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Diet and Nutrition in Orthopedics
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2. Diet and Nutrition in Orthopedics
Sotiria Everetta
, Rupali Joshib
, Libi Galmera
, Marci Goolsbya
and Joseph Lanea
*
a
Dietary Service Metabolic Bone Disease Service, Hospital for Special Surgery, New York, NY, USA
b
Physical Therapy Department Metabolic Bone Disease Service, Hospital for Special Surgery, New York, NY, USA
Abstract
Nutritious diet and a balanced lifestyle are important to maintain good health. Nutritional status
becomes even more important in individuals undergoing small surgical procedures or major
surgeries. In individuals undergoing surgeries, nutritional status is an essential determinant of
bone health. Despite considerable evidence on significance of nutrition, there exists a substantial
percentage of who are malnourished patients with orthopedic diseases and those undergoing
orthopedic surgery (Koval et al. 1999; Patterson et al., J Bone Joint Surg Am. 74:251–60, 1992).
Moreover, nutritional status and malnutrition incidences may not be recognized by healthcare
practitioners. Therefore it is critical that a detailed nutritional assessment be conducted at baseline
on all patients undergoing surgery to identify individuals who are at risk or are currently malnour-
ished in order to achieve successful surgical outcomes and enhance patient care.
Abbreviations
A/P Anterior/posterior
AI Adequate intake
AN Anorexia nervosa
ASBMR American Society for Bone and Mineral Research
BMC Body mass composition or bone mineral concentration
BMD Bone mineral density
BMI Body mass index
CDC Center for Disease Control and Prevention
FAT Female athlete triad
FHA Functional hypothalamic amenorrhea
FRAX Refers to the World Health Organization Fracture Risk Assessment Tool
GALT Gut-associated lymphoid tissue
GERD Gastroesophageal reflux disease
GI Gastrointestinal
IGF-1 Insulin-like growth factor 1
IOM Institute of Medicine
IU International units
KCAL Kilocalories
KG Kilograms
L Liter
LH Luteinizing hormone
*Email: Lanej@hss.edu
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3. MALT Mucosa-associated lymphoid tissue
MG Milligrams
NGT Nasogastric tube
NOF National Osteoporosis Foundation
NRS Nutritional risk screening
NTX Cross-linked N-telopeptide
OC Osteocalcin
ONS Oral nutritional supplements
OZ Ounce
PEG Percutaneous endoscopic gastrostomy
PICP Procollagen type 1 C-terminal propeptide
PPI Proton pump inhibitor
PTH Parathyroid hormone
PUD Peptic ulcer disease
RD Registered dietitians
RDA Recommended daily allowance
SGA Subjective global assessment
T3 Triiodothyronine
THR Total hip replacement
TKR Total knee replacement
TPN Total parenteral nutrition
UL Upper limit
VDR Vitamin D receptor
Introduction
Nutritional status of the orthopedic patient is an important determinant of bone health, treatment of
orthopedic and metabolic bone diseases, and successful orthopedic surgical outcomes. Several
studies have indicated considerable rates of malnutrition in patients with orthopedic diseases and
those undergoing orthopedic surgery (Patterson et al. 1992). Furthermore, nutritional status and
malnutrition occurrences may not be recognized by healthcare practitioners (National Institute of
Health 2012).
Although malnutrition can be seen in any age group, the risk is greater in populations older than
65 years, and in the orthopedic setting, those patients with hip fractures are particularly prone to
detrimental outcomes secondary to poor nutritional status (Symeonidis and Clark 2006). The
literature indicates that 20–60 % of patients admitted with hip fractures are malnourished, described
as protein depletion (low albumin, prealbumin, total lymphocyte count), anthropometric indicators
(body weight, triceps skinfolds, arm circumference measures, and/or body mass index), and
preoperative poor nutrient intake (Patterson et al. 1992; Ozkalkanli et al. 2009). In patients with
hip fractures, malnutrition has been shown to be both a cause and a major determinant of outcome
following injury (Avenell and Handoll 2010). Poor preoperative nutritional status delays wound
healing, increases risk of surgical site infections and development of pressure ulcers and thrombosis,
and increases postoperative mortality (Symeonidis and Clark 2006; Ozkalkanli et al. 2009). Fur-
thermore, postoperative complications resulting from poor nutritional status prolong hospital stay
and rehabilitation time, increase hospital costs, and can be overwhelming for patients and their
families (Symeonidis and Clark 2006).
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4. Malnutrition may also occur postoperatively in hospitalized patients, leading to similarly
unwanted surgical outcomes. The body’s catabolic response to surgery coupled with the perioper-
ative fasting regimen may exacerbate the occurrence of suboptimal nutrient intake, further
compromising the nutrition status of such patients.
There are numerous factors that contribute to poor nutrition in orthopedic patients. These factors
may serve as predictors of surgical outcomes, in addition to playing a role in the development of
diseases such as arthritis and osteoporosis, and orthopedic trauma. Meeting the nutritional needs of
these patients can help avoid the consequences of malnutrition leading to poor surgical outcomes.
We will address these factors and examine interventions to prevent and manage malnutrition in
orthopedic patients. Additionally, we will address micronutrient recommendations that should be
considered during the care of orthopedic patients in the nonsurgical setting.
Important Micronutrients for Orthopedic Patients
Vitamin D
Mechanisms and Effects on Bone
Regulation of calcium homeostasis and bone metabolism occurs through the action of vitamin D on
its target tissues including the intestine, kidneys, and bone (DeLuca 2004). Vitamin D can act at
genomic and non-genomic levels. Genomic effects occur via binding of 1,25(OH)2D to its nuclear
receptor, which leads to alteration in gene transcription of messenger RNA and consequent protein
synthesis (Geusens et al. 1997). Most recently, vitamin D receptor (VDR) polymorphisms have been
found to play a role in osteoporosis (Kelly et al. 1997) and muscle function (Geusens et al. 1997).
