© Springer International Publishing Switzerland 2016
Marinella Astuto and Pablo M Ingelmo (eds.)Perioperative Medicine in Pediatric AnesthesiaAnesthesia, Intensive Care and Pain in Neonates and Children10.1007/978-3-319-21960-8_2525. Prevention of Chronic Postsurgical Pain
(1)
Department of Anesthesia, Clinica Las Condes, Santiago, Chile
(2)
Chronic Pain Service, Department of Anesthesia, The Montreal Children’s Hospital, McGill University, 2300 Tupper Street, Room C1117, Montreal, QC, H3H 1P3, Canada
25.1 Background
Chronic postsurgical pain (CPSP) is conceptualized as pain that extends beyond the period of normal tissue healing, and it is not explained by the initial pathology or surgical complications [1]. In practice, a time frame of pain for more than 2–3 months has gained acceptance as operative definition. The reported prevalence rates range from 5 to more than 50 % in adult surgical population, depending mainly on the type of surgery [2]. CPSP can occur after surgeries such as thoracotomy, extremity amputation, and hysterectomy. However, all procedures including relatively “minor” surgeries (e.g., appendectomy or inguinal hernia repair) have been associated with this condition [3, 4].
Even though CPSP is a well-known entity in the adult literature, this is a relatively unstudied complication in the pediatric population [5]. Considering the growing number of children who undergo surgery every year, there is a necessity to understand the population at risk, possible predisposing risk factors involved, and the eventual long-term effects in functionality and development [6].
25.2 Magnitude of the Problem
The prevalence varies with the nature of the surgical insult and time since surgery but also with the definition criteria used to classify patients with CPSP. Higher prevalence rates are reported in studies that include any report of pain regardless of intensity. Lower rates are typically seen when other criteria than pain (e.g., disability) are also included in the classification [7]. Overall, studies on different pediatric settings suggest that young age at the time of surgery is associated with lower risk of developing CPSP [8].
It has been reported that 1 year after surgery, 22 % of children developed moderate to severe (NRS, ≥4) CPSP. This study included children aged 8–18 years who underwent major orthopedic or general surgery, including thoracotomies and laparoscopies. The relative risk of having moderate to severe pain 1 year after surgery was 2.5 (CI 0.9–7.5) if patients experience pain ≥3 out of 10 two weeks after discharge [7].
In a retrospective study, 113 children and their parents were enrolled to answer telephone interviews regarding persistence and characteristic of pain after surgery in the preceding 3–10 months. Children between ages of 2 and 17 years who had undergone general, orthopedic, and urologic surgeries were included. Thirteen percent of patients reported the existence of CPSP (average pain level of 4.2 ± 1.5 on a 0–10 NRS) with a median duration of 4.1 months [9].
More specifically, groin pain after inguinal hernia repair is reported to be present in 3.2–13.5 % (severe pain in 2 %) of patients after 3.2–49 years follow-up [10–12]. The prevalence of CPSP after inguinal hernia repair seems to be lower when surgery is performed in childhood since adult reported a 10 % incidence of CPSP [6].
Similarly, results from studies of CPSP after sternotomy and thoracotomy have shown that surgeries during childhood have promising results compared with same procedures in adults in terms of chronic pain. A recent report on CPSP after sternotomy during childhood has shown that pain is present in 21 % of patients (10 % ≥4 on the NRS) after a mean follow-up period of 4 years. In adults, sternotomy is followed by CPSP in 20–50 % of patients [8]. Comparably, very young age at the time of surgery was associated with shorter duration of postoperative pain after thoracotomy due to coarctation of the aorta. The prevalence of postsurgical pain (>3 months) after thoracotomy was 3.2 % in the youngest group (0–6 years at the time of surgery), 19.4 % in children aged 7–12 years at the time of surgery, and 28.5 % among those aged 13–25 years at the time of surgery [13].
Spine surgery is associated with variable rates of pain before and after surgery and has been reported with prevalence rates of CPSP ranging from 11 to 68 %, 1–6 years after surgery [6, 14]. Interestingly, Siebert and colleagues have shown that adolescents who experienced no pain before and after spine surgery (“no pain trajectory”) were significantly younger than other groups of patients who experienced pain either before or after surgery [15].
