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15 Parenteral Solutions Overview 169
9. Calder PC, Waitzberg DL, Klek S, Martindale RG. Lipids in parenteral nutrition: biological
aspects. J Parenter Enter Nutr. 2020;44:S21–7.
10. Puder M, Valim C, Meisel JA, et al. Parenteral fish oil improves outcomes in patients with
parenteral nutrition-associated liver injury. Ann Surg. 2009;250:395–402. https://doi.org/10.
1097/SLA.0b013e3181b36657.
11. Ganousse-Mazeron S, Lacaille F, Colomb-Jung V, et al. Assessment and outcome
with intestinal failure referred for intestinal transplantation. Clin Nutr. 2015;34:428–35. https://
doi.org/10.1016/j.clnu.2014.04.015.
12. Zaloga GP. Phytosterols, lipid administration, and liver disease during parenteral nutrition. J
Parenter Enter Nutr. 2015;39:39S–60S. https://doi.org/10.1177/0148607115595978.
13. Carter BA, Taylor OA, Prendergast DR, et al. Stigmasterol, a soy lipid-derived phytosterol, is
an antagonist of the bile acid nuclear receptor FXR. Pediatr Res. 2007;62:301. https://doi.org/
10.1203/PDR.0b013e3181256492.
14. Carpentier YA, Dupont IE. Advances in intravenous lipid emulsions. World J Surg. 2000;24:
1493.
15. Kirk C, Haigh L, Thompson NP, et al. The effects of different parenteral nutrition lipid
formulations on clinical and laboratory endpoints in patients receiving home parenteral nutrition: a systematic review. Clin Nutr. 2022;41:80–90. https://doi.org/10.1016/j.clnu.2021.
11.009.
16. Llop-Talaverón JM, Novak A, Negre JMS, et al. Phytosterol determination in lipid emulsions
for parenteral nutrition. Farm Hosp. 2018;42:116–9. https://doi.org/10.7399/fh.10954.
17. Wretlind A. Development of fat emulsions. Nutrition. 1999;15:641–5. https://doi.org/10.1016/
S0899-9007(99)00102-1.
18. Sadu Singh BK, Narayanan SS, Khor BH, et al. Composition and functionality of lipid
emulsions in parenteral nutrition: examining evidence in clinical applications. Front Pharmacol.
2020;11:506. https://doi.org/10.3389/fphar.2020.00506.
19. Iacone R, Scanzano C, Santarpia L, et al. Macronutrients in parenteral nutrition: amino acids.
Nutrients. 2020;12:772. https://doi.org/10.3390/nu12030772.
20. Vilstrup H, Gluud C, Hardt F, et al. Branched chain enriched amino acid versus glucose
treatment of hepatic encephalopathy. J Hepatol. 1990;10:291–6. https://doi.org/10.1016/0168-
8278(90)90135-E.
21. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of
nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine
(SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). J Parenter
Enter Nutr. 2016;40:159–211. https://doi.org/10.1177/0148607115621863.
22. Bischoff SC, Bernal W, Dasarathy S, et al. ESPEN practical guideline: clinical nutrition in liver
disease. Clin Nutr. 2020;39:3533–62. https://doi.org/10.1016/j.clnu.2020.09.001.
23. Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive
care unit. Clin Nutr. 2019;38:48–79. https://doi.org/10.1016/j.clnu.2018.08.037.
24. Compher C, Bingham AL, McCall M, et al. Guidelines for the provision of nutrition support
therapy in the adult critically ill patient: the American Society for Parenteral and Enteral
Nutrition. J Parenter Enter Nutr. 2022;46:12–41. https://doi.org/10.1002/jpen.2267.
25. Weimann A, Braga M, Carli F, et al. ESPEN practical guideline: clinical nutrition in surgery.
Clin Nutr. 2021;40:4745–61. https://doi.org/10.1016/j.clnu.2021.03.031
26.
Berger MM, Shenkin A, Schweinlin A, et al. ESPEN micronutrient guideline. Clin Nutr.