Non-genomic effects of vitamin D occur as a result of membrane-bound VDR (Norman et al. 1992).
Vitamin D production in the skin depends on various factors such as age, latitude, time of day, season
of the year, and pigmentation. A person older than 70 years produces less than 30 % of the amount of
vitamin D when exposed to the same amount of sunlight as compared to a young adult (Holick
1999).
It is evident that vitamin D plays a fundamental role in bone metabolism (Need 2006). Deficiency
of vitamin D can therefore impair bone metabolism, thus affecting fracture healing. Vitamin
D deficiency has been observed in hip fracture patients, as well as pediatric patients undergoing
orthopedic surgery (Unnanuntana et al. 2013). Poor vitamin D status has been linked to cases of
fracture nonunions, stress fractures, Blount’s disease, and slipped femoral epiphysis (McCabe
et al. 2012). Diamond et al. reported that the prevalence of vitamin D deficiency (<20 ng/mL)
and hypogonadism (serum free testosterone, 11 pg/mL) was higher among men over 60 years of age
who sustained osteoporotic hip fractures as compared to their age-matched controls (Diamond
et al. 1998). Brinkler et al. studied 37 cases of nonunions and documented that 84 % of these
patients were found to have metabolic or endocrine abnormalities. Bony union occurred in 8 of these
84 % patients by medical management alone (Brinker et al. 2007). Consequently it is important to
screen for metabolic or endocrine abnormalities in all patients with impaired fracture healing.
Several studies in community-dwelling older adults have also reported a direct link between
vitamin D status and physical performance. Multiple investigators have found that vitamin D levels
<20 ng/mL result in increased risk of physical performance decline over three years compared to
those with vitamin D levels 30 ng/mL (Wicherts et al. 2007). The National Institutes of Health
considers 20 ng/mL or more to be adequate for bone and overall health in healthy individuals. The
Institute of Medicine (IOM) has released a document stating that 20 ng/mL of vitamin D level is
“generally considered adequate for bone and overall health in healthy individuals.” Low vitamin
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5. D levels (10 ng/mL) have been linked to a higher risk of repeated falling (Snijder et al. 2006;
LeBoff et al. 2008; Suzuki et al. 2008). Furthermore vitamin D 46 ng/mL results in superior
physical performance as compared to levels 32 ng/mL (Dam et al. 2009), and levels between
20 and 30 ng/mL are considered to be insufficient. This is consistent with the 2013 guidelines
published by the National Osteoporosis Foundation, which state that vitamin D level should be at
least 30 ng/mL (Cosman et al. 2013). Hence, many clinicians now recommend vitamin D levels
higher than 35 ng/mL for optimal bone health (Binkley et al. 2011).
Vitamin D3 (Sato et al. 2006) or vitamin D2 supplementation along with calcium is more effective
in preventing falls as compared to calcium alone. Evidence suggests that vitamin D3 (derived from
animal source) supplemented at 1,600 IU daily or 50,000 IU monthly is slightly, but significantly,
more effective than D2 (derived from vegetable source) for increasing vitamin D levels (Binkley
et al. 2011).
Vitamin D Metabolism and Toxicity
Vitamin D is initially generated in the skin from nonenzymatic conversion of provitamin D3. Dietary
intake of vitamin D is usually relatively limited, since few foods with the exception of some types of
fish, contain sizable amounts. It is common practice, therefore, to use supplements to treat vitamin
D deficiency. Vitamin D is either stored in adipose tissue or converted in the liver to
25-hydroxyvitamin D3, the form that circulates in highest concentrations and reflects solar and
dietary exposure. It is converted to the active metabolite 1,25-dihydroxyvitamin D, or calcitriol, in
the kidney, although other tissues can also activate provitamin D3. The synthesis of calcitriol is
enhanced by increasing levels of parathyroid hormone (PTH), which rise in response to lower levels
of serum calcium. Reduced levels of serum phosphate can also increase the production of calcitriol
(Bischoff et al. 2003). Toxicity from vitamin D supplementation is extremely rare and consists
principally of acute hypercalcemia, which results from doses that exceed 10,000 IU per day;
associated serum levels of 25-hydroxyvitamin D are well above 150 ng/mL (Jones 2008). The
tolerable upper level of daily vitamin D intake recently set by the Institute of Medicine (IOM) is
4,000 IU However, patients with malabsorption syndromes may require higher doses of vitamin
D (4,000 IU/day). The long-term effects of supplementation at doses above 4,000 IU per day are
not known. Recent observational studies have suggested associations between serum levels of
25-hydroxyvitamin D above 60 ng/mL and increased risk of pancreatic cancer, vascular calcifica-
tion, and death, but the observational nature of these studies precludes an assessment of cause and
effect (Stolzenberg-Solomon et al. 2010). Table 1 provides recommended daily values and food
sources for vitamin D.
