The neurosurgical wound and factors that can affect cosmetic, functional, and neurological outcomes

Abstract

Surgically accessing pathological lesions located within the central nervous system (CNS) frequently requires creating an incision in cosmetic regions of the head and neck. The biggest factors of surgical success typically tend to focus on the middle portion of the surgery, but a vast majority of surgical complications tend to happen towards the end of a case, during closure of the surgical site incisions. One of the most difficult complications for a surgeon to deal with is having to take a patient back to the operating room for wound breakdowns and, even worse, wound or CNS infections, which can negate all the positive outcomes from the surgery itself. In this paper, we discuss the underlying anatomy, pharmacological considerations, surgical techniques and nutritional needs necessary to help facilitate appropriate wound healing. A successful surgery begins with preoperative planning regarding the placement of the surgical incision, being cognizant of cosmetics, and the effects of possible adjuvant radiation therapy on healing incisions. We need to assess patient's medications and past medical history to make sure we can optimise conditions for proper wound reepithelialisation, such as minimizing the amount of steroids and certain antibiotics. Contrary to harmful medications, it is imperative to optimise nutritional intake with adequate supplementation and vitamin intake. The goals of this paper are to reinforce the mechanisms by which surgical wounds can fail, leading to postoperative complications, and to provide surgeons with the reminder and techniques that can help foster a more successful surgical outcome.

1. INTRODUCTION

Surgically accessing pathological lesions located within the central nervous system (CNS) frequently requires creating an incision in the cosmetic regions of the head and neck. Proper surgical technique and understanding of the underlying anatomy is essential in not only obtaining the maximum cosmetic result but also in avoiding serious complications such as cerebrospinal fluid leakage or superficial infection capable of spreading into the CNS. In addition, cosmetic and wound‐healing concern does not end with closure of the skin in the operating room. For example, neurosurgical patients with a depressed level of consciousness have increased risk of adverse events related to wound healing and breakdown. There are many factors during the postoperative course that can be modified or managed to achieve optimal wound healing. Our literature review includes various aspects of incision planning, postoperative wound management, nutritional and pharmacological considerations, and other detrimental factors that should be considered in order to maximise the likelihood of successful postoperative wound closure.

2. VASCULAR COMPROMISE

Without an adequate vascular supply, healing tissue from a surgical wound is unable to obtain the vital oxygen and nutrients needed for tissue reconstruction. In addition, proper venous and lymphatic drainage is essential for the removal of both wound by‐products and inflammatory processes intrinsic to tissue damage. Since ancient times, it has been well documented that tissue cannot survive without an intact pedicle providing rich arterial blood supply. Early texts describing a surgeon utilising a flap pedicle with adequate vascular supply for a superficial wound were written in 600 BC by an Indian Surgeon called Sushruta. Pioneering the surgical frontier, he performed rhinoplasty on a woman whose entire nose had been cut off as a penalty for adultery. He utilised a forehead scalp pedicle flap that had adequate vascular supply to reconstruct a new nose. Even without a full understanding of 21st century medicine, Sushruta was able to appreciate the importance of how a well‐vascularised pedicle ensures tissue flap survival. Although the patient likely did not have a cosmetically pleasing postoperative appearance compared with modern approaches, the large defect was successfully masked because of the surgeon's understanding of the relationship between the vascular supply and its inherent need for appropriate surgical wound healing. Continuing into the present day, an accurate understanding of the vascular anatomy of the scalp allows surgeons to minimise transecting critical vessels during a surgical incision.