2022;41:1357–424. https://doi.org/10.1016/j.clnu.2022.02.015.
27. Alfonso JE, Berlana D, Ukleja A, Boullata J. Clinical, ergonomic, and economic outcomes with
multichamber bags compared with (hospital) pharmacy compounded bags and multibottle
systems: a systematic literature
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28.
Newton DW,
Pharm. 2008;65:1761–6. https://doi.org/10.2146/ajhp080015.
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30. Ferguson TI, Emery S, Price-Davies R, Cosslett AG. A review of stability issues associated with
vitamins in parenteral nutrition. ESPEN J. 2014;9:e49–53. https://doi.org/10.1016/j.clnme.
2014.01.001.
Chapter 16
Complications Associated with Parenteral
Nutrition
Luca D’Alessandro and Francesco Barbani
Introduction
Parenteral nutrition (PN) is a vital intervention involving the intravenous delivery of
essential nutrients when oral or enteral nutrition (EN) is not feasible or sufficient to
meet a patient’s caloric and protein needs. In the intensive care unit (ICU), PN may
serve as a short-term solution durin g temporary contraindications to EN, such as
acute illness or post-surgery, or as a long-term option for patients with
non-modifiable diseases or intestinal failure [1, 2]. PN solutions typically comprise
macronutrients (e.g., glucose, amino acids, lipids), electrolytes, and micronutrients
(e.g., vitamins, trace elements) and are administered through central vascular access
devices (CVAD) to prevent fluid overload [3–6].
Complications associated with PN can be categorized as follows:
• Metabolic complications
• Hyperglycemia
• Hypertriglyceridemia
• Liver diseases: steatosis, cholestatic disea se, gallbladder stones
• Refeeding syndrome
• Mechanical complications
• Vascular access device (VAD)-related issues
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_16.
L. D’Alessandro (
Ortho-neurological Department, Division of Anesthesia and Intensive Care, Azienda
Ospedaliera di Rilievo Nazionale “Ospedali dei Colli” – Ospedale C.T.O, Naples, Italy
F. Barbani
Department of Anesthesia and Critical Care, University of Florence, Azienda Ospedaliera
Universitaria “Careggi”, Florence, Italy
Author(s), under exclusive license to Springer Nature Switzerland AG 2024
© The
A. Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
https://doi.org/10.1007/978-3-031-66541-7_16
✉)
171
172 L. D’Alessandro and F. Barbani
• Short-term and positioning-related complications: arterial puncture, pleural punc-
ture (pneumothorax, hemothorax)
• Long-term complications: venous thrombosis, VAD tip dislodgement, catheter-
related bloodstream infections (CRBSI)
• Infectious complications
• Catheter-related bloodstream infections (CRBSI)
The incidence of these complications depends on various factors including the
timing of PN initiation, dosage, duration, proper positioning and maintenance of
vascular access devices, and the potential integration with EN [3].
To mitigate potential PN-related complications, it is essential to avoid unnecessary PN or, at the very least, minimize PN dosage and volume [1–3]. The concept of
supplemental parenteral nutrition (SPN), which combines EN and PN to achieve
caloric and protein goals, offers a strategy to reduce PN usage. This approach not
only helps in infection reduction due to the beneficial aspects of EN but also
facilitates the optimal timing for weaning off SPN and transitioning to exclusive
EN, particularly in short-term PN scenarios. Swift discontinuation of PN upon
recovery from intestinal failure can lead to the removal of CVAD, significantly
reducing the risk of time-dependent infectious and mechanical complications [7, 8].