Table 1 Vitamin D recommendations
AI
(ug/day)
UL
(ug/day) Sources
Children and adults
31–50 years
5 25 (0–12
months)
Fish liver oils, flesh of fatty fish, liver and fat from seals and polar bears,
eggs from hens that have been fed vitamin D, fortified milk products, and
fortified cereals
50 1 year
50–70 years 10–30 50 “
70 years 15–30 50 “
Source: Institute of Medicine (IOM) Dietary Reference Intakes (DRIs) 2010, Cosman National Osteoporosis
Foundation (NOF) Clinician’s Guide 2013
Pregnancy and lactation: AI, 5 ug/day; UL, 50 ug/day
AI adequate intake, UL upper limit
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6. Calcium
Calcium and vitamin D influence bone health and insufficient intake and levels of these
micronutrients are linked to osteoporosis and bone fractures (Nurmi-Luthje et al. 2009). All
orthopedic patients should be screened for vitamin D deficiency and appropriate supplementation
should be initiated. Calcium and vitamin D supplementation has been indicated in elderly patients
with hip fractures to reduce postoperative complications and minimize bone loss (Nurmi-Luthje
et al. 2009; Lanham-New 2008). In patients with profound vitamin D deficiency (20 ng/mL),
vitamin D should be prescribed and corrected prior to surgery. Vitamin D3 of up to 4,000 IU should
be prescribed daily and reevaluation of vitamin D levels should be assessed in 2–4 weeks (Table 4).
For calcium deficiencies, supplementation of calcium citrate is recommended and goal supplemental
calcium amount should lead to target PTH level of 50–20 pg/mL (Fig. 1). Low calcium intake is
associated with increased osteoporosis and fracture risk (Chapuy et al. 1992). Current recommended
dietary allowances for calcium are indicated in Table 2 and recommended sources of dietary calcium
in Table 3. Research suggests that calcium ingested in dietary form along with carbohydrates, lipids,
and other nutrients present in food enhances calcium absorption; therefore dietary calcium is
preferred over supplemental calcium (Emkey and Emkey 2012). Exact mechanisms of enhanced
calcium absorption in dietary form are not clear; however dietary fats and carbohydrates coingested
with dairy may increase intestinal transit time and intracellular absorption. Low-fat diets may
decrease serum estradiol concentrations in women, reducing calcium absorption and in turn bone
health.
Many factors (disease states, medications, etc.) influence intestinal absorption, and supplemental
calcium may be recommended if calcium requirements are not met. Conditions such as celiac
disease and lactose intolerance may interfere with the ability to meet the calcium recommendations.
Chronic glucocorticoid treatment, proton pump inhibitors, hyperthyroidism, malabsorptive bariatric
surgery, cigarette smoking, and chronic alcoholism inhibit calcium absorption. Aging can also lead
Fig. 1 *Values based on corrected calcium (mg/dL) = measured total Ca (mg/dL) +0.8 (4.0–serum albumin [g/dL]).
**Supplementation for decreased intake based on 2013 National Osteoporosis Foundation Guidelines (Cosman
et al. 2013) and decreased absorption and increased excretion based on expert opinion Joseph Lane, MD
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7. Table 2 Calcium recommendations
AI
(mg/day) UL (mg/day) Sources
0–6 months 210 – Milk, cheese, yogurt, corn tortillas, calcium-set tofu, Chinese
cabbage, kale, broccoli
7–12 months 270 – “
1–3 years 500 1,500–2,500 (for all
ages)
“
4–8 years 800 1,500–2,500 “
9–18 years 1,300 1,500–2,500 “
19–50 years 1,000 1,500–2,500 “
50–70 years;
70 years
1,200 1,500–2,500 “
Source: Institute of Medicine (IOM) Dietary Reference Intakes (DRIs) 2010, Cosman National Osteoporosis
Foundation Clinician’s Guidelines 2013
Pregnancy and lactation: AI: /= 18 years, 1,300 mg/day; 19–50 years, 1,000 mg/day; UL, 2,500 mg/day
AI adequate intake, UL upper limit
Table 3 Common food sources of calcium
Food Portion Calcium (mg)
Cereal, calcium fortified ½ cup 200–670
Cheese, American 1 oz 160
Cheese: cheddar, mozzarella, muenster 1 oz 300
Cheese: provolone, jack, Swiss 1 oz 205
Fish, salmon canned with bones 3 oz 180
Greens, collards ½ cup 135
Kale, raw 1 cup 90
Milk, fat-free 1 cup 305
Milk, reduced fat 1 cup 285
Milk, whole 1 cup 275
Orange juice, calcium fortified ½ cup 175–200
Soy milk or rice milk, calcium fortified 1 cup 300–370
Spinach ½ cup 135
Tofu, fortified with calcium sulfate or lactate ¼ cup 215
Yogurt, fruit or plain 8 oz 275–450
Source: US Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard
Reference
mg milligrams, oz ounce
Table 4 Vitamin D replacement schedulea
Vitamin D level (ng/mL) Weeks 1–2 Weeks 2–4 Maintenance Recheck labs
20 4,000 IU/day 4,000 IU/day 2,000 IU/day 4 weeks
20–30 4,000 IU/day 2,000 IU/day 2,000 IU/day 6 weeks
30–40 2,000 IU/day 2,000 IU/day 2,000 IU/day 3 months
40 No supplement needed
a
Source: Expert opinion Joseph Lane, MD
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8. to a decline in small intestinal absorption of calcium. If adequate dietary calcium intake is not
possible, supplemental calcium is recommended. Numerous forms of supplemental calcium are
available; however, calcium citrate is the preferred source of calcium supplementation. Calcium
citrate is better absorbed and is associated with fewer side effects related to calcium supplementation
use (i.e., constipation, gastrointestinal distress). The effect of calcium supplementation on bone
health is best observed when calcium is combined with vitamin D and when plasma concentrations
of calcium increases, suppressing plasma PTH and renal production of 1,25(OH)2D3. Low levels of
serum PTH and 1,25(OH)2D3 reduce stimulus for osteoclastic bone resorption (Need 2006). The
dose-absorption saturation point of calcium is approximately 500 mg; therefore 500 mg doses
ingested every 6–8 h until recommended total daily intake is achieved are recommended. Goal
supplemental calcium amount should lead to target PTH level of 50–20 pg/mL. Due to recent data
that may suggest a link between supplemental calcium and heart disease (Bolland et al. 2010), the
PTH window should be slightly wider than previously recommended. Patients who have resistance
to calcium absorption or intolerance to supplementation may require additional supplementation
with 1,25-OH vitamin D to increase gastrointestinal efficiency.