The scalp is among the highly vascularised tissues of the human body. It receives vascular supply from both internal and external segments of the carotid artery. The four main branches off of the external carotid artery (ECA) are the superficial temporal, angular, occipital, and posterior auricular arteries and the supraorbital and supratrochlear arteries, which are the terminal branches of the ophthalmic artery.1 The front portion of the scalp is supplied by the supratrochlear (also known as the frontal artery) and supraorbital arteries, which arise from the supratrochlear notch and supraorbital foramen, respectively.2 These vessels extend up towards the vertex of the skull and provide one of the anastomotic points between internal and external carotid circulation by joining with the frontal segments of the superficial temporal arteries.3 The superior temporal artery, a terminal branch of the external carotid, supplies the middle portion of the scalp by ascending anterior to the ear. This artery then splits into the frontal branch, as specified above, and the parietal branch, which supplies the temporalis muscle and parietal scalp. The parietal branch of the superficial temporal artery has an anastomosis with its counterpart from the opposite side as well as the ipsilateral occipital arteries, which supply the posterior scalp. Of note, the arteries of the scalp, especially the frontal temporal artery, can produce an arteriovenous malformation called a cirsoid aneurysm.4 These aneurysms are considered to be hemangiomas of the arterial vessel and can occur because of trauma.5 The occipital and posterior auricular arteries, both of which are branches of the ECA, supply the posterior scalp. Upon branching from the ECA, the occipital artery traverses through the trapezius muscle and continues towards the vertex of the scalp. The greater occipital nerve typically accompanies the occipital artery. The posterior auricular arteries pass along the styloid process between the mastoid and the ear and supply the scalp posterior to the auricle. Since Miller et al, recommendations on microvascular replantation have stated that two or more arterial connections and as many veins as possible should be anastomosed.6

Venous drainage of the scalp is divided into three groups: superficial, diploic, and emissary. The superficial veins run alongside their arterial counterparts. The diploic veins are found within the diploe, the space between the inner and outer tables of the skull. The diploe and superficial veins are both connected to the intracranial venous sinuses by means of the valve‐less emissary veins, which pass through tiny foramina within the bones.7 These veins provide bidirectional flow, typically flowing from external to internal, but can change direction in abnormal pathologies such as increased intracranial pressure. The four main groups of emissary veins are posterior condyloid, mastoid, occipital, and parietal emissary veins. One of the most important emissary veins is the vein of Vesalius, which connects the pterygoid venous plexus with the cavernous sinus via the sphenoidal emissary foramen. Having the veins void of valves permits infections from extra‐cranial sources to spread intra‐cranially and lead to septic thrombi. Consideration of such vascular networks is vital in more extensive incisions where a continuous blood supply is needed to provide maximum healing.

Incisions transecting a larger surface area may diminish wound healing as such approaches carry a higher risk of compromising vascular supply. For example, in a larger craniotomy, it is ideal to place an incision approximately 1 cm anterior to the tragus to avoid transecting the proximal main trunk of the superficial temporal artery and the emerging branches of the facial nerve. However, such an approach may not align with the primary goal of a craniotomy for tumour resection, which is to individualise the incision based on the location of the underlying pathology. Ultimately, considerations with regard to any surgical incisions should focus on both preserving an adequate vascular pedicle to perfuse the wound and fully addressing the area of disease.

3. POSTOPERATIVE RADIATION

In the modern era, most physicians are accustomed to ordering or obtaining tissue samples from a location of questionable pathology. Frequently, an intraoperative biopsy of a specimen suspected to be a neoplasm is promptly sent for pathology, and if the diagnosis is confirmed to be malignant, then radiation therapy can routinely be a treatment. With regard to cerebral pathology, radiation oncology frequently treats high‐grade CNS tumours and metastatic lesions with radiation therapy. Unfortunately, the effects of radiation are not localised exclusively to the area of pathology.

The healing of a surgical wound occurs in a highly organised sequence of complex, energy‐requiring cellular and biochemical interactions. The early inflammatory and proliferative phases of surgical wound healing are inhibited by ionising radiation. Ionising radiation interferes with transforming factor beta (TGFB), vascular endothelial growth factor (VEGF), interferon‐gamma (IFN‐Gamma), and other pro‐inflammatory cytokines such as various interleukins.8 In the late proliferative stage, ionising radiation inhibits matrix metalloproteinase (MMP), granulation tissue formation, reepithelialisation, and neovascularization.9 Because of the increased metabolic demand required for wound healing, it is advised that, when possible, the smallest optimal incision be utilised to not only improve wound healing but also to maximise cosmetic outcomes.

