Right 2 Flashcards

(96 cards)

1
Q

The average energy intake is

A

~2600 kcal/d for American
men and ~1800 kcal/d for American women, though these estimates
vary with body size and activity level.

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2
Q

Formulas for roughly estimating
REE are useful in assessing the energy needs of an individual whose
weight is stable. Thus,

A

for males, REE = 900 + 10m, and for females,

REE = 700 + 7m, where is m mass in kilograms

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3
Q

The calculated REE

is then adjusted for physical activity level by multiplying by

A

1.2 for

sedentary, 1.4 for moderately active, or 1.8 for very active individuals.

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4
Q

The nine essential

amino acids are

A

histidine, isoleucine, leucine, lysine, methionine/

cystine, phenylalanine/tyrosine, threonine, tryptophan, and valine

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5
Q

For adults, the recommended dietary allowance (RDA) for protein

A

is ~0.6 g/kg desirable body mass per day, assuming that energy needs
are met and that the protein is of relatively high biologic value. Current
recommendations for a healthy diet call for at least 10–14% of calories
from protein

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6
Q

Fats are a concentrated source of energy and
constitute, on average, 34% of calories in U.S. diets. However, for
optimal health, fat intake should total

A

no more than 30% of calories.
Saturated fat and trans fat should be limited to <10% of calories and
polyunsaturated fats to <10% of calories, with monounsaturated fats
accounting for the remainder of fat intake

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7
Q

least 45–55% of total

calories should be derived from carbohydrates. The brain requires

A

~100 g of glucose per day for fuel; other tissues use about 50 g/d. Some
tissues (e.g., brain and red blood cells) rely on glucose supplied either
exogenously or from muscle proteolysis. Over time, adaptations in
carbohydrate needs are possible during hypocaloric states. Like fat
(9 kcal/g), carbohydrate (4 kcal/g), and protein (4 kcal/g), alcohol
(ethanol) provides energy (7 kcal/g)

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8
Q

For adults, 1–1.5 mL of water per kilocalorie of energy expenditure
is sufficient under usual conditions to allow for normal variations
in physical activity, sweating, and solute load of the diet.

A

Water
losses include 50–100 mL/d in the feces; 500–1000 mL/d by evaporation
or exhalation; and, depending on the renal solute load, ≥1000
mL/d in the urine. I

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9
Q

Fever increases water losses by

~200 mL/d per °C; diarrheal losses vary but may be as great as

A

5 L/d

in severe diarrhea.

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10
Q

When renal function is normal and solute
intakes are adequate, the kidneys can adjust to increased water intake
by excreting up to

A

18 L of excess water per day

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11
Q

Increased water needs during pregnancy are ~30 mL/d.

A

During lactation, milk production increases daily water requirements
so that ~1000 mL of additional water is needed, or 1 mL for each milliliter
of milk produced

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12
Q

benchmark recommendations regarding

nutrient intakes have been developed to guide clinical practice.

A

These
quantitative estimates of nutrient intakes are collectively referred to
as the dietary reference intakes (DRIs

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13
Q

Thiamine deficiency is therefore

more common in cultures that rely heavily on a

A

rice-based diet.
Tea, coffee (regular and decaffeinated), raw fish, and shellfish contain
thiaminases, which can destroy the vitamin

drinking large
amounts of tea or coffee can theoretically lower thiamine body stores.

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14
Q

In Western countries, the primary causes of

thiamine deficiency are alcoholism and chronic illnesses such as cancer.

A

Alcohol interferes directly with the absorption of thiamine and
with the synthesis of thiamine pyrophosphate, and it increases urinary
excretion. Thiamine should always be replenished when a patient with
alcoholism is being refed, as carbohydrate repletion without adequate
thiamine can precipitate acute thiamine deficiency with lactic acidosis

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15
Q

Wet beriberi presents primarily
with cardiovascular symptoms that are due to impaired myocardial
energy metabolism and dysautonomia

A

; it can occur after 3 months
of a thiamine-deficient diet. Patients present with an enlarged heart,
tachycardia, high-output congestive heart failure, peripheral edema

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16
Q

dry beriberi present with a symmetric
peripheral neuropathy of the motor and sensory systems, with
diminished reflexes.