Metabolic Complications
Hyperglycemia
Hyperglycemia during parenteral nutrition (PN) infusion is a common occurrence,
even among noncritically ill patients. In critically ill individuals, hyperglycemia can
be more pronounced, especially during metabolic stress-response states where
insulin resistance makes it challenging to maintain plasma glucose levels within
the optimal range. Factors such as severe infections, a history of diabetes, or
concomitant administration of glucocorticoids further elevate the risk of
hyperglycemia [9]
Over the past decades, numerous randomized control trials (RCTs) have explored
strategies for achieving better glycemic control and improving outcomes in critically
ill patients. Initially, tight glycemic control aiming for levels below 110 mg/dL was
associated with reduced mortality and morbidity. However, subsequent RCTs
yielded inconsistent results, with concerns arising regarding an increased risk of
hypoglycemic events and mortality. Consequently, glycemic control targeting levels
below 180 mg/dL has shown to be more beneficial for critically ill patients, leading
to lower mortality rates and improved outcomes [10–12]. To optimize glycemic
control during PN infusion, initiating PN at a low flow rate is advisable, especially
during the early stages of critical illness when metabolic stress responses are
ongoing. PN administration may also be coupled with insulin infusion, and glucose
levels should be monitored more frequently, particularly during the initial stages of
.
16 Complications Associated with Parenteral Nutrition 173
PN infusion. Although hyperglycemia is more common, hypoglycemia represents a
severe event that can exacerbate morbidity and mortality outcomes. Hypoglycemia
may occur during insulin infusion or when the PN infusion rate is rapidly reduced or
discontinued [
3, 12].
Hypertriglyceridemia
Hypertriglyceridemia is a common complication associated with parenteral nutrition
(PN) administration and may occur due to factors such as glucose overload and
excessive infusion of intravenous fat emulsion (IVFE). It occurs when the amount of
lipids infused exceeds the metabolic capacity for plasma clearance and
metabolization [3, 5].
The recommended dosage of IVFE is typically below 1.5 g/kg/day, considering
additional nutritional sources such as propofol infusion. In critically ill and stressed
patients, metabolic capacity may be compromised, warranting a more conservative
approach with a dosage of 1 g/kg/day, particularly in conditions like shock, sepsis,
multiple organ failure, acute kidney injury, liver failure, hyperglycemia, corticosteroid use, and propofol-based sedation [1, 2]. Monitoring triglyceride levels aims to
maintain plasma concentrations below 500 mg/dL, with adjustments made to the
IVFE infusion amoun t or discontinuation if necessary [13]. To effectively control
plasma lipid concentrations, overfeeding should be avoided and closely monitored.
Evidence suggests that fish oil and medium-chain triglycerides (MCT) may help
reduce the risk of hypertriglyceridemia by accelerating lipid clearance. Additionally,
omega-3 polyunsaturated fatty acids from fish oil, compared to soybean-based lipids
rich in phytosterols, may improve cholestatic liver dysfunction as the latter are
associated with reduced intrahepatic bile flow [14]. If IVFE infusion needs to be
reduced due to hypertriglyceridemia, there is a risk of developing a state of energy
underfeeding, which must be taken into consideration and managed accordingly.
Liver Disease: Steatosis, Cholestatic Disease, and Gallbladder Stones
Liver disease in patients receiving parenteral nutrition (PN) may manifest as
steatosis, cholestatic disease, or gallbladder stones, often accompanied by mildly
elevated liver enzymes. Steatosis typically occurs due to overfeeding, regardless of
the route of infusion (PN and/or EN), with excessively high rates of intravenous fat
emulsion (IVFE) administration leading to fat accumulation in hepatocytes. Cholestasis, characterized by elevated levels of conjugated bilirubin, results from impaired
bile flow due to the absence of enteral nutrition digestion stimuli, which normally
trigger the release of cholecystokinin (CCK) and stimulate gallbladder contraction
174 L. D’Alessandro and F. Barbani
and emptying. Additionally, gallbladder contractility may be depressed, leading to
bile stasis, clotting, and the formation of sludge and stones. The risk and probability
of developing PN-related liver disease increase with the duration of PN administration, with laboratory abnormalities potentially becoming evident within a week of
full PN. Diagnostic criteria are met when at least two of the following tests show
values 1.5 times the upper limit of normal: alkali
transferase, and/or serum direct bilirubin.