Focusing on aesthetics, the early effects of ionising radiation on a surgical wound can produce erythema, dry desquamation, alopecia, and hyperpigmentation. The later effects of ionising radiation include skin atrophy, dehydration of the wound bed, microvascular changes including telangiectasia and progressive vascular stenosis because of neo‐intimal hyperplasia, fibrosis, ulceration, and depigmentation. As the vessel stenosis progresses and the vascular calibre diminishes, the irradiated tissue receives progressively less oxygenated blood and nutrients. Therefore, a well‐tailored short incision confined to the optimal area will lead to maximal healing when radiation is needed postoperatively.

4. GLUCOCORTICOIDS

Certain neoplastic pathological lesions of the CNS produce vasogenic oedema through the breakdown of the blood–brain barrier. This produces significant swelling, causing mass effect with a tandem increase in intracranial pressure. Glucocorticoids inhibit inflammation, fibroblast proliferation, angiogenesis, and reepithelialization.10 The use of vitamin A can restore the inflammatory response and promote wound healing, epithelialisation, and collage synthesis. Unfortunately, vitamin A in large doses is contraindicated in neurosurgical patients as retinoid can markedly increase intracranial pressure (ICP), which can have catastrophic results. Moreover, glucocorticoids, while useful for combating cerebral oedema globally, can impair the healing process if used postoperatively.

Glucocorticoids can predispose a surgical wound to infection not only through breakdown and dehiscence, which has a higher probability in longer incisions, but also by inhibiting the immune system on a molecular level. Glucocorticoids directly inhibit subcutaneous dendritic cells and their signalling cytokines molecules, such as interleukin‐12.11 Dexamethasone has been shown to inhibit U937 cell adhesion and neutrophil release, thereby inhibiting the immune system's ability to fight infection in the surgical wound.12 Moreover, it is important to take into consideration how a patient's medication use for chronic conditions may affect their postoperative outcome.

Long‐term treatment with glucocorticoids is not uncommon in neurosurgical patients, especially in patients with rheumatological disease. These patients are predisposed to developing glucocorticoid‐induced osteoporosis, and this is the most common iatrogenic cause of secondary osteoporosis in the United States.13 In neurosurgery, osteoporosis can be detrimental when surgical instrumentation is placed in the skull or cervical spine. Because of the loss of trabecular bone and the inhibition of new bone formation, these patients are predisposed to fractures, pseudoarthrosis, and instrumentation dislodgement, which can affect the soft tissue wound closure. It is important to consider that surgical wound healing in and around underlying bone can be impaired in up to 32% of patients on dexamethasone.14 Likewise, a common adverse effect of high‐dose or prolonged glucocorticoid use can also reduce the efficiency of wound closure.

The use of glucocorticoids can cause profound hyperglycaemia and can exacerbate baseline diabetes. Poorly controlled diabetes can produce further systemic and local wound immunosuppression, increasing the likelihood of wound infection.15 Poorly controlled diabetes also reduces the antioxidant activity of cells and molecules responsible for free radical scavenging.16 Excessive free radicals not only impair local wound healing but can also produce negative neurological outcomes in an injured brain.17, 18, 19 Free radicals also inhibit the healing metabolic function of keratinocytes in wound healing.20 Poorly controlled diabetes further impairs healing of fractures, which can affect neurosurgery patients with traumatic injuries to the skull and spine.21 High serum glucose levels inhibit human fibroblast cell migration in wound healing, causing a decrease in collage deposition, which reduces the tensile strength of the wound.22 In cases of increased incision length, the force on the wound edges is greater because there are less fixated portions of skin. It is the authors' opinion that an insulin sliding scale should be mandatory in any patients on glucocorticoids postoperatively.