A

The neuropathy affects the legs most markedly,

and patients have difficulty rising from a squatting position

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17
Q

Alcoholic patients with chronic thiamine deficiency also may have
central nervous system (CNS) manifestations known as

A

Wernicke’s
encephalopathy, which consists of horizontal nystagmus, ophthalmoplegia
(due to weakness of one or more extraocular muscles),
cerebellar ataxia, and mental impairment (Chap. 467). When there
is an additional loss of memory and a confabulatory psychosis, the
syndrome is known as Wernicke-Korsakoff syndrome. Despite the
typical clinical picture and history, Wernicke-Korsakoff syndrome is
underdiagnosed.

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18
Q

The laboratory diagnosis of thiamine deficiency usually is made by
a functional enzymatic assay of transketolase activity measured before
and after the addition of thiamine pyrophosphate.

A

A >25% stimulation
in response to the addition of thiamine pyrophosphate (i.e., an activity
coefficient of 1.25) is interpreted as abnormal.

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19
Q

In acute thiamine deficiency with either cardiovascular or neurologic signs,

A

200 mg of thiamine three times daily should be given intravenously
until there is no further improvement in acute symptoms;
oral thiamine (10 mg/d) should subsequently be given until recovery
is complete.

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20
Q

niacin refers to nicotinic acid and nicotinamide and their
biologically active derivatives. Nicotinic acid and nicotinamide serve
as precursors of two coenzymes,

A

nicotinamide adenine dinucleotide
(NAD) and NAD phosphate (NADP), which are important in numerous
oxidation and reduction reactions in the body.

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21
Q

Niacin deficiency causes

A

pellagra, which is found
mostly among people eating corn-based diets in parts of China,
Africa, and India.

Pellagra in North America is found mainly
among alcoholics; among patients with congenital defects of intestinal
and kidney absorption of tryptophan (Hartnup disease

Bright red glossitis then ensues and is
followed by a characteristic skin rash that is pigmented and scaling,
particularly in skin areas exposed to sunlight. This rash is known as
Casal’s necklace because it forms a ring around the neck

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22
Q

The primary
manifestations of this syndrome are sometimes referred to as “the
four D’s”:

A

dermatitis, diarrhea, and dementia leading to death.

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23
Q

Treatment of pellagra consists of oral supplementation with

A

100– 200 mg of nicotinamide or nicotinic acid three times daily for 5 days.
High doses of nicotinic acid (2 g/d in a time-release form) are used
for the treatment of elevated cholesterol and triglyceride levels and/
or low high-density lipoprotein cholesterol levels

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24
Q

is also important for connective tissue
metabolism and cross-linking (proline hydroxylation), and it is a component
of many drug-metabolizing enzyme systems, particularly the
mixed-function oxidase systems.