Proton pump inhibitors (PPIs) and histamine2-receptor (HR2) antagonists are acid-suppressive
medications widely used for the management of acid-related diseases such as gastroesophageal
reflux disease (GERD) and peptic ulcer disease (PUD). PPIs were introduced more recently and have
a longer and more potent action than HR2 antagonists; however both medications are among the
most commonly prescribed in the world. Recent concerns have been raised about the long-term
safety and adverse affects of these drugs, particularly the association identified with increased
fracture risk. Recent meta-analyses revealed an increased risk of fractures with PPIs but not with
HR2 antagonists (Yu et al. 2011). These studies observed that PPIs modestly increased the risk of
hip, spine, and any-site fractures. The exact mechanism for this increased risk is unknown and has
not been proven. Studies have pointed to potential mechanisms, such as PPI-induced hypergas-
trinemia and inhibition of calcium absorption. PPIs increase serum gastrin by inhibiting acid
secretions, which stimulates parathyroid glands and increases PTH levels, inducing excessive
bone remodeling (Yang 2012). This may contribute to increased bone loss of calcium, making
patients on PPIs prone to fractures. Some studies have found decreased serum calcium levels,
suggesting PPIs may impair calcium absorption from meals and supplements; however further
investigation of this relationship is necessary (Yang 2012). Due to the concern related to PPIs and
fracture risk, practitioners should only prescribe these medications for appropriate indications and
they should frequently revisit the need and duration of PPI therapy.
Calcium supplements have recently been linked to an increased risk of myocardial infarction
(Bolland et al. 2010). It should however be noted that the dietary calcium is not associated with
increased risk of heart disease. The exact mechanism is unclear, but it may be due to the calcium
peaks, which occur with supplements, and the more gradual rise in serum calcium levels that occur
with dietary sources. A literature review revealed that calcium supplementation was associated with
a 30 % increased risk in myocardial infarction (Bolland et al. 2010). Possible explanations for this
increased risk include an increased serum calcium level, calcium vascularization, and primary
hyperparathyroidism although further research must be done. Given the widespread use of calcium
supplements, healthcare providers must evaluate patients’ intake of calcium from diet and supple-
ments in order to avoid excess consumption and higher cardiovascular risk.
Foods and beverages that contain tannins (tea, coffee), oxalates (spinach, rhubarb, beet greens),
and phytate (pinto and navy beans, peas, wheat bran) form insoluble complexes with calcium and
interfere with intestinal absorption of calcium (Emkey and Emkey 2012). Although foods such as
beans and leafy greens contain abundant amount of calcium, the availability of calcium from these
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9. foods is largely reduced due to their content of oxalates and phytates. The interference of calcium
absorption of these foods only involves the calcium absorption of the same food but will not affect
calcium absorption in other foods consumed at the same time, for instance, spinach consumed with
milk. Fiber intake can impact calcium absorption when fiber significantly exceeds calcium intake
(Emkey and Emkey 2012). Additionally, high intake of sodium and caffeine intake may also
interfere with the body’s ability to absorb calcium (Emkey and Emkey 2012). Nutrients that increase
calcium absorption include vitamin D, lactose, and prebiotics/probiotics (Emkey and Emkey 2012).
High Sodium and protein intake can lead to excessive calcium loss from the Kidney (Bihuniak
et al. 2013).
Vitamin K
Vitamin K is a fat-soluble vitamin that functions as a coagulation factor and, for the skeleton, acts as
a cofactor in carboxylation of osteocalcin. Low vitamin K contributes to under-carboxylated
osteocalcin, leading to low bone mass density. Vitamin K refers to a family of compounds with a
common chemical structure. Phylloquinone (vitamin K1) is present in plant foods. Menaquinones
(vitamin K2) are the bacterial form of vitamin K. Phylloquinones are present in abundant amounts in
plant-based foods, such as leafy greens and cruciferous vegetables, and in smaller amounts in fish,
meat, eggs, and cereals. The role of vitamin K in the prevention and treatment of osteoporosis
requires more research; however studies indicate vitamin K supplementation, in combination with
calcium and vitamin D supplementation, increases BMD and bone mineral content (Lanham-New
2008). In a study of postmenopausal women, supplementation of vitamin K1 with vitamin D,
calcium, magnesium, and zinc resulted in significant reduction in femoral neck bone loss compared
with placebo (Lanham-New 2008). A recent meta-analysis shows a beneficial effect of pharmaco-
logic dose of vitamin K2 on reducing vertebral and hip fractures (Lanham-New 2008). Patients at
risk for low vitamin K levels, whether by disease, diet, or drugs, may benefit from supplementation.
Vitamin C
Vitamin C is a powerful antioxidant that studies suggest may have positive effects on bone health.
Vitamin C deficiency is known to cause scurvy and also to contribute to osteoporosis and fragility
fractures. The Framingham Osteoporosis Study showed a 40 % decrease in hip fracture among those
who took 250–500 mg of vitamin C per day from diet and supplements (Sahni et al. 2009). The exact
mechanism in which vitamin C contributes to a lower fracture risk is unknown. Antioxidant
properties of vitamin C and its effect in decreasing oxidative damage may be protective against
decreases in bone mass, as oxidation can increase bone resorption. Additionally, collagen is the
primary protein of bone matrix and vitamin C is also involved in the hydroxylation of lysine, the
critical first step for collagen biosynthesis (Munday 2003).