5. PHARMACOLOGICAL CONSIDERATIONS

On discharge, the patient and associated caregivers should be informed about avoiding use of non‐steroidal anti‐inflammatory drugs (NSAIDS). Aspirin, ibuprofen, and other NSAID's inhibit the inflammatory phase of wound healing and inhibit platelet function.23 As a result, these medications can predispose patients to potential postoperative bleeding. In addition to inhibiting local superficial wound healing, NSAIDs inhibit bone arthrodesis, which can be detrimental in spinal fusion procedures.24 There is a high incidence of cervical spine pathology in patients with rheumatoid arthritis, and many of these patients tend to require surgery.25 The use of disease‐modifying anti‐rheumatic drugs (DMARDS) has become the standard of care in the treatment of patients with progressive rheumatoid arthritis.26 While these drugs may be beneficial in hindering the progression of rheumatoid arthritis, they also cause immunosuppression, predisposing to wound infections and inhibition of postoperative spinal fusion.27, 28

The annual incidence of metastatic cerebral lesions is approximately 10 per 100 000 people, and brain metastases can be found in up to 15% of patients on autopsy who have died because of systemic cancer.29 Several studies have shown increased overall survival rates in patients who have undergone surgical resection of one to three cerebral metastases, particularly when followed by postoperative radiation.30, 31 A high number of patients undergoing craniotomy for resection of cerebral metastases will have undergone chemotherapy during, before, or after surgery. Chemotherapy use is not restricted to cerebral metastases and is also used in certain high‐grade primary brain neoplasms. An example that illustrates this is the increased rates of survival in patients with World Health Organization Stage IV Glioblastoma Multiforme (GBM) who receive the chemotherapeutic agent temodar.32 It has long been established that systemic chemotherapy creates an immunocompromised state that can interfere with surgical wound healing.33, 34 The incidence of postoperative wound complications in patients receiving chemotherapy can be as high as 11%.35 The American Cancer Society informs postoperative patients who are on chemotherapy and their caregivers to look for redness, bruising, scaly broken skin, crusts, scabs, cuts, bleeding, swelling, drainage, pus, warmth, pain, and tenderness in the surgical wound while on chemotherapy.36 Chemotherapeutic agents can have a highly detrimental effect on surgical wound healing as they interfere with the proliferation and division of cells such as fibroblasts, macrophages, epithelial cells, keratinocytes, endothelial cells, cytokine‐producing lymphocytes, neutrophils, and other leukocytes.

A new class of monoclonal antibodies that prevent the proliferation of blood vessels through the inhibition of angiogenesis are being used to treat many systemic cancers that metastasise to the brain as well as for certain high‐grade primary CNS tumours such as GBM. Bevacizumab is a monoclonal antibody that inhibits VEGF and has been found to cause an increase in wound‐healing complications in patients who have had brain tumours resected.37 While these medications are effective in preventing the recruitment of new blood vessels to supply enlarging tumours, they also inhibit the formation of new blood vessels needed to supply the tissues of a healing wound.

Patients who have sustained severe multi‐system traumatic injuries may become haemodynamically unstable because of ongoing haemorrhage from different sites throughout the body. In cases of hypovolemic shock, it is often necessary to provide vasoconstricting pressors to maintain an adequate blood pressure to perfuse vital organs. In cases of severe life‐threatening shock, the body will shunt blood towards the internal organs to provide adequate life‐sustaining perfusion, simultaneously causing decreased perfusion to areas such as the skin. A patient who has recently undergone a decompressive hemicraniectomy for resection of a traumatic subdural haematoma and is simultaneously going into hypovolemic shock from haemorrhage into the thoracic and abdominopelvic cavities may require vasoconstrictive pressors in addition to fluid resuscitation and transfusion of blood products. Vasoconstricting pressors can produce tissue hypoxia in the craniotomy surgical wound through reduced microcirculation perfusion, leading to impaired healing. The use of vasoconstrictive pressors is not only limited to hypovolemic shock from haemorrhage but is also commonly used in patients with septic shock. An example that illustrates this is a patient recovering in the intensive care unit after undergoing a craniotomy for resection of a brain tumour and who is now in septic shock from a urinary tract infection secondary to an indwelling catheter. Prior to receiving vasoconstrictive pressors, the surgical wound is already under‐perfused from the hypotension of the septic shock state. Cancer patients recovering in the ICU after receiving chemotherapy have an increased incidence of sepsis from being immunosuppressed and may require vasoconstrictive pressors.