A

Vitamin C

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25
Administration of vitamin C (200 mg/d) improves the symptoms | of scurvy within several days.
High-dose vitamin C supplementation (e.g., 1–2 g/d) may slightly decrease the symptoms and duration of upper respiratory tract infections.
26
Vitamin C supplementation has also | been reported to be useful in
Chédiak-Higashi syndrome (Chap. 80) | and osteogenesis imperfecta
27
Taking g of vitamin C in a single dose may result in abdominal pain, diarrhea, and nausea. Since vitamin C may be metabolized to oxalate, it is feared that chronic high-dose vitamin C supplementation could result in an increased prevalence of kidney stones. However, except in patients with preexisting renal disease, this association has not been borne out in several trials
>2
28
is a water-soluble vitamin that plays a role in gene expression, gluconeogenesis, and fatty acid synthesis and serves as a CO2 carrier on the surface of both cytosolic and mitochondrial carboxylase enzymes.
Biotin
29
is believed to have caused the “burning feet syndrome” seen in prisoners of war during World War II.
Pantothenic acid deficiency
30
is a precursor for acetylcholine, phospholipids, and betaine. Choline is necessary for the structural integrity of cell membranes, cholinergic neurotransmission, lipid and cholesterol metabolism, methyl-group metabolism, and transmembrane signaling
Choline
31
Retinaldehyde (11-cis) is the essential form of vitamin A that is required for normal vision, whereas
retinoic acid is necessary for normal morphogenesis, | growth, and cell differentiation.
32
is the most prevalent carotenoid | with provitamin A activity in the food supply
β-Carotene
33
VIt A deficiency This condition includes milder stages of night blindness and conjunctival xerosis (dryness) with Bitot’s spots (white patches of keratinized epithelium appearing on the sclera) as well as rare, potentially blinding corneal ulceration and necrosis.
Keratomalacia (softening of the cornea) leads | to corneal scarring
34
Any stage of xerophthalmia should be treated with
60 mg (or RAE) of vitamin A in oily solution, usually contained in a soft-gel capsule. The same dose is repeated 1 and 14 days later. Doses should be reduced by half for patients 6–11 months of age. Mothers with night blindness or Bitot’s spots should be given vitamin A orally–either 3 mg daily or 7.5 mg twice a week for 3 months
35
Infants 6–11 months of age should | receive 30 mg vitamin A;
children 12–59 months of age, 60 mg. For reasons that are not clear, vitamin A supplementation has not proven useful in high-risk settings for preventing morbidity or death among infants 1–5 months of age.
36
vit a toxicity
``` Acute toxicity is manifested by increased intracranial pressure, vertigo, diplopia, bulging fontanels (in children), seizures, and exfoliative dermatitis ```
37
represents the classic disease of vitamin D deficiency. Signs of deficiency are muscle soreness, weakness, and bone pain. Some of these effects are independent of calcium intake.
Rickets
38
There are two natural forms of vitamin K:
vitamin K1, also known as phylloquinone, from vegetable and animal sources, and vitamin K2, or menaquinone, which is synthesized by bacterial flora and found in hepatic tissue. Phylloquinone can be converted to menaquinone in some organs.
39
Vitamin K is required for the posttranslational carboxylation of glutamic acid,
which is necessary for calcium binding to γ-carboxylated proteins such as prothrombin (factor II); factors VII, IX, and X; protein C; protein S; and proteins found in bone (osteocalcin) and vascular smooth muscle (e.g., matrix Gla protein).
40
Vitamin K is found in
green leafy vegetables such as kale and spinach, and appreciable amounts are also present in margarine and liver. Vitamin K is present in vegetable oils; olive, canola, and soybean oils are particularly rich sources
41
The symptoms of vitamin K deficiency are due to hemorrhage;
newborns are particularly susceptible because of low fat stores, low breast milk levels of vitamin K, relative sterility of the infantile intestinal tract, liver immaturity, and poor placental transport. Intracranial bleeding as well as gastrointestinal and skin bleeding can occur in vitamin K–deficient infants 1–7 days after birth. Thus, vitamin K (0.5–1 mg IM) is given prophylactically at delivery.
42
Vitamin K deficiency
is treated with a parenteral dose of 10 mg. For patients with chronic malabsorption, 1–2 mg/d should be given orally or 1–2 mg per week can be taken parenterally
43
