Introduction to Surgical Principles

Condition

kcal/kg/day

Adjustment above baseline energy expenditure

Grams of protein/kg/day

Normal

Mild stress

25–30

1.2

Moderate stress

1.4

1.5

Severe stress

30–35

1.6

Burns

35–40

2.5

The goal for nutritional support in a surgical patient is to prevent and reverse the catabolic state associated with injury. It is of crucial importance to evaluate each patient’s nutritional status prior to and after any surgical intervention to optimize the success of the treatment. While a detailed physical exam is extremely useful to determine nutritional status, certain lab values are helpful in establishing objective values. These studies include albumin, pre-albumin, and transferrin levels. Concentrations of serum albumin less that 3.0 g/dl are an indicator of malnutrition. Albumin has a half-life of 14–18 days, demonstrating the patient’s recent nutritional status, whereas pre-albumin (half-life 3–5 days) and transferrin (half-life 7 days) may show more rapid changes in nutritional status. These serum markers can guide clinical decisions and serve as a benchmark for nutritional optimization. Furthermore, an individual’s energy requirements can be measured by indirect calorimetry and trends in serum markers as well as estimated from urinary nitrogen excretion [4]. In addition to supplying sufficient calories and protein to prevent the catabolic state and allow for protein synthesis and tissue repair, some patients may require essential vitamin and mineral supplementation.

In terms of nutritional supplementation, enteral feeding is preferred over parenteral, not only based on the cost and avoidance of vascular access-associated complications but also for the benefits attained from feeding the intestine directly [5]. There are numerous routes for enteral feeding including temporary ones such as Dobhoff tubes to more permanent methods that involve surgical placement of feeding tubes (Table 2.2). Using the gastrointestinal tract prevents diminished secretory IgA production, bacterial overgrowth, and altered mucosal defenses associated with parenteral nutrition.

Table 2.2

Common feeding routes

Access option	Comments
Nasogastric tube	Only for short-term use, increase risk of aspiration, frequently dislodged
Dobhoff tube	May use slightly longer than NG tube, although it is a temporary feeding route. Decrease risk of aspiration due to post-pyloric placement. More challangening to place than NG tube. Easily dislodged
Percutaneous endoscopic gastrostomy (PEG)	Placed via endoscope, can be used for longer periods of time. Aspiration risks due to pre-pyloric placement. Can have complications related to placement and site leaks
Surgical gastrostomy	Requires surgery, procedure may allow placement of extended duodenal/jejunal feeding port which allow for gastric decompression and post-pyloric feeding
Fluoroscopic gastrostomy	Blind placement using needle and T-prongs to anchor to the stomach, can thread smaller catheter through gastrostomy into duodenum/jejunum under fluoroscopy
PEG-jejunal tube	Jejunal placement with regular endoscope is operator dependent, jejunal tube often dislodges retrograde, two-stage procedure with PEG placement, followed by fluoroscopic conversion with jejunal feeding tube through PEG
Surgical jejunostomy	Requires surgery, allows for post-pyloric feeds, less risk of aspiration

Patients that benefit from nutrition supplementation are those that have poor preoperative nutritional statuses [6, 7]. Healthy patients without malnutrition undergoing elective surgery can tolerate partial starvation for up to 10 days before any clinically significant protein catabolism occurs. However, in the critically ill patient, early enteral feeding has become the standard of care and has been shown to reduce both morbidity and mortality [8]. Furthermore, early intervention with supplement nutrition is favored for patients who show preoperative protein-calorie malnutrition (Table 2.3).