Therefore, vitamin C is essential in strengthening bone structure and preventing fractures. Patients
with low bone mineral density should be encouraged to consume fruit and vegetables that are high in
vitamin C. Patients with joint hypermobility may also benefit from higher vitamin C intake from diet
and supplementation. Adequate intake of vitamin C for adults 19 years and older is 75 mg/day for
women and 90 mg/day for men. Vitamin C deficiency is seen in patients whose plasma level of
vitamin C is less than 11.4 mmol/L (Johnston and Thompson 1998).
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10. Applications to Critical or Intensive Care
The importance of maintaining adequate nutritional status of the orthopedic patient in the critical
care setting is crucial for patients with serious orthopedic injuries and those requiring complex
orthopedic surgeries. Failure to recognize patients’ degree of malnutrition in the critical care setting
may significantly impair rehabilitation and add to the morbidity and mortality risk. Hip fracture,
multi-trauma, and complex spinal surgery patients are the most frequent type of patients requiring
critical care in an orthopedic surgical setting.
Nutritional status of critical care patients can be evaluated using a variety of methods, including
laboratory data, anthropometric data, patient demographics, and medical history. A thorough nutri-
tional screening and/or assessment should be conducted at baseline on all patients undergoing
orthopedic surgery to identify patients who are malnourished or at risk for malnutrition. Examples
of nutritional screening tools validated for use in hospitalized patients include the Nutritional Risk
Screening 2002 (NRS 2002) and the Subjective Global Assessment (SGA) (Kondrup et al. 2013).
These screening tools identify at-risk patients by assessing anthropometric measurements (low BMI,
significant weight loss, muscle wasting), reduced dietary intake, and presence of severe illness
(Ozkalkanli et al. 2009). For accuracy of anthropometric assessments, self-reported heights and
weights should be avoided; precise measurements should be obtained by trained healthcare pro-
fessionals. Classification of BMI is a useful indication of nutrition status; however this measurement
should be interpreted with caution and within the context of the individual patient’s condition.
Edema, high muscle mass, short stature, and ethnicity are some conditions which may skew how
BMI values are classified. Nonetheless, BMI is a useful component of nutritional screening tools for
orthopedic patients.
Nutritional screenings and assessments should be conducted before planned orthopedic interven-
tions to ensure sufficient recovery and prevention of the stated postoperative complications.
Indicators of malnutrition include underweight status (BMI 18.5), depleted albumin levels
(3.4 mg/dL), depleted prealbumin stores (15 mg/dL), and significant weight loss in 6 months
(10 % unintentional weight loss in a 6-month period). When these malnutrition indicators are
identified, a nutrition intervention should be initiated. Nutrition interventions in nonemergency
situations may include prescription for oral supplements until goal weight and serum protein
markers are met.
Perioperative Nutrition Care Planning
In determining the nutrition intervention strategy for orthopedic patients, provision of energy and
protein should be individualized and determined by comprehensive nutrition assessments conducted
by the healthcare team. In the critical care setting, efforts should be made quickly to assess the
nutritional status of orthopedic patients, and nutritional interventions should begin early to minimize
postoperative complications. The elements of a nutrition intervention program are often conducted
by a registered dietitian and include:
1. Assessment of the patient’s status and needs
2. Calculation of macro- and micronutrient requirements (i.e., calorie, protein, lipid, fluid, vitamin,
mineral, and electrolyte requirements)
3. Prescription and initiation of the nutrition plan (i.e., oral nutritional supplements, enteral nutri-
tional support, parenteral nutritional support)
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11. 4. Careful monitoring of clinical status, biochemical status, and patient’s compliance and tolerance
to nutrition plan
5. Accurate documentation of plan and monitoring
Typical energy requirements for orthopedic patients range from 25 to 35 kcal/kg/day and protein
requirements range from 1.2 to 2.0 g/kg/day; however these values vary based on patients’ weight
status, surgery, and health history. Nutrition therapy for the orthopedic patient consists of early
postoperative feedings by means of oral diets (with or without the use of oral nutritional supple-
ments), enteral nutrition support via tube feedings (nasogastric or orogastric), gastrostomy or
jejunostomy feedings, or parenteral routes. Micronutrient supplementation in the form of vitamins,
minerals, and specific amino acids indicated for wound healing may also be required for nutrition
therapy of the critically ill orthopedic patient. Additionally, fluid status should be optimized.
Nutritional treatments will be discussed in details below. Registered dietitians (RDs) have the
necessary skills for determining nutrition status and nutrient requirements and can assist in the
selection, administration, and monitoring of appropriate nutrition support.
Oral Nutritional Supplements
Oral nutritional supplements (ONS) are commonly used in the preoperative or perioperative period
to meet nutrient needs of patients. The use of ONS in elderly patients is often indicated to achieve
favorable outcomes in hip fractures (Volkert et al. 2006). ONS are recommended in elderly patients
after hip fracture and orthopedic surgery to minimize complications and reduce risk of pressure ulcer
development (Volkert et al. 2006). ONS are also indicated in patients who are well nourished if it is
anticipated that nutritional intake will be suboptimal during the perioperative period. Most ortho-
pedic patients face periods of fasting and liquid diets; therefore ONS has a role in supplementing
nutrient intake to minimize nutrient depletion while oral intake is suspended (due to NPO status) or
insufficient (during liquid diet phases).
ONS have been shown to increase perioperative nutrient intake and promote wound healing and
favorable postoperative outcomes in hip fracture patients, trauma patients, and spine surgery patients
(Avenell and Handoll 2010. Several studies indicate that the use of ONS in elderly patients with hip
fractures may lead to increased nutrient intake, reduced proximal femur bone loss, enhanced
recovery of plasma proteins, and shorter rehabilitation hospital stays (Avenell and Handoll 2010;
Foss et al. 2007). It is important to note that several servings of ONS may be required daily to meet
the nutrient needs of orthopedic patients and to be effective in achieving the desired outcomes.