is an integral component of many metalloenzymes in the body; it is involved in the synthesis and stabilization of proteins, DNA, and RNA and plays a structural role in ribosomes and membranes
Zinc
44
mild chronic zinc deficiency can cause stunted growth in children, decreased taste sensation (hypogeusia), and impaired immune function. Severe chronic zinc deficiency has been described as a cause of hypogonadism and dwarfism in several Middle Eastern countries. In these children, hypopigmented hair is also part of the syndrome.
Acrodermatitis enteropathica is a rare autosomal recessive disorder characterized by abnormalities in zinc absorption.
45
Zinc (20 mg/d until recovery) may be an effective adjunctive
therapeutic strategy for diarrheal disease and pneumonia in children ≥ 6 months of age.
46
is an X-linked metabolic disturbance of copper metabolism characterized by mental retardation, hypocupremia, and decreased circulating ceruloplasmin
Menkes kinky hair syndrome
47
The diagnosis of is usually based on low serum levels of copper (<65 μg/dL) and low ceruloplasmin levels (<20 mg/ dL).
copper deficiency
48
Serum levels of copper may be elevated
in pregnancy or stress conditions since ceruloplasmin is an acute-phase reactant and 90% of circulating copper is bound to ceruloplasmin.
49
is an endemic cardiomyopathy found in children and young women residing in regions of China where dietary intake of selenium is low (<20 μg/d).
Keshan disease
50
Malnutrition can arise from primary or secondary causes, resulting in the former case from inadequate or poor-quality food intake and in the latter case from
diseases that alter food intake or nutrient | requirements, metabolism, or absorption.
51
Primary malnutrition occurs mainly in developing countries and under conditions of political unrest, war, or famine.
Secondary malnutrition, the main form encountered in industrialized countries, was largely unrecognized until the early 1970s, when it was appreciated that persons with adequate food supplies can become malnourished as a result of acute or chronic diseases that alter nutrient intake or metabolism, particularly diseases that cause acute or chronic inflammation
52
Marasmus is the end result of | a long-term deficit of dietary energy, whereas kwashiorkor
has been | understood to result from a protein-poor diet
53
is a state in which virtually all available body fat stores have been exhausted due to starvation without systemic inflammation
Marasmus (starvation–related malnutrition)
54
is a state that involves substantial loss of lean body mass | in the presence of chronic systemic inflammation
Cachexia (chronic disease–related | malnutrition)
55
Acute ↓ energy and protein intake with substantial systemic inflammation
Kwashiorkor (Acute Disease– or Injury– Related Malnutrition)
56
kwashiorkor
The major sine qua non is severe reduction of levels of serum proteins such as albumin (<2.8 g/dL) and transferrin (<150 mg/dL) or of iron-binding capacity (<200 μg/dL). Cellular immune function is depressed, as reflected by lymphopenia (<1500 lymphocytes/μL in adults and older children) and lack of response to skin test antigens (anergy
57
After ~10 days of total starvation, an unstressed individual loses about 12–18 g of protein per day (equivalent to ~60 g of muscle tissue or ~2–3 g of nitrogen). I
In contrast, in injury and sepsis, protein breakdown accelerates in proportion to the degree of stress, reaching 30–60 g/d after elective surgery, 60–90 g/d with infection, 100–130 g/d with severe sepsis or skeletal trauma, and >175 g/d with major burns or head injuries
58
is the only fuel that can be utilized by hypoxemic tissues (anaerobic glycolysis), white blood cells, and newly generated fibroblasts.
Glucose
59
remains prevalent, causing | goiter, hypothyroidism, and cretinism.
Iodine deficiency
60
is endemic in many populations, producing growth retardation, hypogonadism, and dermatoses and impairing wound healing
Zinc deficiency
61
Nutritional Deficiency: The High-Risk Patient
Underweight (body mass index <18.5) and/or recent loss of ≥10% of usual body mass Poor intake: anorexia, food avoidance (e.g., psychiatric condition), or NPOa status for more than ~5 days Protracted nutrient losses: malabsorption, enteric fistulas, draining abscesses or wounds, renal dialysis Hypermetabolic states: sepsis, protracted fever, extensive trauma or burns Alcohol abuse or use of drugs with antinutrient or catabolic properties: glucocorticoids, antimetabolites (e.g., methotrexate), immunosuppressants, antitumor agents Impoverishment, isolation, advanced age
62
BMI values <18.5 are | considered underweight;