Certain antibiotics have pharmacological effects that can inhibit wound healing, such as tetracycline and erythromycin that inhibit leukocyte chemotaxis, gentamicin that delays reepithelialisation, and mupirocin that inhibits wound contraction.38

A deficiency in vitamin C and zinc can inhibit the formation of collagen, which is essential during the initial stages of tissue granulation. Trace levels of zinc, copper, and selenium are essential in surgical tissue wound healing, and it is helpful to provide these elements as supplements during the postoperative period.39 Nutrition and receiving proper amounts of vitamins are essential as cancer patients are often in a hyper‐metabolic state causing cachexia; the rapidly dividing and proliferating cancer cells deprive the body of key nutrients, vitamins, and elements that would be used by the wound‐healing cell populations.40

6. TECHNIQUE

The primary goal of most surgeons, regardless of specialty, is to plan an optimal incision that permits ease of access to the intended area of concern. Although the site of the incision can be planned using anatomical landmarks, stereotactic neuronavigation allows for confirmation of the precise location of the pathology that will influence the size and location of the incision. If the patient has a subcutaneous port reservoir for infection entering into a vessel or the CNS, the incision should be as far away from the port site as feasible. An example that illustrates this is an Omaya Reservoir attached to an intraventricular catheter that can be used for the administration of chemotherapeutic agents to the CNS. The vascular supply to the surrounding musculature and nearby nerves should also be bypassed in tandem, avoiding the aforementioned hardware and anatomy. For maximum healing, the incision should not be over the edge of an uneven craniotomy defect or over an area with an underlying metallic plate fixation device from previous surgeries.

In terms of incision size versus vasculature preservation, the best vascular supply should be maintained, and the smallest incision possible should be made, but large enough to prevent any struggling intra‐operatively. Preservation of the temporal branch of the facial nerve located in the interfascial fat pad prevents postoperative paralysis of fibres supplying the frontalis, orbicularis oculi, and corrugator supercilli muscles. Facial asymmetry because of paralysis of these facial muscles can produce an undesirable functional and cosmetic outcome. It is ideal to keep the majority of the superficial skin incision behind the hairline as this reduces visibility of the scar. This is more difficult in patients with male pattern baldness and cancer patients suffering from alopecia while on chemotherapy. Certain anterior skull base lesions can be accessed by a supraorbital craniotomy where the incision can be buried in the edge of the eyebrow to minimise the visibility of the scar. As a substitute to a traditional linear incision, an alternating zig zag wavy line incision decreases tension and allows for a more cosmetically appealing re‐approximation of the scalp behind the hair line. In terms of subfrontal craniotomies, one can insert a subgaleal drain intra‐operatively, which will reduce the amount of subgaleal haematoma, which can distort the appearance of the head postoperatively. While the type of incision is important with regard to cosmetic healing, the size of the incision requires equal consideration.

The incision size must give easy access to the lesion but must also be as small as possible. Large “C”‐shaped incisions or large reverse question mark incisions are not necessary for a small intra‐cerebral lesion. However, a large decompressive hemicraniotomy or hemicraniectomy may be absolutely essential in cases of an expanding traumatic subdural or epidural haematoma. In cases where the intraoperative swelling is significant, the bone flap may be removed, and the patient will have an unsightly cephalic appearance because of the cranial defect postoperatively. These can usually be corrected with a synthetic or autologous cranioplasty within a few weeks to months once the swelling has subsided. Even when a large decompressive hemicraniotomy versus craniectomy is performed, the majority of the incision can still be placed behind the hair line. Although the lesion heals side to side as described, a longer incision requires more energy to heal and more tensile strength to hold the wound together and is thus prone to more complications.