Table 2.3

Comparison of tube feed products

Product	Caloric density (kcal/ml)	Protein (%kcal)	Features
Crucial	1.5	25	Promotes absorption and tolerance in critically ill patients with GI dysfunction
Diabetisource AC	1.2	20	For patients with diabetes or stress-induced hyperglycemia
Glucerna 1.2	1.2	20	Nutrition for glycemic control
Impact	1	22	Supports immune defense in patients at risk for infections
Jevity 1.2	1.2	18.5	18 g of dietary fiber/L
Optimental	1	20.5	For malabsorptive conditions
Pivot 1.5	1.5	25	Very high-protein calorically dense for metabolic stress
Peptamen 1.5	1.5	18	High-caloric GI formula
Perative	1.3	20.5	Peptide-based semi-elemental protein for easier absorption
Promote	1	25	For patients with lower calorie needs but higher protein needs

Table was adapted from the original and provide the full AMA citation, used by permission

Indications for parenteral nutrition are limited to patients that have a contraindication in using the gastrointestinal tract or have failed enteral supplementation. It comes in two forms: total parenteral nutrition (TPN) and peripheral parenteral nutrition (PPN). TPN requires central venous access because it has a high osmolarity from high dextrose content, whereas PPN can be administered through the peripheral intravenous line because of much lower dextrose and protein concentrations. Some nutrients cannot be concentrated into the small volumes required for PPN, thereby making it inappropriate for patients with severe malnutrition [1]. PPN can be considered if central access is unavailable or it is used to augment oral nutrition. It should only be used for short periods after which TPN should be considered. Complications related to parenteral nutrition include sepsis from catheter site infection, cholestasis and gallstone formation as well as intestinal atrophy leading to impaired gut immunity, bacterial overgrowth, and reduced IgA production [1]. The best way to avoid these complications is to feed enterally whenever possible.

Inflammation and Injury

In order to provide the optimal care and surgical treatment, we must approach and understand the patient on a variety of levels, whether it is related to the molecular level of injury and its related systemic response or to the metabolism involved in healing. All aspects must be considered to achieve the best outcome. Injury to the patient results in an inflammatory process that is triggered on a local level. Inflammation describes the process in which fluid and circulating leukocytes accumulate in the extravascular tissue [1]. It describes not only the localized effects but also the triggered systemic response. The inflammatory response is closely associated with healing and repair and therefore closely interrelated to every aspect of surgery.

Inflammation is fundamentally a protective response that allows for removal of harmful agents and cellular debris as well as repair damage. However, excess inflammation can be pathological and harmful. The initiation, maintenance, and termination of inflammation are highly complex and coordinated process mediated by a myriad of cells as well as cytokines.

Cytokines mediate a broad range of cellular activities and function locally at the site of injury to promote wound healing and eradicate infection [8–12]. Cytokines can have both proinflammatory and anti-inflammatory actions, and their balance is a well-coordinated system. Some of the important cytokines involved in this process include tumor necrosis factor (TNF), interleukins, and interferon.

The release of cytokines from damaged cells not only plays a role on a local level but also can trigger a systemic response. This can induce a response from the central nervous system via the hypothalamic-pituitary-adrenal axis in the form of released hormones [1]. The two principle hormones that are involved are glucocorticoids and catecholamines. During injury, there is an increase in the production of cortisol, which plays an important role in decreasing the inflammatory process and limiting the harmful aspect of inflammation [13–15]. Catecholamine release in the form of epinephrine and norepinephrine activates increased cellular metabolism throughout the body and mobilization of glucose via glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis. The catecholamine release also helps to reestablish and maintain homeostasis [16]. Critically ill patients who suffer from severe stress often have insulin resistance leading to hyperglycemia [17]. Hyperglycemia during these periods often leads to increased morbidity and mortality. Tight management of blood sugars has been shown to decrease complications [18].

Wound Healing

All tissue heals in four divided phases, which can overlap. These four phases are (1) hemostasis/inflammation, (2) cellular migration, (3) proliferation, and (4) remodeling. The first step in the process consists of the initial injury leading to a disruption of tissue integrity. This triggers platelet aggregation in order to form a clot and the release of a variety of growth factors and cytokines from the platelet granules. Furthermore, the fibrin clot serves as the scaffold for the migration inflammatory cells, including polymorphonuclear leukocytes (neutrophils) and monocytes [19].