25.3 General Mechanisms and Clinical Presentation
The pivotal factor seems to be the nerve damage during the procedure. However, the development of CPSP involves biological, psychological, surgical, and genetic factors interacting in a specific moment [16].
Inflammatory mediators are released by damaged tissue and an inflammatory cascade is triggered after surgery. Several molecules and compounds act directly on the primary afferent terminals, decreasing their excitation threshold (peripheral sensitization) [3]. This response is normal and produces the major part of the acute postsurgical pain. However, one of the triggers of pain chronicity is thought to be the peripheral nerve damage. When nerves are transected or stretched during surgical manipulation, they discharge trains of impulses using glutamatergic neurotransmission via NMDA receptors to sensitize nociceptive pathways in the CNS [16]. This effect produces excitotoxic neuronal destruction and neuroimmune inflammation causing central macrophage activation [17]. All the process of central sensitization is also accompanied by alterations in gene expression resulting in changes in function and synaptic connections in the spinal cord [18].
Interestingly, changes derived by this phenomenon are not limited to the spinal cord. Important alterations in the cortex gray matter and descending systems have also been documented [17].
While mechanisms of peripheral and central sensitization are initially physiologic and protective, under unknown conditions, they become maladaptive and deleterious. The transition is complex and not completely understood. From clinical and epidemiological studies, it is possible to observe that psychosocial and genetic factors have relevant roles in the occurrence of CPSP in an individual.
Clinically, CPSP can have both inflammatory and neuropathic characteristics. Usually, inflammatory symptoms (e.g., swelling, redness) decay over time and respond satisfactorily to NSAIDs. However, neuropathic component may persist for longer periods and is commonly refractory to regular analgesics [19].
Neuropathic pain is usually continuous, like a superficial burning sensation or painful cold. It is also described like paroxystic electric shock or very brief stabbing pain. The neuropathic pain could be spontaneous or elicited by light mechanical (friction, pressure) or thermal stimulation [20]. One of the cardinal manifestations of neuropathic pain is allodynia, in which a non-painful stimulus (e.g., touch) produces pain. A second manifestation is known as secondary hyperalgesia, in which an increase in pain sensitivity occurs in non-injured areas beyond the area of initial injury [21]. In the clinical setting in a patient who is suspected to suffer from CPSP, all these clinical features should be related with the surgical area or scar.
25.4 Factors Associated with CPSP in Children
It is obvious that only a fraction of patients develop CPSP after surgery. However, there is no clear way to know what patient in what situation will evolve with CPSP. In this regard, available literature has highlighted some risk factors for developing CPSP. Since the majority of the information is provided from studies performed in adults, the interpretation of these data in the context of child care should be done carefully.
Arbitrarily, it is possible to group the associated factors for developing CPSP into three main groups: surgical, psychosocial, and patient-related factors.
25.4.1 Surgical Factors
The following surgical factors are linked with an increased likelihood of developing CPSP: type of surgery (e.g., spine surgery, thoracotomy, amputation, etc.), increased duration of surgery, low surgical load in a specific surgery center, open surgeries (vs. video-assisted procedures), pericostal stitches, and evidence of nerve damage. Whether these factors are causally related to the development of CPSP is not completely known [16]. Nevertheless, it seems evident that there is a relation between the magnitude of injured tissues, the probability of nerve damage, and the occurrence of CPSP. As a result, adequate training in less invasive surgical techniques appears warranted. Avoiding an unnecessary surgery is always advisable.
25.4.2 Psychosocial Factors
Preoperative anxiety, post-traumatic stress disorder, introverted personality, pain catastrophizing, poor social support, and emotional numbness have been associated with CPSP or with chronic postsurgical disability in adults [22]. There are no clues to know whether these factors may have the same effect in children. However, it has been reported that anxiety 6 months after surgery is associated with the maintenance of pain after 12 months [7]. It is also interesting that parental catastrophizing scores 48–72 h after surgery can predict pain intensity in their children 12 months later [23]. Adolescents with idiopathic scoliosis who have greater expectations about changes in self-appearance before spine surgery report more pain and experienced less reduction in preoperative pain after surgery [14]. Those findings stand out the intimate relationship between the effect of the psychological “environment” during perioperative period and the occurrence of persistent pain after surgery. The role of eventual psychological interventions or therapies in modifying CPSP remains to be elucidated.