The pathophysiology of PN-related
understood. Critically ill patients may have coprecipitating factors exacerbating liver
dysfunction, including sepsis, shock, fluid overload, infections, invasive procedures,
and exposure to potentially hepatotoxic medications. Overfeeding, even through EN,
can lead to steatosis and hepatitis, especially in states of hypoperfusion, which may
cause ischemic hepatitis.
The composition of IVFE may contribute to cholestasis genesis, with soybeanoil-based IVFE rich in omega-6 polyunsaturated fatty acids and phytosterols potentially reducing bile flow and promoting sludge formation. Conversely, fish oil, rich
in omega-3 fatty acids and poor in phytosterols, may reverse cholestatic disease.
Preventing PN-related liver disease involves avoiding energy overfeeding, considering extra-nutritional caloric sources such as lipids from propofol or citrate for
continuous renal replacement therapy. Encouraging low-flow EN, or trophic dose
EN, may stimulate bile flow and clearance, reducing the risk of cholestatic disease.
Overall, efforts to minimize PN administration and promote enteral nutrition tolerance are essent ial for mitigating the risks associated with PN-related liver disease.
liver disease is multifactorial and not fully
ne phosphatase, gamma-glutamyl
Refeeding Syndrome
Refeeding syndrome, marked by metabolic and electrolyte changes along with
corresponding clinical manifestations, occurs shortly after reintroducing or increasing caloric intake post-food restriction [
or oral refeeding [16]. Despite its complexity, refeeding syndrome often goes
undiagnosed, with hypophosphatemia as a main but not sole indicator
[17, 18]. First described during World War II, it results from metabolic adaptation
during prolonged fasting [19, 20].
During fasting, metabolic and hormonal changes allow the body to utilize lipids
and proteins as the main energy source, with a decrease in basal metabolism
[21]. Intracellular ions are reduced despite normal blood levels, explaining their
physiological range maintenance [22].
Refeeding
anabolism, triggered by insulin secretion in response to increased blood glucose
levels during refeeding [23, 24]. This leads to heightened intracellular demands for
phosphate, potassium, and magnesium, causing hypophosphatemia, hypokalemia,
and hypomagnesemia. Additionally, sodium retention and thiamine deficiency contribute to salt and water retention [25,
syndrome’s pathophysiology involves metabolic reactivation towards
15]. It can manifest after parenteral, enteral,
Phosphorus is crucial for intracellular
26].
16 Complications Associated with Parenteral Nutrition 175
processes, cell membrane integrity, ATP storage, and oxygen transport via hemoglobin [25]. Potassium and magnesium, major intracellular cations, play vital roles in
enzymatic systems and membrane potential maintenance [25]. Refeeding-induced
suppression of gluconeogenesis and onset of lipogenesis further affect metabolic
balance [25, 26]. Thiamine deficiency, particularly critical during prolonged fasting,
can lead to various neurological symptoms and cardiovascular complications
25, 2
6]. Clinical manifestations of refeeding syndrome vary widely, ranging from
[
neurological to cardiac, respiratory, gastrointestinal, and muscular symptoms
[25, 26]. Electrolyte imbalances contribute to these manifestations, with hyperglycemia potentially causing hepatic steatosis and respiratory complications
]. Thiamine deficiency manifests primarily through neurological symptoms
[25, 26
such as encephalopathy, neuropathy, dementia, and psychosis, potentially leading to
Wernicke’s syndrome characterized by diplopia, nystagmus, ataxia, and confusion.