A layered surgical closure of the scalp is an essential component of closing after intracranial surgery. A meticulous re‐approximation of the galea aponeurotica, the fibrous layer of dense connective tissue responsible for the final tensile strength of the wound, is the foundation for creating a durable closure that will maintain the structural integrity of the wound. Located above the galea, the subcutaneous layer is quite fragile, and tightly tied sutures, when approximated, can easily tear through this tissue. In the final layer, the primary epithelial skin incision can be closed in a variety of ways, including but not limited to staples or a running stitch. However, the preferred method remains a subcutaneous sutured closure with application of skin glue; consequently, this method is also known to provide the best cosmetic result.

In larger bi‐coronal craniotomies, many neurosurgeons utilise a wavy smooth zig zag incision or suture line.41 As a result, the final closure disperses the tension across the incision. In addition, this technique allows the surgeon to align the incision with the vector of hair growth, minimising trauma to the follicle and thus reducing the amount of hair loss at the site. During the postoperative period, it is essential that the patient does not have significant pressure on the surgical wound. For example, such considerations are particularly important in comatose patients with suboccipital lesions as they are more likely to lie in a supine position that places greater pressure on the wound. These patients require meticulous wound care with frequent repositioning of the head.

6.1. Nutrition

Nutritional management in the postoperative neurosurgical patient, particularly the patient with traumatic brain injury, is medical treatment. While the human brain accounts for just 2% of total body weight, it consumes over 20% of serum glucose for energy needs at baseline without the presence of injury or pathology.42 In the neurotrauma patient with significant traumatic brain injury (TBI), the brain enters a hyper‐metabolic state where cerebral energy stores are rapidly consumed at a cellular level.43 The level of metabolism in the injured brain can increase from 32% to 200% depending on the severity of the injury.44 Even in the most severe cases of TBI where a patient is placed into a barbiturate coma for neuroprotection by reducing cerebral metabolism, the cerebral metabolic demand is still 100%–120% greater than resting baseline energy expenditures.45 A systemic hyper‐metabolic state occurs in TBI with a depletion of whole body energy stores.46 The healing neurosurgical wound from a craniotomy incision competes with cerebral and systemic metabolic consumption, which can deprive the wound from receiving adequate nutritional support. TBI patients have a marked increase in gluconeogenesis; hepatic protein synthesis; and usage of protein, carbohydrates, and fat with hyper metabolism in the mitochondria.47 Patients with obesity have copious stores of fat in adipose cells that can serve as an energy source during periods of malnutrition. However, the process of fat oxidation causes an excess of free radical production. which further leads to secondary damage to an already injured CNS.48, 49 Protein malnutrition impairs the immune systems response and results in a decreased ability to produce antibodies and cytokines.50, 51 Protein energy malnutrition can impair the proliferation of CD8 T lymphocytes responsible for suppressing infection.52 In the neurosurgical patient, a superficial wound infection can have potentially catastrophic complications, such as meningitis.53 There is strong evidence that the level of caloric intake can affect the patient's final neurological outcome.54, 55 Prolonged protein malnutrition causes the catabolism of muscle fibres, leading to muscle atrophy and subsequent decreased strength.56 This can be detrimental in a craniotomy that depends on the tensile wound strength from surgically approximating certain muscle groups such as the temporalis, occipitofrontalis, and its aponeurosis.

It is not uncommon for the neurosurgical patient to have postoperative nausea and vomiting because of medications, chemotherapy, CNS pathology, or other factors. Such changes in appetite can also become a serious health issue when paired with acute changes in mental status. To illustrate, an abulic patient may not have the desire to eat because of a frontal lobe or limbic lesion causing an amotivational state. Moreover, a patient may not be able to adequately feed themselves because of motor weakness or discoordination or may be verbally unable to communicate their hunger because of language impairment from pathology in their dominant cerebral hemisphere. A postoperative patient with significant cognitive and other neurological impairment may develop malnutrition from receiving suboptimal attention from a caregiver in a skilled nursing facility. It is imperative to have proper nutrition for a craniotomy wound to successfully heal.57