<17, significantly underweight; and <16, severely wasted. Values of 18.5–24.9 are normal; 25–29.9, overweight; and ≥30, obese.
63
The triceps is a convenient site that is generally | representative of the body’s overall fat level.
A thickness <3 mm | suggests virtually complete exhaustion of fat stores
64
(the half-life of serum albumin is
~21 days, whereas those of prealbumin and retinol-binding protein are ~2 days and ~12 h, respectively), some of these proteins
65
Multiplying by 1.1–1.4 yields a range 10–40% above basal that estimates the 24-h energy expenditure of the majority of patients.
The lower value (1.1) is used for patients without | evidence of significant physiologic stress; the higher value (1.4) is
66
can also be useful in patients who have difficulty weaning from a ventilator and whose energy needs therefore should not be exceeded to avoid excessive CO2 production. Patients at the extremes of weight (e.g., obese persons) and/or age are good candidates as well, because the Harris-Benedict equations were developed from measurements in adults with roughly normal body weights
Indirect calorimetry
67
2.8–3.5 g/dL: Protein depletion or systemic inflammation
<2.8 g/dL: Possible acute malnutrition or severe | inflammation
68
Body Mass Index (BMI), Muscle Mass, and Protein Energy Malnutrition (PEM)
``` >30 Normal Obese 25–29.9 Normal Overweight 20–24.9 Normal Normal >18.5 Decreased PEM despite adequate or excessive adipose tissue store >18.5 Decreased Moderate PEM <16 Decreased Severe PEM <13 Decreased Lethal in men <11 Decreased Lethal in women ```
69
is the provision of liquid formula meals through a tube | placed into the gut.
Enteral SNS
70
is the direct infusion of complete mixtures of crystalline amino acids, dextrose, triglyceride emulsions, and micronutrients into the bloodstream through a central venous catheter or (rarely in adults) via a peripheral vein.
Parenteral SNS
71
The chief disadvantage of tube feeding in acute illness is | intolerance due to gastric retention, risk of vomiting, or diarrhea.
The presence of severe coagulopathy is a relative contraindication to the insertion of a feeding tube. In adults, parenteral nutrition (PN) almost always requires aseptic insertion of a central venous catheter with a dedicated port.
72
A previously well-nourished person can tolerate whereas the degree of tolerance to prolonged starvation is much less in patients whose skeletal muscle mass is already reduced, whether from PEM, from the muscle atrophy of old age (sarcopenia), or from muscle atrophy due to neuromuscular disease.
~7 days of starvation without harm, even in the | presence of a moderate systemic response to inflammation (SRI),
73
In general, unintentional weight loss of >10% during the previous 6 months or a weight-to-height ratio that is <90% of standard, when associated with physiologic impairment, crudely predicts that the patient has moderate PEM.
Weight loss | >20% of usual or <80% of standard makes severe PEM more likely
74
is a negative acute-phase protein and hence a | marker of the SRI.
Serum albumin
75
A major disadvantage of enteral SNS is that the amounts of protein and calories provided to critically ill patients commonly fail to reach target goals within the first
7–14 days after SNS is initiated. This problem is compounded by the lack of enteral products that allow the provision of the recommended protein target of 1.5–2.0 g/kg without simultaneously inducing potentially harmful caloric overfeeding.
76
The bowel and its associated digestive organs derivesecretion of gastrointestinal hormones that stimulate gut trophic activity
70% of their required nutrients directly from nutritional substrates absorbed from the intestinal lumen. Enteral feeding also supports gut function by stimulating splanchnic blood flow, neuronal activity, IgA antibody release, and
77
In renal disease, except for brief periods, protein intakes should approach the required level for normal adults of at least
0.8 g/kg and should aim for 1.2 g/kg as long as severe azotemia does not occur Patients with severe renal failure who require SNS need concurrent renal replacement therapy.
78
In hepatic failure, protein intakes of
1.2–1.4 g/kg (up to 1.5 g/kg) should be provided as long as encephalopathy due to protein intolerance does not occur. In the presence of protein intolerance, formulas containing 33–50% branched-chain amino acids are available and can be provided at the 1.2- to 1.4-g/kg level
79
Cardiac patients and many other severely stressed patients often benefit from fluid and sodium restriction