Diagnosis may involve MRI highlighting lesions in the medial thalamus and
periaqueductal regions. Thiamine deficiency can also result in Korsakoff syndrome,
presenting as retrograde and anterograde amnesia and confabula
impairs ATP biosynthesis, impacting myocardial contractility and potentially leading to congestive heart failure [
leading to diffuse edema, acute pulmonary edema, and heart failure. Diagnosing
refeeding syndrome is challenging due to its heterogeneous clinical presentation and
lack of specific markers. Identifying high-risk patients is crucial for early intervention. Risk factors include AIDS, chronic alcoholism or drug addiction, advanced
age, dysphagia, eating disorders, psychiatric disorders, uncontrolled diabetes
itus, chronic renal failure, homelessness, abuse, military service, professional
mell
athletics, vomiting, surgical interventions, malabsorption, cancer, neurological conditions, bariatric surgery, fasting, protein malnutrition, and critical care. ASPEN’s
2020 consensus provides criteria for stratifying the risk of refeeding syndrome based
on various parameters, facilitating its identification and management [
high-risk patients are identified, it is crucial to reintroduce food cautiously, gradually
increasing calorie and protein intake to support weight recovery and restore the
functionality of vital organs, musculoskeletal systems, and psycho-behavioral abilities. In conclusion, regular monitoring of vital parameters, laboratory tests, and
clinical evaluation is necessary to prevent and promptly address nutrient imbalances,
thereby mitigating the onse
27–3
0]. Sodium retention can induce fluid overload,
t of clinical manifestations associated with the syndrome.
tion. Moreover, it
15]. Once
Mechanical Complications
Mechanical complications related to vascular access devices (VADs) are common
during parenteral nutrition (PN) infusion, particularlyin the ICU setting [31, 32]. Critical illness often necessitates the placement of central venous access for various
purposes such as antibiotic administration, vasoactive medication infusion, and
hemodynamic monitoring. Given the need for hyperosmotic and concentrated nutritional solutions, central lines are preferred for PN administration, with a multiple
176 L. D’Alessandro and F. Barbani
lumen central venous access device (CVAD) being highly recommend ed. CVADs
are categorized based on duration (short-, mid-, or long-term) and insertion site
(central vs. peripheral) [31, 32
]. Centrally inserted central catheters (CICCs) are
placed in central veins like the internal jugular, subclavian, thoracic axillary, or
common femoral vein. Peripherally inserted central catheters (PICCs) are placed in
the upper arm deep venous system or at the femoral venous axis. Both CICCs and
PICCs can serve as short- or long-term vascular access, with measures taken to
minimize dislodgement and infection risks. CVADs are essential for infusing PN
formulations
with an osmolarity >900 mOsm/L, while peripheral vascul ar access
devices can suffice for PN formulations with osmolarity ranging from
750 to 9 00 mOsm/L [
31]. Peripheral parenteral nutriti on (PPN) formulations contain
fewer osmotically active molecules and require a larger volume of fluids for equivalent macronutrient delivery compared to central PN. Consequently, PPN may pose
a risk of fluid overload, especially in patients requiring fluid restriction. PPN is
typically used to supplement oral or enteral nutrition when a smaller volume is
prescribed. For administering hyperosmolar parenteral formulations (Osmolar
ity
>900 mOsm/L), the use of a central venous access device (CVAD) is necessary to
mitigate thrombosis risk [
31, 3
2]. Short-term complications from CVADs primarily
stem from the insertion procedure itself. The use of ultrasound to identify the optimal
vein for puncture and for guidance during insertion significantly reduces the risk of
mechanical complications such as arterial puncture, pneumothorax, or hemothorax
[33]. Additionally, considering peripherally inserted central catheters (PICCs) can
help mitigate the consequences of arterial puncture at the neck or chest level.
Previously considered to have a higher risk of thrombotic complications, recent
studies reviewed by Balsorano et al. indicate a PICC-related thrombosis incidence of
2.4% (95% CI 1.5 – 3.3), comparable to that of CICCs [
34]. Various insertion
bundles, designed to enhance patient safety, have been described for both CICCs
and PICCs. These bundles typically involve ultrasound-based selection of the
optimal insertion site, which minimizes the risk of pleural puncture and arterial
hematoma formation. PICCs may be preferable for PN infusion, especially when
considering the vessel-to-catheter diameter ratio, which affects the risk of venous
thrombosis [35–37].