Nutrition Support Therapy
Enteral Nutrition Support
Enteral nutrition support or tube feeding is a means of providing nutrients to patients who are unable
to consume sufficient nutrients orally. Among orthopedic patients, this may include patients who
present with dysphagia (preexisting dysphagia or dysphagia that has occurred postoperatively),
malnourished patients, trauma patients with elevated metabolic demands, patients with dementia,
patients suspected to require prolonged intubation periods, and patients who have surgeries that
interfere with eating. Perioperative complications and dementia have been shown to contribute to
low nutrient intake in hip fracture patients (Foss et al. 2007); therefore these conditions may
predispose patients to require intensive nutrition regimens, such as ONS, enteral tube feeding, or
parenteral nutrition. Enteral nutrition therapy in elderly hip fracture patients has been shown to
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12. increase plasma protein stores and improve mobility and anthropometric parameters after surgery
(Volkert et al. 2006).
Further research on the use of enteral feeding in orthopedic surgical patients is required to
establish guidelines in this setting; however the use of tube feeding has been shown to improve
outcomes in patients who are critically ill. Enteral nutrition support should be initiated early, even in
patients who are not considered severely malnourished, if it is anticipated that patients will not be
able to eat for a for more than 7 days perioperatively (Weimann et al. 2006). Patients with severe
trauma, those who are malnourished, and those with anticipated inadequate oral intake (60 % of
estimated needs) for more than 10 days may benefit from early enteral nutrition support to minimize
postoperative complications (Weimann et al. 2006).
Enteral nutrition is the preferred method over parenteral nutrition for critically ill patients who
require nutrition support therapy. Enteral nutrition can help maintain integrity of gut-associated
lymphoid tissue (GALT) and mucosa-associated lymphoid tissue (MALT) (Kang and Kudsk 2007).
When compared to parenteral nutrition, enteral nutrition has been associated with lower incidence of
infection and reduced costs in critically ill patients (McClave et al. 2009). Enteral nutrition support
should not be used, however, in patients with a nonfunctioning gut, intestinal obstructions, severe
ileus, severe shock, and intestinal ischemia (Weimann et al. 2006) or patients with terminal illnesses
who decline nutrition support (Volkert et al. 2006).
Enteral feeding route is determined by duration of nutrition support therapy and available access.
Percutaneous endoscopic gastrostomy (PEG) feedings are preferred over nasogastric tube (NGT)
feedings for long-term (4 week) nutrition support (Weimann et al. 2006). Nasogastric tubes should
be placed postpylorically in critically ill patients or patients with high aspiration risk. Head of bed
should be elevated for critically ill patients to minimize aspiration risk and feedings should be
initiated at low rates and gradually increased to goal. Precautions such as monitoring for aspiration
and feeding intolerance and administering feeds at appropriate rates should be carried out to ensure
safety.
Parenteral Nutrition Support
The administration of total parenteral nutrition (TPN) has been studied as a means to mitigate
nutrient depletion in orthopedic patients, particularly in patients undergoing spinal surgery
(Lapp et al. 2001). Spine surgery patients are prone to protein and calorie malnutrition due to
prolonged delays in postoperative diet progression and inability to tolerate oral and/or enteral intake
after surgery. Although total parenteral nutrition has historically been used to optimize nutrition
status in patients undergoing complex spine surgery, use of this modality should be restricted due to
the inherent risks associated with feeding via central venous access. The benefits of enteral nutrition
support over the use of parenteral nutrition support are well documented (McClave et al. 2009).
Several studies suggest reductions in infectious morbidity, length of hospital stay, and cost of
nutrition therapy with regard to enteral nutrition compared to parenteral nutrition (McClave
et al. 2009). In the event that enteral nutrition is not feasible, parenteral nutrition should be initiated
in patients who have been unable to receive adequate nutrition at least 5–7 days postoperatively.
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13. Applications to Other Conditions
Underweight Status
Low Body Mass Index
Orthopedic patients who present with low body weight and low body mass index are at increased
risk of developing osteoporosis and fragility fractures (Kanis et al. 2005). According to the FRAX
index (fracture risk assessment tool), a low BMI is a risk factor for bone fracture, and a BMI less than
19 is a strong risk factor for fracture (Kroger 2013). Patients that are determined to have a BMI
below 18.5 are considered underweight and face increased risk for decreased bone mineralization
and bone fractures (Kanis et al. 2005). A higher weight and increased muscle and fat mass may be
protective against bone loss and fracture. Weight loss and low body weight may indicate reduction in
lean muscle and fat mass, in addition to conditions (illness, infection, etc.) that may influence
osteoporosis and fracture risk. If surgery is indicated for fracture repair, those patients who are found
to be underweight on admission have higher mortality, incidences of delayed healing, decreased
mobility and recovery, and decreased physical function (Gumieiro et al. 2013).
Low Body Weight and the Female Athlete Triad
The female athlete triad refers to the interrelationship between energy availability, menstrual
function, and bone health (Nattiv et al. 2007). It is estimated that between 15 % and 62 % of the
female athletic population exhibit eating disorders and between 3 % and 66 % (Otis 1992) have
menstrual irregularities. Reproductive abnormalities such as delayed menarche and/or secondary
amenorrhea are highly prevalent in female athletes (O’Donnell and De Souza 2004), dancers
(Warren et al. 2002), and patients with anorexia nervosa (Roze et al. 2007). The female athlete
triad is more commonly seen in endurance and aesthetic sports (Nattiv et al. 2007), termed leanness
sports (Sherman and Thompson 2004), and thus, a heightened awareness should be present with
these athletes. The main treatment for the female athlete triad is nutrition counseling and education
on the consequences of continued low energy availability. Accurate diagnosis and appropriate
treatment require a team approach and may involve physicians, dietitians, and mental health
professionals who will work with the athlete, athletic trainer, coaches, parents, and teammates.
