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W2011796135 abstract "A 33-year-old woman with chronic and severe abdominal pain refractory to all prior treatments was referred by her primary care physician. She first developed recurrent episodes of abdominal pain at age 6 years, which led to school absences, and the frequency and severity of these episodes increased after menarche. At age 19 after traveling through Mexico, she developed an acute gastroenteritis with worsening abdominal pain, diarrhea, fever, and vomiting and was diagnosed to have irritable bowel syndrome (IBS). During the last 10 years the pain has become more frequent, and for the last 5 years the pain is constant and associated with abdominal bloating and constipation. Additional diagnoses include fibromyalgia and occasional migraine headaches treated with sumatriptan. Antispasmodics, protein pump inhibitors, gabapentin, and tegaserod were not helpful in relieving the pain. Diagnostic studies including 2 colonoscopies, an esophagogastroduodenoscopy, a computed tomography scan, capsule endoscopy, pelvic ultrasound, and abdominal magnetic resonance imaging were negative. An exploratory laparotomy 5 years earlier suggested endometriosis, leading to an unsuccessful trial of leuprolide acetate. She also had a cholecystectomy 3 years ago as a result of a low ejection fraction on hepato-iminodiacetic acid scan. The patient has had more than 30 emergency department visits during the last 10 years, where she usually receives IV morphine and promethazine and is discharged with a week's supply of oral narcotics, hydrocodone or oxycodone. Her family physician often needs to refill these prescriptions to prevent visits back to the emergency department. She has had 5 hospitalizations for the abdominal pain when emergency department treatments were unsuccessful. Her most recent hospitalization 1 month ago led to a second diagnostic laparotomy with negative findings. Postoperatively, increasing dosages of IV morphine sulfate up to 60 mg/day was required to treat the pain. Because of difficulty in relieving the pain and implementing a hospital discharge, a psychiatry consult was called. The consultant noted that the patient carries a diagnosis of major depression, with post-traumatic stress disorder resulting from an early childhood history of family conflict and deprivation and sexual and physical abuse. The parents divorced when she was 12. At age 16 the patient left home before finishing high school, and after becoming pregnant she married at age 17. After 4 years she left her spouse when he became physically abusive. The patient and her daughter are currently living with her mother. For the last 2 years she has been unable to work as a fast food clerk and is currently receiving disability payments. The psychiatrist recommended treatment with paroxetine 20 mg/day and follow-up at a local mental health center. She was discharged with paroxetine and also oxycodone 10 mg 3 times a day. On presentation, the patient is lying on her side on the examination table with hips flexed. She complains of severe cramping abdominal pain in the mid and lower abdomen with nausea. The physical exam is notable for her squinting in pain with mild palpation of the abdomen and a positive Carnett's test. She is asking to be hospitalized to find out the cause of the pain and to get IV medication to relieve it. Although the patient admits to having infrequent hard stools, there is no relationship of the pain to eating, defecation, menses, or physical activity. There is general agreement that for practicing gastroenterologists, this clinical presentation is often difficult to understand and one of the most challenging to manage. But here, diagnosis is not the problem; in fact, the risk is that some physicians not recognizing or accepting the diagnosis will pursue additional studies, still hoping to find some specific etiology possibly more responsive to treatment. The record shows that this patient's functional abdominal pain syndrome (FAPS) “breeds true” in its clinical features, and in fact although the disorder is relatively uncommon, it is well-recognized by gastroenterologists. The patient fits Rome III criteria for FAPS, with years of continuous abdominal pain that is not related to eating, defecation, or menses, and there is a loss of daily functioning. The multiple negative studies are confirmatory. Notably she has constipation, which is not a diagnostic feature of FAPS, and thus she also has Rome III criteria for a diagnosis of functional constipation and/or a complication of chronic narcotic use. Because the pain is not relieved by defecation, she does not have IBS. The physical examination can provide supportive evidence for the diagnosis by excluding other conditions. “Alarm signs” such as significant weight loss, an abdominal mass, or blood in the stool should prompt further investigation. However, these findings commonly occur with comorbid depression, inspissated stool in the colon, or