Ultrasound-guided
venipuncture with a microintroducer kit improves the first
attempt success rate and reduces vein endothelium trauma and platelet aggregation,
lowering the risk of thrombosis. Intra-procedural systems for tip location, such as
echocardiography with micro-bubble tests or intracavitary ECG, virtually eliminate
the risk of primary malposition during CVAD placement [
35]. Sterile conditions
must be maintained throughout the procedure for both CICCs and PICCs, including
measures for operators, ultrasound probes, and patients [
33, 35, 38].
Catheter lum en
obstruction is another mechanical complication worth noting. If the PN solution is
combined with incompatible medications or salts at critical concentrations, precipitations may occur within the infusion line or catheter lumen. To prevent lumen
occlusion or precipitation infusion in the patient’s venous circulation, it is crucial to
administer PN solutions exclusively in dedicated lines or lumens. If the nutritional
16 Complications Associated with Parenteral Nutrition 177
solution infusion is paused, the lumen should be flushed with 20 mL of NaCl 0.9%
and then locked [32, 34, 35].
Infectious Complications
Catheter-related bloodstream infection (CRBSI) poses a significant risk to patients
with either centrally or peripherally inserted vascular access devices (VADs), potentially leading to sepsis or septic shock with high mortality rates [32, 33]. Given that
many critically ill patients require a CVAD for various indications such as hemodynamic monitoring and drug infusions, CRBSIs can occur with varying incidence
rates across all types of VADs. Microorganisms, predominantly fungi and bacteria,
can contaminate a catheter following colonization of an infusion solution, infusion
line, or catheter port through contact. Therefore, it is crucial for all VAD management operators to undergo training and adhere to evidence-based guidelines to
minimize infection risks [33, 38].
through the insertion site on the skin. Utilizing preliminary echographic assessment
to identify the optimal site helps reduce infective complications by selecting an exit
site with the lowest skin microbial load, such as the upper arm (suitable for PICCs)
and the chest (suitable for axillary vein CICCs) [39]. In cases where an optimal veinto-catheter diameter ratio is lacking, inserting the catheter into a more proximal and
larger vein and then placing the exit site at the most suitable location through
tunneling is advisable. This practice effectively reduces the risk of infections by
moving the exit site away from the catheter’s entrance into the vessel [40]. During
catheter insertion, strict adherence to evidence-based prevention bundles is essential.
This includes using a checklist to enhance adherence to hygiene protocols,
employing ultrasound to assess the best insertion and exit sites and guide VAD
insertion, utilizing antiseptic barrier caps and needleless secure devices, opting for
catheters with the lowest lumen number as per therapy requirements, and considering the use of antiseptic or antibiotic-impregnated catheters for patients at higher risk
of CRBSI or those who are extremely frail and vulnerable [32, 33, 38].
patients who no longer require VADs, including for PN, as early as possible is the
most effective strategy for minimizing the risk of CRBSI.
Another
route for catheter-related infections is
ifying
Ident
Conclusions
In conclusion, the management of refeeding syndrome and the administration of
parenteral nutrition require careful consideration of metabolic, electrolyte, and
mechanical complications to ensure patient safety and optimal outcomes. Refeeding
syndrome presen ts a complex array of metabolic and electrolyte changes, often with
heterogeneous clinical manifestations, necessitating early identification of high-risk
patients for prompt intervention. Understanding the pathophysiology of refeeding
178 L. D’Alessandro and F. Barbani
syndrome, including metabolic reactivation and electrolyte shifts, is essential for
effective prevention and treatment strategies. Mechanical complications associated
with vascular access devices for parenteral nutrition administration highlight the
importance of proper insertion techniques, device selection, and infection prevention
measures. Strategies such as ultrasound guidance, adherence to sterile procedures,
and dedicated line usage help miti
gate the risk of catheter-related bloodstream
infections and other mechanical issues. Furthermore, addressing patient-specific
factors and comorbidities, along with adherence to evidence-based guidelines, is
paramount in minimizing complications associated with parenteral nutrition and
vascular access devices. Collaborative efforts among healthcare providers, ongoing
training, and adherence to best practices are essential components of ensuring patie
safety and reducing adverse outcomes in the management of refeeding syndrome
and parenteral nutrition administration.
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