Screening for components of the female athlete triad should be done as part of the annual
pre-participation examination. Identification of one component or risk factor should trigger further
evaluation for the other components (Nattiv et al. 2007). Depending on the number and severity of
issues identified, the athlete may need to be restricted from participation. In this situation, it is critical
that a team of providers decide together on the best plan for treatment, which may include visits with
nutrition and mental health practitioners. A contract should be used to ensure patient compliance
with the treatment plans and goals before she is allowed to return to participation. The best treatment
is prevention and can be achieved by providing education about the female athlete triad to the
athletes and those involved in their care and encouraging safe, healthy athletic participation with
healthy nutrition and body image practices.
Relationship Between Disordered Eating, Reproductive Abnormalities, and Bone
An association between eating disorders and reproductive abnormalities specifically
oligomenorrhea and amenorrhea has been well established. Low energy availability, which is an
imbalance of dietary calorie intake compared to exercise energy expenditure, may be inadvertent,
intentional, or even pathologic as is seen in eating disorders. This low energy availability disrupts the
normal hypothalamic-pituitary-gonadal axis function, which leads to menstrual irregularities and
negative effects on bone health (Ihle and Loucks 2004). Absence of menses caused by this
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14. disruption of hormonal function is known as functional hypothalamic amenorrhea (FHA). These
energy deficient conditions both in the long term (Williams et al. 2001) and short term (Loucks
et al. 2006) have been reported to affect reproductive function. Reproductive function is mediated
through luteinizing hormone (LH) pulsatility, and energy availability is crucial to its proper function
in the adolescent population (Loucks et al. 2006). This pulsatility is disrupted only below a threshold
of energy availability (30 kcal kg Lean Body Mass ( 1) day ( 1)) (Loucks and Thuma 2003).
Several studies have investigated athletes, patients with anorexia nervosa, and ballet dancers and
reported a link between disordered eating, menstrual irregularities, and stress fractures (Kaga
et al. 2004). It is estimated that between 15 % and 62 % (Kiernan et al. 1992) of the female athletic
population exhibit eating disorders and around 3–66 % (Otis 1992) have menstrual irregularities.
Athletes with later age of menarche and decreased menses per year have lower bone mineral density
and more stress fractures (Drinkwater 1990). In particular, runners with a history of oligomenorrhea
were six times more likely to sustain a stress fracture in a retrospective study (Myburgh et al. 1990).
A relationship between menstrual abnormalities such as amenorrhea and oligomenorrhea and bone
mineral density (BMD) has been identified (Cobb et al. 2003), and this relationship is independent of
body weight and composition. In ballet dancers, osteopenia has been correlated with amenorrhea
and poor nutritional habits (Kaufman et al. 2002). It has been documented that female dancers and
professional ballerinas consumed below 70 % and 80 % (20–30 % food restriction), respectively, of
the recommended daily allowance (RDA) of energy intake to meet body weight targets (Koutedakis
and Jamurtas 2004). Furthermore, it has also been confirmed that menarche occurred at a later age in
ballet dancers as compared to non-dancers without having any effect on height or weight (Warren
1980). Energy deficiency results in hypothalamic suppression that can then affect the reproductive
axis and bone health (Zanker and Swaine 1998).
A study that recently modeled female athlete triad in animals reported severely low energy levels,
anestrous, and significant decreases in body weight, body mass composition (BMC), estrogen, and
leptin levels (Dimarco et al. 2007). Animal model of delayed puberty reported decreased serum
estradiol levels along with decreased cortical thickness and a decreased trabecular number and an
increase in trabecular separation and lower bone strength (Yingling and Khaneja 2006).
Anorexia nervosa is an eating disorder characterized by low body weight (least 15 % of
predictable body weight) and low bone mass (bone density between 1 and 2.5 SD below the
young adult mean) (defined low body weight and low bone mass) (Misra and Klibanski 2006).
Moreover, menstrual irregularities, such as delayed menarche, are a critical factor in predicting low
bone mass in this population and are seen in 35 % of patients with AN (Misra et al. 2004).
Studies have demonstrated low bone formation markers in adolescents with AN that may lead to
osteopenia (Soyka et al. 2002), but in spite of the fact that 83 % of anorexics partially recover, only
33 % actually recover weight and menstrual regularity (Herzog et al. 1999).
There exists a dose-response relationship between energy availability and hormones like cross-
linked N-telopeptide of type I collagen (NTx) and estradiol, for procollagen type 1 C-terminal
propeptide (PICP) and insulin, and for osteocalcin (OC), triiodothyronine (T3), and insulin-like
growth factor (IGF)-1 (Loucks and Thuma 2003). Furthermore, Loucks and Ihle et al. showed that
low energy availability results in uncoupling of bone resorption, and formation in that bone
resorption is affected before formation in regularly menstruating, habitually sedentary, young
women of normal body composition.
Delayed Puberty and Catch-Up Growth
It is critical to prevent bone loss resulting from disordered eating and/or reproductive abnormalities
during adolescence as it may have effects on bone health in adulthood. There exists a correlation
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15. between bone mineral density and body mass index along with age of onset and duration of anorexia
(Bachrach et al. 1990). Skeletal maturation was compensated by an increase in height velocity
towards the end of puberty in elite female rhythmic gymnasts aged 12–23 years (Georgopoulos
et al. 2001). However, data from athletes and ballet dancers suggest that bone mass cannot be
regained after delayed puberty and amenorrhea during young adulthood (Warren et al. 2002),
thereby suggesting that there is a permanent lack of catch-up growth in these women.
