the Victorian Infant
Collaborative Study Group, et al. Association between postnatal
dexamethasone for treatment of bronchopulmonary dysplasia
and brain volumes at adolescence in infants born preterm. J
Pediatr. 2014;164(4):737.
32. Chessex P, Harr ison A, Khashu M, et al. In preterm neonates, is
the risk of developing bronchopulmonary dysplasia influenced
by the failure to protect total parenteral nutrition from exposure to ambient light? J Pediatr. 2007;151(2):213.
33. Chessex P, Laborie S, Nasef N, Masse B, Lavoie JC. Shielding
parenteral nutrition from light improves survival rate in premature infants. J Parenter Enteral Nutr. 2017;41(3):378.
34. Christensen RD, Henry E, Wiedmeier SE, et al. Identifying
patients, on the first day of life, at high risk of developing parenteral nutrition-associated liver disease. J Perinatol. 2007;27(5):284.
35. Chryssanthou E, Broberger U, Petrini B. Malassezia pachydermatis fungaemia in a neonatal intensive care unit. Acta Paediatr.
2001;90(3):323.
36. Clark RH, Thomas P, Peabody J. Extrauterine growth restriction remains a serious problem in prematurely born neonates.
Pediatrics. 2003;111(5 pt 1):986.
37. Coleman MM, Spear ML, Finkelstein M, et al. Short-term
use of umbilical artery catheters may not be associated with
increased risk for thrombosis. Pediatrics. 2004;113(4):770.
38. Dahl GB, Svensson L, Kinnander NJ, et al. Stability of vitamins
in soybean oil fat emulsion under conditions simulating
intravenous feeding of neonates and children. JPEN J Parenter
Enteral Nutr. 1994;18(3):234.
39. Darlow BA, Graham PJ, Rojas-Reyes MX. Vitamin A supplementation to prevent mortality and short and long-term
morbidity in very low birthweight infants. Cochrane Database
Syst Rev. 2016;8:CD000501.
40. Darmaun D, Lapillonne A, Simeoni U, And the Committee
on nutrition of the French Society of pediatrics (CNSFP)
and French Society of Neonatology (SFN), et al. Parenteral
nutrition for preterm infants: issues and strategies. Arch Pediatr.
2018;25(4):286.
41. Denne SC, Poindexter BB. Evidence supporting early nutritional support with parenteral amino acid infusion. Semin
Perinatol. 2007;31(2):56.
42. Dinerstein A, Nieto RM, Solana CL, et al. Early and aggressive
nutritional strategy (parenteral and enteral) decreases postnatal
growth failure in very low birth weight infants. J Perinatol.
2006;26(7):436.
43. Drenckpohl D, McConnell C, Gaffney S, Niehaus M, Macwan
KS. Randomized controlled trial of very low birth weight infants
receiving higher rates of infusion of intravenous fat emulsions
during the first week of life. Pediatrics. 2008;122(4):743.
44. Dudrick SJ. Early developments and clinical applications of
total parenteral nutrition. J Parenter Enteral Nutr. 2003;27(4):291.
45. Ehrenkranz RA. Early, aggressive nutritional management for
very low birth weight infants: what is the evidence? Semin
Perinatol. 2007;31(2):48.
46. Ehrenkranz RA, Dusick AM, Vohr BR, et al. Growth in the
neonatal intensive care unit influences neurodevelopmental
and growth outcomes of extremely low birth weight infants.
Pediatrics. 2006;117(4):1253.
47. Embleton ND. Optimal protein and energy intakes in preterm
infants. Early Hum Dev. 2007;83(12):831.
48. Faessler B, McCombie G, Biedermann M, Felder F, Subotic IJ.
Leaching of plasticizers from polyvinylchloride perfusion lines
by different lipid emulsions for premature infants under clinical
conditions. Int J Pharm. 2017;520(1–2):119.
49. Farrag HM, Cowett RM. Glucose homeostasis in the micropremie. Clin Perinatol. 2000;27(1):1.
50. Finch CW. Review of trace mineral requirements for preterm
infants: what are the current recommendations for clinical
practice? Nutr Clin Pract. 2015;30(1):44.
51. Furdon SA, Horgan MJ, Bradshaw WT, et al. Nurses’ guide to
early detection of umbilical arterial catheter complications in
infants. Adv Neonatal Care. 2006;6(5):242.
52. Gargasz A. Neonatal and pediatric parenteral nutrition. AACN
Adv Crit Care. 2012;23(4):451.
53. Gorski LA, Hadaway L, Hagle M, et al. 2016 Infusion therapy
standards of practice. J Infus Nurs. 2016;39(suppl 1):S1.
54. Grant J. Recognition. prevention, and treatment of home total
parenteral nutrition central venous access complications. JPEN
J Parenter Enteral Nutr. 2002;26(suppl 5):S21.
55. Gura KM, Duggan CP, Collier SB, et al. Reversal of parenteral
nutrition-associated liver disease in two infants with short
bowel syndrome using parenteral fish oil: implications for future
management. Pediatrics. 2006;118(1):e197.