hemorrhoids, respectively. Unlike acute pain, there is no autonomic arousal with abdominal palpation. Surgical scars indicating previous laparotomies might be present. The paradoxical “closed eyes” sign as seen with this patient occurs when the patient closes the eyes when the abdomen is palpated, thus communicating pain. In contrast, patients with acute pain are quite anxious and keep their eyes open. Abdominal wall pain must be excluded by using the Carnett's test. When present, the pain from palpation increases with raising the head and contracting the rectus abdominus muscle, whereas with visceral pain it decreases. As noted here, FAPS might also produce increased pain reporting, with abdominal wall contraction caused by central sensitization with viscerosomatic referral. If the examination is negative, no further diagnostic studies, particularly in view of the long history of negative testing, are indicated. Further testing only reinforces the concept that another diagnosis is being missed, and invasive studies might increase the risk of aggravating the visceral hypersensitivity. How can individuals encounter such severe and disabling pain in the absence of a structural diagnosis? With this patient there was a confluence of factors beginning early in life, which when taken together might have contributed to her current chronic pain condition. In recent years there has been considerable research evaluating brain-gut interactions, looking at peripheral measures such as intestinal inflammation and altered mucosal immune function and the central effects of stress on neural signaling, and this is beginning to help us understand this question. This patient's clinical presentation demonstrates the contribution of both central and peripheral factors, ultimately leading to her chronic pain. This patient has an early childhood history of recurrent episodes of pain (previously called recurrent abdominal pain in children or RAP), with worsening at the time of menses. Her symptoms became aggravated in a setting of family distress and emotional, physical, and sexual abuse. Additional factors include the history of postinfectious IBS, which develops usually after a bacterial enteric infection in a setting of psychological distress, and she also had several abdominal surgeries and invasive diagnostic procedures. Abdominal surgeries can lead to abdomen-pelvic nerve injury, and mucosal inflammation from infection can activate mucosal mast cells and other immune cells, which can secrete proteases, cytokines, and other mediators, which in turn activate sensory neurons and contribute to visceral hypersensitivity. In addition, the history of abuse might amplify pain as a result of activation of certain brain regions such as the mid-cingulate cortex that leads to disinhibition, an inability to down-regulate incoming sensory input from the viscera. Even in the absence of an abuse history, it is likely that the combination of pain associated with noxious experiences can encode the linkage of emotional distress with the pain in regions like the mid-cingulate. A simple example might be a young child having a difficult experience in the dentist's office, and later in life that distressing retained memory leads to continued difficult painful experiences at the dentist's office. With chronic and severe pain, peripheral contributing factors such as visceral hypersensitivity become secondary to central sensitization, the alteration of central pain control centers as is evident with this patient. Here, management strategies must shift to centrally targeted treatments. The patient's condition is complicated by the development of narcotic bowel syndrome. This is another commonly recognized, although not often diagnosed, condition characterized by chronic or frequently recurring abdominal pain associated with escalating dosages of narcotics. Although more often seen in patients with functional gastrointestinal disorders, this condition can also develop in patients with structural disorders in which the nature and severity of the pain are not explained by the evident disease pathology. Continued use of narcotics over time leads to a progression in the frequency, duration, and intensity of the pain episodes. Recent studies suggest that chronic narcotic use paradoxically produces visceral hyperalgesia caused by activation of excitatory antianalgesic pathways in the opioid regulatory system, descending facilitation of pain at the rostral ventral medulla, and dorsal horn glial cell activation that produces morphine tolerance via inflammatory effects. Thus, the combination of early childhood trauma with ongoing stress, gastrointestinal infection leading to postinfectious IBS, multiple operations and procedures, and the escalating use of narcotics are together generative of the increased frequency and severity of pain episodes that eventually lead to a chronic and refractory pain condition. Table 1 lists the criteria for FAPS and narcotic bowel syndrome.Table 1Diagnostic