Overweight and Obese Status
Obesity is a global health concern and orthopedic patients who are overweight or obese are more
likely to experience osteoarthritis and other musculoskeletal ailments. Overweight and obese adults
are more likely to experience joint pain and back pain and have more difficult rehabilitation courses.
Obesity is also gaining prevalence in pediatric populations. Obesity influences the skeletal structure
in developing children and adolescence. The orthopedic effect of obesity in pediatric populations is
seen in the incidences of Blount’s disease and slipped capped femoral epiphysiodesis, and increased
BMI is associated with higher risk of lower extremity fractures in children (Kessler et al. 2013).
Orthopedic injury and osteoarthritis are more prevalent in obese patients than nonobese patients.
With respect to orthopedic injuries, proximal humerus fractures and low-energy knee dislocations
are more frequently observed in obese patients compared to nonobese patients (Prieto-Alhambra
et al. 2012; Georgiadis et al. 2013). Additionally, vascular injuries are commonly associated in knee
dislocations in obese patients (Georgiadis et al. 2013), further complicating treatment of the
dislocation. Osteoarthritis is a major comorbidity in obese patients and there is a direct relationship
between obesity and risk of total knee replacement (Samson et al. 2010). Higher BMI levels are also
associated with total hip replacement (THR), although there is a weaker relationship than total knee
replacement (TKR) (Franklin et al. 2009). In orthopedic surgical patients, there is an increased risk
of infection, developing wound complications, and thrombotic events in obese patients.
Diabetes
The presence of diabetes may lead to unique challenges in managing orthopedic patients in the
surgical setting. It is well known that poor glycemic control has been associated with several
perioperative complications that contribute to increased morbidity and mortality. Orthopedic surgi-
cal patients with uncontrolled diabetes mellitus may be at a significant increased risk of developing a
cerebrovascular event, ileus, wound infection, increased length of stay, and death, in both type I and
type II diabetes (Kerkhoffs et al. 2012; Marchant et al. 2009). The exact relationship between
glycemic control and perioperative outcomes in not clearly understood. However, it is well know
that elevated blood sugar concentration can acutely influence the body’s ability to heal wounds and
maintain optimal physiological stability. Diabetes also contributes to the risk of femoral neck
fractures since insulin resistance affects bone strength and integrity (Ishii et al. 2012).
Evaluation of orthopedic patients should include diabetes evaluation and screening when surgery
is planned. This includes obtaining blood glucose levels and hemoglobin A1c levels during
presurgical screening. In patients with preexisting diabetes, a thorough assessment of glycemic
control and self-management should be done. In patients with a hemoglobin A1C level greater than
10 %, orthopedic surgery should be postponed if possible, until improved glycemic control and
hemoglobin A1C levels are achieved. A target hemoglobin A1C level of 8 % should be achieved
before a planned elective surgery for optimal postoperative outcomes (Umpierrez et al. 2012).
Perioperative management of diabetes in orthopedic patients should include the glycemic target
levels of a premeal glucose level of 140 mg/dL and a random glucose level of 180 mg/dL;
however these glycemic targets should be modified according to patients’ clinical status (Umpierrez
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16. et al. 2012). Medical nutrition therapy, including providing patients with a consistent amount of
carbohydrates at each meal, and administering coordinated doses of rapid-acting insulin to carbo-
hydrate ingestion should be a component of inpatient management.
Guidelines and Protocols
I. Obtain a thorough history paying particular attention to:
• Past medical history including GI or rheumatologic conditions
• Asthma or other chronic corticosteroid exposure
• Gastric bypass surgery and lactose and gluten sensitivity
• Smoking and alcohol use
• Eating disorders and delayed or irregular menses in women
II. Physical exam: Look for signs of collagen disorder or hypermobility
• Short 5th digit or 5th digit extension beyond 90
• Bunions or flat feet
• Easily able to touch toes with knees extended
III. Laboratory assessment
• Comprehensive metabolic panel (including serum calcium and albumin)
• Metabolic bone labs: iPTH, bone-specific alkaline phosphatase, urine NTX (goal 35)
• Vitamin D level
• Sprue panel if gluten intolerance is suspected
IV. Nutritional assessment
• Dietary habits and caloric intake
• BMI
• Activity level and energy expenditure
V. Treatment
• Replace micro- or macronutrient deficiencies
– Calcium if PTH less than 20 pg/mL (Fig. 1)
– Vitamin D (Table 4)
– Vitamin C: 500–1,000 mg daily, in patients with osteoporosis, history of fragility fractures,
and particularly in those with signs of hypermobility
• Psychosocial support
• Pharmacological treatment if when indicated
Summary Points
• Healthcare providers should assess the nutritional status of all orthopedic patients, including an
evaluation of anthropometric measures, nutrition-related laboratory markers, and medical history.
• Inadequate intake of vitamin D, calcium, and vitamin C is associated with poor bone quality,
decreased bone healing, and osteoporosis.
• Low serum calcium can be due to decreased intake or increased excretion. Evaluation and
appropriate correction of the cause can lead to improved calcium levels.
• PTH level (goal 20–50) should be used as a marker of adequate calcium intake.
• Orthopedic patients identified with malnutrition or at risk for malnutrition should have a treatment
plan implemented early to minimize postoperative complications.
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17. • Patients undergoing elective surgery who present with malnutrition should have their surgery
postponed until nutritional status is improved when possible.
• In critical care settings, nutrition support may be required to improve nutritional status of patients.
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