It is important that the patient begins receiving nutritional support in the intensive care unit (ICU) during the initial postoperative course.58 Vitamin C has long been known to be critically important in the collagen formation of surgical wound healing; however, recent investigations have shown it plays a role in bone healing as well.59 Selenium is utilised by fibroblasts during the proliferative phase of wound healing and has become an invaluable wound‐healing supplement that is gaining use in postoperative nutritional regimens.60 Elemental zinc is gaining popularity in patients in the ICU with complex surgical wounds that require additional nutritional, vitamin, and elemental support for wound healing. Elemental zinc is an essential cofactor in several important enzymes, such as zinc‐dependent MMPs, which aide in the debridement of devitalised tissue by macrophages and keratinocyte migration during wound repair.61 In the animal model, nutritional caloric restriction has consistently been found to be detrimental to multiple aspects of surgical wound healing, including cellular evidence of increased oxidative damage.62 Nutrition is not only important to superficial surgical wound healing but is also critically important to the area of the brain affected by surgery and underlying pathology.63 Adequate postoperative nutrition will result in a better cosmetic, functional, and neurological outcome.

6.2. Wound breakdown

Neurosurgery patients often receive comprehensive and meticulous care in the ICU during the immediate postoperative period. Some will have an altered mental status postoperatively, ranging from mild confusion to a deep comatose state, because of sedation and the area of the CNS affected by the offending pathology. As they improve clinically, they are often downgraded to telemetry units and eventually to the general floor. After the hospital course is completed, some may not be able to be discharged home and require placement in a skilled nursing facility or long‐term acute care facility. While in a facility, a primary concern is that prolonged immobility can lead to the development of pressure ulcers. Although pressure ulcers are common in the sacrum and other dependent regions, they are not uncommon on the scalp and around incision sites. Scalp pressure ulcers can contribute to wound breakdown and progress to dehiscence. A superficial wound infection can eventually spread underneath to critical structures. Intraoperatively, a tight approximation of the galea is essential to provide a barrier in order to prevent the spread of infection and initiate proper healing. A superficial wound infection that spreads to the CNS can have catastrophic consequences, particularly in patients with pre‐existing neurological impairment as it can be difficult to detect an acute change in mental status. Consequences of superficial infections that invade the CNS include meningitis, cerebritis, encephalitis, ventriculitis, abscess, and empyema; if these are not identified in a rapid manner, they can become fatal. Early detection can be very difficult as these patients are more prone to pneumonia from aspiration and prolonged ventilation, urinary tract infections from prolonged catheterisation, and poor sanitary conditions secondary to being in an immobilised state. Inflammatory markers such as erythrocyte sedimentation rate and C‐reactive protein are neither sensitive nor specific in the postoperative period because of expected post‐surgical inflammatory changes.

6.3. Conclusions

Neurosurgery patients typically have many factors that can adversely affect wound healing of a craniotomy incision. As mentioned throughout our review, glucocorticoids, radiation, chemotherapy, poor nutrition, cachexia from advanced metastatic process, or even pressure ulcers because of the inability to move can all contribute to poor wound healing. Therefore, intraoperative measures, including a meticulous layered wound closure, can enhance not only the final cosmetic and functional result but prevent a negative neurological outcome. Instructions for meticulous and specific wound care at the time of discharge can be paramount in preventing the breakdown of a neurosurgical wound. Early postoperative clinic visits, with wound checks, can potentially identify a superficial wound dehiscence before a superficial infection has the opportunity to spread to the CNS. Discharge instructions given to the patient, family, caregiver, primary care physician, or skilled nursing facility staff should include specific wound instructions, with special attention to any wound dehiscence, erythema, discharge, induration, fluctuance, or warmth. If any of these are discovered, they should be reported promptly. Further instructions should be given to promptly report any fevers, chills, myalgias, neck pain, photophobia, new or worsening headache, neck stiffness, or altered mentation from baseline. By approaching wound care in a holistic manner, starting in the operating room and continuing through the patient's final destination, we can make sure that each step of the wound‐healing process is fully assessed and properly treated.

Berry JAD, Miulli DE, Lam B, et al. The neurosurgical wound and factors that can affect cosmetic, functional, and neurological outcomes. Int Wound J. 2019;16:71–78. 10.1111/iwj.12993