CriteriaFAPSaFrom Clouse RE, Mayer EA, Aziz Q, et al. Functional abdominal pain syndrome. Gastroenterology 2006;130:1492–1497. Presence for at least 3 months, with onset at least 6 months before diagnosis of: 1Continuous or nearly continuous abdominal pain; and 2No or only occasional relationship of pain with physiologic events (eg, eating, defecation, or menses); and 3Some loss of daily functioning; and 4The pain is not feigned (eg, malingering); and 5Insufficient symptoms to meet criteria for another disorder of gastrointestinal function that would explain the pain.Narcotic bowel syndromebFrom Grunkemeier DMS, Cassara JE, Dalton CB, Drossman DA. The narcotic bowel syndrome: clinical features, pathophysiology and management. Clin Gastroenterol Hepatol 2007;5:1126–1139. Chronic or frequently recurring abdominal pain that is treated with acute high-dose or chronic narcotics and all of the following: 1There is marked worsening of pain when the narcotic dose wanes and improvement when narcotics are reinstituted (“soar and crash”). 2There is a progression of the frequency, duration, and intensity of pain episodes. 3The nature and intensity of the pain are not explained by a current or previous gastrointestinal diagnosis.a From Clouse RE, Mayer EA, Aziz Q, et al. Functional abdominal pain syndrome. Gastroenterology 2006;130:1492–1497.b From Grunkemeier DMS, Cassara JE, Dalton CB, Drossman DA. The narcotic bowel syndrome: clinical features, pathophysiology and management. Clin Gastroenterol Hepatol 2007;5:1126–1139. Open table in a new tab The cornerstone of management depends on an effective physician-patient relationship. Clinicians might feel challenged in the least, frustrated, or even angry when caring for patients with chronic and painful disorders; that is understandable. The diagnosis might seem uncertain, and some physicians feel less capable than when treating a structural diagnosis, although this might be more perception than reality. The patient's lack of improvement might be perceived as a personal failure to not find the proper treatment. The patient's urgent requests for pain relief might create personal conflict as to whether to prescribe narcotics for a nonmalignant condition. Furthermore, there are also pressures relating to time and low reimbursement rates, particularly when diagnostic procedures appropriately are not ordered. Thus, it is important for the treating physician to first treat himself or herself: (1) accept that these are positive diagnoses and that further studies are not needed, (2) recognize their chronicity and reduce expectations for cure or rapid recovery, (3) understand that the physician's role for these disorders is to provide support, guidance, and hope while facilitating the patient's acceptance of this as a chronic disorder that requires personal responsibility for the management. Table 2 lists some features that lead to a more effective physician-patient relationship when caring for patients with FAPS.Table 2Guidelines to Enhance the Physician-Patient RelationshipListen actively Focus on the patient's world, ie, “Sit where the patient sits” Allow the patient to tell his/her story without interruption Seek to understand the symptom experience within a biopsychosocial contextIdentify and respond to the patient's concerns and expectations What do you think is going on? What are your worries and concerns? What are your expectations from me?Validate the patient and illness Acknowledge the pain Acknowledge the impact of the illness Provide a physiologic explanation for the symptomsSet realistic and consistent limits when ordering tests “Don't just do something, stand there” Order tests on the basis of objective data rather than pain severityPsychosocial assessment Why is the patient coming now? Is there a history of traumatic life events? What is the impact of the pain on quality of life? What is the role of family or culture? What are the patient's psychosocial resources?Help the patient take on responsibility for the care Involve patient in treatment options “How are you managing with your pain?” rather than “How is your pain?”Provide some continuity of care (along with primary care provider) Open table in a new tab As with this patient, when the FAPS is complicated by narcotic bowel syndrome, the narcotics must first be discontinued. Usually this can occur on an outpatient basis. However, inpatient withdrawal might be considered if the narcotic usage is high, and there are secondary effects like ileus, pseudo-obstruction, or electrolyte imbalances, or if there is limited patient motivation or family support. The time frame of the withdrawal is influenced by the duration of the narcotic usage and the dosage. In general, withdrawal can occur between several days to 2 or 3 weeks. A general guideline is to start a tricyclic antidepressant (TCA) or serotonin-norepinephrine reuptake inhibitor (SNRI) at least several days before withdrawal begins. When instituting the withdrawal, the patient should