56. Hall AR, Arnold CJ, Miller GG, Zello GA. Infant parenteral
nutrition remains a significant source for aluminum toxicity.
JPEN (J Parenter Enteral Nutr). 2017;41(7):1228.
57. Hardy IJ, Gillanders L, Hardy G. Is manganese an essential
supplement for parenteral nutrition? Curr Opin Clin Nutr Metab
Care. 2008;11(3):289.
58. Hay WW Jr. Strategies for feeding the preterm infant.
Neonatology. 2008;94(4):245.
59. Hay WW Jr, Rozance PJ. Neonatal hyperglycemia—causes,
treatments, and cautions. J Pediatr. 2018;200:6.
60. Hay WW Jr, Thureen P. Protein for preterm infants: how much
is needed? How much is enough? How much is too much?
Pediatr Neonatol. 2010;51(4):198.
61. Hu F, Tang Q, Wang Y, et al. Analysis of nutrition support in
very low birth weight infants with extrauterine growth restriction. Nutr Clin Pract. 2019;34(3):436.
62. Ibrahim HM, Jeroudi MA, Baier RJ, Dhanireddy R, Krouskop
RW. Aggressive early total parenteral nutrition in low-birthweight infants. J Perinatol. 2004;24(5):482.
63. Karlowicz MG, Hashimoto LN, Kelly RE, et al. Should central
venous catheters be removed as soon as candidemia is detected
in neonates? Pediatrics. 2000;106(5):e63.
64. Kaufman SS. Prevention of parenteral nutrition associated liver
disease in children. Pediatr Transplant. 2002;6(1):37.
UNIT THREE Metabolic and Nutritional Care of the Neonate478
https://t.me/medicina_free
65. Kerner JA, Garcia-Carenga MG, Fisher AA, et al. Treatment of
catheter occlusion in pediatric patients. JPEN J Parenter Enteral
Nutr. 2006;30(1):S73.
66. Khashu M, Harr ison A, Lalari V, et al. Photoprotection of
parenteral nutrition enhances advancement of minimal enteral
nutrition in preterm infants. Semin Perinatol. 2006;30(3):139.
67. Khashu M, Harr ison A, Lalari V, et al. Impact of shielding
parenteral nutrition from light on routine monitoring of blood
glucose and triglyceride in preterm neonates. Arch Dis Child
Fetal Neonatal Ed. 2009;94(2):F111.
68. Kilbride HW, Power s R, Wirtschafter DD, et al. Evaluation and
development of potential better practices to prevent neonatal
nosocomial bacteremia. Pediatrics. 2003;111(4 pt 2):e504.
69. Kilbride HW, Wirtschafter DD, Powers RJ, et al.
Implementation of evidence-based potentially better practices to
decrease nosocomial infections. Pediatrics. 2003;111(4 pt 2):e519.
70. Klein GL. Aluminum in parenteral solutions revisited—again.
Am J Clin Nutr. 1995;61(3):449.
71. Klevebro S, Westin V, Stoltz Sjostrom E, et al. Early energy and
protein intakes and associations with growth, BPD, and ROP in
extremely preterm infants. Clin Nutr. 2019;38(3):1289 (Epub
ahead of print).
72. Kline AM. Pediatric catheter-related bloodstream infections: latest strategies to decrease risk. AACN Clin Issues.
2005;16(2):185.
73. Lapillionne A. Enteral and parenteral lipid requirement of
preterm infants. World Rev Nutr Diet. 2014;110:82.
74. Lee MD, Yoon JF, Kim SI, et al. Stability of total admixtures in
reference to ambient temperatures. Nutrition. 2003;19(10):886.
75. Lee S, Gura KM, Kim S, et al. Current clinical applications of
omega-6 and omega-3 fatty acids. Nutr Clin Pract. 2006;21(4):323.
76. Lehmann CU, Conner KG, Cox JM. Preventing provider
errors: online total parenteral nutrition calculator. Pediatrics.
2004;113(4):748.
77. Leick-Rude MK, Haney B. Midline catheter use in the intensive care nursery. Neonatal Netw. 2006;25(3):189.
78. Leitch CA, Denne SC. Energy expenditure in the extremely
low-birth weight infant. Clin Perinatol. 2000;27(1):181.
79. Lucas A, Morley R, Cole TJ. Randomised trial of early
diet in preterm babies and later intelligence quotient. BMJ.
1998;317(7171):1481.
80. MacKay M, Anderson C, Boehme S, Cash J, Zobell J. Frequency
and severity of parenteral nutrition medication errors at a large
Children’s hospital after implementation of electronic ordering
and compounding. Nutr Clin Pract. 2016;31(2):195.
81. Matlow AG, Kitai I, Kirpalani H, et al. A randomized trial
of 72- versus 24-hour intravenous tubing set changes in
newborns receiving lipid therapy. Infect Control Hosp Epidemiol.