to 1000 mL of PN formula and | 5–20 meq of sodium per day.
80
Normal adults require
~30 mL of fluid/kg of body weight from all sources each day as well as the replacement of abnormal losses such as those caused by diuretic therapy, nasogastric tube drainage, wound output, high rates of perspiration (which can be several liters per day during periods of extreme heat), and diarrhea/ostomy losses.
81
Fluid restriction may be necessary in | patients with fluid overload.
Total fluid input can usually be limited to 1200 mL/d as long as urine is the only significant source of fluid output. In severe fluid overload, a 1-L central vein PN solution of 7% crystalline amino acids (70 g) and 21% dextrose (210 g) can temporarily provide an acceptable amount of glucose and protein substrate in the absence of significant catabolic stress
82
For normally nourished, | healthy individuals, the total energy expenditure is
~30–35 kcal/kg.
83
Critical illness increases resting energy expenditure, but this increase is significant only in initially well-nourished individuals with a robust SRI who experience, for example, severe multiple trauma, extensive burns, sepsis, sustained high fever, or closed head injury. In these situations, total energy expenditure can reach
40–45 kcal/kg
84
The chronically starved patient with adapted PEM has a reduced energy expenditure and is inactive, with a usual total energy expenditure of
~20–25 kcal/kg.
85
SNS is at least as effective as 100% for the first
10 days of critical illness, actual measurement of energy expenditure generally is not necessary in the early period of SNS
86
Insulin resistance due to the SRI is associated with
increased gluconeogenesis and reduced peripheral glucose utilization, with resulting hyperglycemia. Hyperglycemia is aggravated by excessive exogenous carbohydrate administration from SNS.
87
Hypocaloric nutrition, with provision of
~1000 kcal and 70 g protein per day for up to 10 days, requires less fluid and reduces the likelihood of poor glycemic control, although a higher protein intake would be optimal. During the second week of SNS, energy and protein provision can be advanced to 20–25 kcal/kg and 1.5 g/kg per day, respectively, as metabolic conditions permit
88
The daily protein recommendation for healthy adults is
0.8 g/kg, but body proteins are replenished faster with 1.5 g/kg in patients with PEM, and net protein catabolism is reduced in critically ill patients when 1.5–2.0 g/kg is provided.
89
In patients who are not critically ill but who require SNS in the acute-care setting, at least
1 g of protein/ kg is recommended, and larger amounts up to 1.5 g/kg are appropriate when volume, renal, and hepatic tolerances allow.
90
Iron is a highly reactive catalyst of oxidative reactions and thus is not included in PN mixtures. The parenteral iron requirement is normally
only ~1 mg/d.
91
Peripheral PN may be enhanced by
small amounts of heparin (1000 U/L) and co-infusion with parenteral fat to reduce osmolarity, but volume constraints still limit the value of this therapy, especially in critical illness
92
The subclavian approach is best tolerated by the patient and is the easiest to dress.
The jugular approach is less likely to cause a pneumothorax. Femoral vein catheterization is strongly discouraged because of the risk of catheter infection
93
to the daily parenteral formula for hospitalized patients with temporary catheters reduces the risk of fibrin sheath formation and catheter infection.
The addition of 6000 U of heparin
94
The most common problems caused by parenteral SNS | are fluid overload and hyperglycemia (Table 98e-7).
Hypertonic dextrose stimulates a much higher insulin level than meal feeding. Because insulin is a potent antinatriuretic and antidiuretic hormone hyperinsulinemia leads to sodium and fluid retention
95
Infections of the central access catheter rarely occur in the
first 72 h. Fever during this period is usually attributable to infection elsewhere or another cause. Fever that develops during parenteral SNS can be addressed by checking the catheter site and, if the site looks clean, exchanging the catheter over a wire, with cultures taken through the catheter and at the catheter tip
96
If cultures are positive for more pathogenic bacteria or for fungi like Candida albicans, it is generally best to replace the catheter at a new site.
Whether antibiotic treatment is required is a clinical decision, but C. albicans grown from the blood culture in a patient receiving PN should always be treated with an antifungal drug because the consequences of failure to treat can be dire.