be covered with the maximal dose of a medium- to long-acting narcotic to achieve comfort, usually the dose chronically or currently being used. This dosage is then decreased by 10%–33% and is given in equally divided daily dosages. It is given in a noncontingent fashion rather than as circumstances might require to prevent acute withdrawal and to avoid urgent requests for medication. Short-acting agents (eg, oxycodone) should be converted to equivalent dosages of longer-acting agents to avoid the “soar-crash” effect of rapid withdrawal. A medium-acting benzodiazepine (eg, lorazepam, 1 mg every 6–8 hours) is started at the time of the withdrawal protocol to reduce anxiety. In addition, clonidine, an α2-adrenergic receptor agonist that blocks the physiologic effects of narcotic withdrawal, is added in doses of 0.1–0.6 mg in divided dosages toward the end of the taper. It might be continued for several days after the withdrawal. It is possible that withdrawal of the narcotic will reduce or eliminate the constipation. If not, polyethylene glycol solution can be used as an osmotic laxative, or lubiprostone, a newer agent that acts on chloride channels to increase secretion, might be prescribed. If there is evidence for pelvic floor emptying difficulties (eg, excessive straining or manual manipulation to empty stool), an anorectal motility study with consideration of biofeedback treatment is indicated. The TCAs (eg, desipramine, nortriptyline, amitriptyline) or the new SNRIs (duloxetine, venlafaxine) are of particular value in treating chronic pain syndromes because of their combined noradrenergic and serotonergic effects. These agents have generally been more successful than selective serotonin reuptake inhibitors (SSRIs), although there are insufficient data with this class of agents to say this with certainty. However, with this patient it is reasonable to reduce or discontinue the paroxetine and switch to or add low dosages of either the TCA or SNRI. To assure treatment adherence, the physician needs to clarify to the patient that these are “central analgesics,” not simply drugs for psychiatric conditions; they have independent effects on pain and can be used in lower dosages than used to treat major depression. Thus, 25–75 mg desipramine or 30 mg duloxetine can be initiated and increased to full dosages if needed, particularly when depression is also present. It usually helps to use diagrams or to otherwise explain to the patient the physiologic basis for treatment: to facilitate descending inhibitory pathways that block afferent visceral conduction. In addition, patients need to be informed that these are not “mind altering,” are not addicting, and can be stopped without major withdrawal effects if needed. Patients might need to stay on these medications indefinitely. Gabapentin and pregabalin are increasingly being prescribed for chronic neuropathic pain conditions including peripheral neuropathies and, more recently, fibromyalgia. Their benefit for visceral or central pain syndromes is not established, although a few case reports have suggested benefit for visceral pain. Long-term treatment with benzodiazepines is not recommended because of their abuse potential and their tendency to interact with other medications. Within psychiatry, patients who are refractory to usual dosages of antidepressants receive additional medications to augment the clinical effect, because they act on different neuroreceptors. Buspirone, a non-benzodiazepine azapirone with antianxiety properties, might enhance the analgesic effect of antidepressants. This is based on clinical experience in our clinic, and no studies have yet been published on this treatment combination. Recently, we have used a low-dose atypical antipsychotic agent (eg, quetiapine 25–100 mg) that acts on dopamine receptors for augmenting treatment in our patients with chronic pain syndromes. This class of agents has antianxiety and sleep benefits and might also have independent analgesic effects. Preliminary data from our clinic show that about 50% of patients with chronic and severe FAPS who previously failed antidepressants and who are prescribed quetiapine with an antidepressant stay on it, and most of those who do achieve some benefit. This agent is not yet approved for this medical condition, and monitoring must be done for side effects such as metabolic syndrome and rarely, liver toxicity or extrapyramidal signs. No psychological treatment has been studied with FAPS. However, studies showing benefit in a wide variety of other painful conditions including IBS, migraines, and fibromyalgia suggest they are also likely to be beneficial for FAPS. Cognitive-behavioral therapy identifies maladaptive thoughts, perceptions, and behaviors and is used to develop new ways to increase symptom control. Stress management attempts to counteract the physiologic effects of stress or anxiety. Hypnosis and dynamic psychotherapy have been used primarily for IBS but also might have theoretical benefit. On