1999;20(7):487.
82. McKinnon BT. FDA safety alert: hazards of precipitation associated with parenteral nutrition. Nutr Clin Pract. 1996;11(2):59.
83. Mermel LA, Farr BM, Sherertz RJ, et al. Guidelines for the
management of intravascular catheter-related infections. Infect
Control Hosp Epidemiol. 2001;22(3):222.
84. Meyer MP, Haworth C, Meyer JH, et al. A comparison of oral
and intravenous iron supplementation in preterm infants receiving recombinant erythropoietin. J Pediatr. 1996;129(2):258.
85. Mirtallo J, Canada T, Johnson D, et al. Safe practices for parenteral nutrition. JPEN (J Parenter Enteral Nutr). 2004;28(6):S39.
86. Moe-Byrne T, Brown JV, McGuire W. Glutamine supplementation to prevent morbidity and mortality in preterm infants.
Cochrane Database Syst Rev. 2016;4:CD001457.
87. Morgan C. Early amino acid administration in very preterm
infants: too little, too late or too much, too soon? Semin Fetal
Neonatal Med. 2013;18(3):160.
88. Moyses HE, Johnson MJ, Leaf AA, et al. Early parenteral
nutrition and growth outcomes in preterm infants: a systematic
review and meta-analysis. Am J Clin Nutr. 2013;97(4):816.
89. Murai DT. Are femoral Broviac catheters effective and safe? A
prospective comparison of femoral and jugular venous Broviac
catheters in newborn infants. Chest. 2002;121(5):1527.
90. Murphy BP, Inder TE, Huppi PS, et al. Impaired cerebral cortical gray matter growth after treatment with dexamethasone for
neonatal chronic lung disease. Pediatrics. 2001;107(2):217–293.
91. Nedergaard J, Cannon B. Brown adipose tissue: development
and function. In: Polin RA, F ox WW, Abman S, eds. Fetal and
Neonatal Physiology. 5th ed. Philadelphia: Saunders; 2016.
92. Ogilvy-Stuart AL, Beardsall K. Management of hyperglycaemia in the preterm infant. Arch Dis Child Fetal Neonatal Ed.
2010;95(2):F126.
93. Phipps K, Modic A, O’Riordan MA, et al. A randomized trial
of the Vein Viewer versus standard technique for placement of
peripherally inserted central catheters (PICCs) in neonates. J
Perinatol. 2012;32(7):498.
94. Pierro A, Eaton S. Metabolism and nutrition in the surgical
neonate. Semin Pediatr Surg. 2008;17(4):276.
95. Premji S, Fenton T, Sauve R. Does amount of protein in
formula matter for low-birthweight infants? JPEN J Parenter
Enteral Nutr. 2006;30(6):507.
96. Putet G. Lipid metabolism of the micropremie. Clin Perinatol.
2000;27(1):57.
97. Puthoff TD. Enhancing parenteral nutrition therapy for the
neonate. Nutr Clin Pract: Pediatrics Neonates. 2007;22(2):183.
98. Qiao L, Tang Q, Wenying Z, et al. Effects of early parenteral
iron combined erythropoietin in preterm infants: a randomized
controlled trial. Medicine (Baltim). 2017;96(9):e5795.
99. Rangel SJ, Calkins CM, Cowles RA, and the 2011 American
pediatric surgical association outcomes and clinical tr ials
Committee, et al. Parenteral nutrition-associated cholestasis: an
American pediatric surgical association outcomes and clinical trials Committee systematic review. J Pediatr Surg. 2012;47(1):225.
100. Reynolds RM, Bas KD, Thureen PJ. Achieving positive protein
balance in the immediate postoperative period in neonates
undergoing abdominal surgery. J Pediatr. 2008;152(1):63.
101. Roberts SA, Ball RO, Moore AM, et al. The effect of graded
intake of glycly-L-tyrosine on phenylalanine and tyrosine
metabolism in parenterally fed neonates with an estimation of
tyrosine requirement. Pediatr Res. 2001;49(1):111.
102. Rowe MI, Rowe SA. The last fifty years of neonatal surgical
management. Am J Surg. 2000;180(5):345.
103. Rozance PJ, Hay WW Jr. Neonatal hyperglycemia. NeoReviews.
2010;11:e632.
104. Sentipal-Walerius J, Dollberg S, Mimouni F, et al. Effect of
pulsed dexamethasone therapy on tolerance of intravenously
administered lipids in extremely low birth weight infants. J
Pediatr. 1999;134(2):229.
105. Sertic AJ, Connolly BL, Temole Mj, et al. Perforations associated with peripherally inserted central catheters in a neonatal
population. Pediatr Radiol. 2018;48(1):109.
106. Shah PS, Shah VS. Continuous heparin infusion to prevent
thrombosis and catheter occlusion in neonates with peripherally placed percutaneous central venous catheters. Cochrane
Database Syst Rev. 2008;2:CD002772.
Соседние файлы в папке Библиотека им академика М.И. Перельмана