Neutrophils are the first cells to enter the wound and peak at 24–48 h. Their role is to remove bacteria and tissue debris as well as to release further inflammatory cytokines (Fig. 2.1). Following the neutrophils, the second kind of inflammatory cell to migrate to the wound is the macrophage. These cells have the highest concentration in the wound at 48–96 h and participate in wound debridement as well as the release of further cytokines and growth factors, which regulate cell proliferation, matrix deposition, and angiogenesis [20, 21].

Fig. 2.1

The cellular, biochemical, and mechanical phases of wound healing (From Wound Healing Schwartz’s principles of surgery, 10e, 2014)

The proliferative phase occurs from day 4 to 12. It is during this time that tissue continuity is reestablished. Fibroblasts are the main cell involved during this phase. The fibroblasts produce collagen and participate in wound contraction. Endothelial cells are also present and partake in angiogenesis. Collagen formation plays an important role in the maturation of the wound. Initially, there is a predominance of type III collagen, which is eventually transformed into type I during the remodeling phase [19].

Maturation and remodeling begin during the fibroblastic phase, characterized by collagen breakdown and reorganization. Several weeks after the injury, the wound reaches a plateau of collagen quantity, while the tensile strength of the wound continues to increase for several months [22]. Scars can take up to 1 year to fully mature, but the strength of the scar never reaches their pre-injury state, usually only approaching 80 % of its former state.

Epithelialization of the wound occurs within 1 day after injury. Cells at the edge of the wound proliferate and migrate until the defect is bridged. This process occurs through a loss of contact inhibition of the cells [23–26]. Re-epithelialization is complete within 48 h after incised wounds but may take significantly longer time for larger wounds.

There are certain factors that affect wound healing that one has to be cognizant of in order to counteract them. Low-oxygen states that are found in hypoxia stemming from peripheral vascular disease, radiation-induced injury, or anemia can have poor outcomes on wound healing. Fibroplasia and collagen synthesis are both decreased in hypoxic wounds. Patients that may suffer from these conditions benefit by increasing the oxygen tension in the tissue, whether it is through revascularization procedures or treatment with hyperbaric oxygen.

Steroids can also have a deleterious impact on wounds. They reduce collagen synthesis and wound strength via inhibition of the inflammatory phase of wound healing [27]. Furthermore, they hinder epithelialization and wound contraction. Vitamin A has been shown to have positive effects in mitigating the harm caused by steroids [28]. In addition, metabolic disorders can cause an increase in wound problems, with diabetes mellitus being the most common disorder encountered. Hyperglycemic states can cause decrease in inflammation, angiogenesis, and overall collagen synthesis. Patients with diabetes often suffer from vascular disorders leading to hypoxemia, confounding the problems [29]. Aggressive glycemic control can improve outcomes.

Surgical Technique

Antiseptic Technique

There are several antiseptics used to clean the skin preoperatively. A review of the current literature has demonstrated that preoperative skin with 0.5 % chlorhexidine in methylated spirits was associated with lower rates of surgical-site infections following clean surgery than alcohol-based povidone-iodine paint [30]. In the Dumville et al. review, no other comparisons of skin antiseptic techniques showed statistically significant differences in surgical-site infection rates [30].

Sutures

Types

There are several types of suture materials currently manufactured. The choice of suture depends on several factors, including the amount of tension on the wound, the number of layers of closure, the depth of suture placement, the anticipated amount of edema, and the anticipated timing of suture removal [31]. The size of the suture material represents the diameter of the suture material [31]. The higher number prior to the 0, the smaller the suture. For example, 5–0 suture is smaller than 2–0 suture. If the suture does not have a “0” in the size, then the size correlates with the increasing number, i.e., size 2 suture is larger than size 1, which is larger than 0 or 2–0. The smaller the diameter of the suture, the less the tensile strength [31].

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