the basis of the literature in IBS, these treatments might not improve the pain as much as the patient's adaptation to the pain and increased coping strategies (“The pain is still there but it doesn't bother me as much”). Critical to implementing psychological treatment is that the referring physician must help the patient accept the value of these treatments as part of their ongoing plan of care. Figure 1 offers a treatment algorithm for FAPS on the basis of the above guidelines. Beginning with an effective patient-physician relationship, treatments are added on the basis of the severity of the symptoms. Constipation if present is treated, and narcotics if present are withdrawn. Next the clinician will likely prescribe a low-dose TCA or SNRI, and after 4–6 weeks this dosage can be increased while monitoring for clinical benefit and side effects. If this is unsuccessful, psychiatric referral should be considered for augmentation treatment with another antidepressant (eg, SSRI, bupropion), buspirone, or an atypical antipsychotic. On occasion, the patient might first be referred to a mental health counselor for psychological treatment. However, with more severe symptoms, combined pharmacologic and behavioral intervention is needed. FAPS is a recently established diagnosis, and emerging evidence suggests that the genesis of the symptoms is more centrally than viscerally determined. Brain-gut research is beginning to understand the mechanisms for the association of psychosocial trauma and stress with pain regulation, and future studies are needed to clarify these associations. Clinical trials have not yet been targeted to this diagnostic entity, so most of our knowledge of treatment relates to other chronic pain disorders (including somatic pain syndromes) or IBS. Furthermore, clinical trials are conducted with single agents, yet FAPS often requires multiple medications along with psychological interventions to reframe patient expectations and establish coping strategies. Drug trials last 8–12 weeks, which might be a long enough period to understand whether long-term benefits can occur with these chronic disorders. In addition, longer antidepressant treatment trials are now being used in psychiatry for post-traumatic stress disorder and major depression to determine their effects on relapse prevention (ie, longer treatments might cause neuroplastic changes that “normalize” brain neurons and prolong remission). Similar long-term studies are needed to determine whether chronic pain can similarly be ameliorated. The physician-patient relationship might be the key to treatment success, yet there is no financial support from federal agencies or pharmaceutical companies to support studies in this area. Efforts to train physicians on communication and patient relationship skills are needed. Finally, even though “quality time” with patients has been shown to increase patient satisfaction, adherence to treatment, and the clinical outcome, insurance reimbursement is inadequate relative to that obtained by ordering additional procedures, and that is counterintuitive and contraindicated for patients with FAPS. In sum, the existing studies do not replicate the chronic, multiple needs of patients with FAPS or severe functional gastrointestinal disorders. Future studies will require the evaluation of multicomponent treatments (eg, the common combination of psychotherapy and pharmacotherapy) and physician treatment behaviors. FAPS is diagnosed according to the Rome III criteria, which endorse a biopsychosocial approach to the understanding of this disorder and the care of the patients. No other guidelines exist. However, the recommended treatment strategies are similar to other chronic pain disorders where similar guidelines exist. Evidence-based reviews and treatment recommendations for related gastrointestinal disorders like IBS are not necessarily appropriate, given that FAPS symptoms are generated primarily by central rather than peripheral (ie, visceral) processes. Finally, guidelines for narcotic bowel syndrome do not exist, although published recommendations from one center that receives referrals to treat these disorders are referenced below. Physicians need to accept a biopsychosocial understanding of FAPS and the care of patients having this disorder, because traditional disease-based strategies are ineffective. Diagnosis is based on Rome III criteria, with minimization of diagnostic testing. Treatment is based on an effective physician-patient relationship that takes into account the biologic and psychosocial determinants of the condition. A graded multicomponent treatment strategy that includes one or more centrally acting pharmacologic agents and behavioral interventions with ongoing care is recommended for maximal benefit." @default.
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W2011796135 title "Severe and Refractory Chronic Abdominal Pain: Treatment Strategies" @default.
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