Pelvic and abdominal pain is a common diagnostic and management dilemma that spans a wide diversity of clinical settings. One of the most significant challenges in the diagnosis and management of these conditions is the lack of consensus for diagnostic criteria.
Pelvic pain refers to pain primarily in the anatomic pelvis, anterior abdominal wall at or below the umbilicus. It is a common presenting symptom in women and, occasionally, in men, both as an acute or a chronic symptom. Chronic pelvic pain is noncyclic pain of a duration of at least 6 months in the pelvis, anterior abdominal wall at or below umbilicus, lumbosacral back, or buttock that is severe enough to cause functional disability requiring medical evaluation.
Abdominal pain is a generic term for focal or general discomfort localized to the abdominal region. Recurrent abdominal pain is defined as at least three separate episodes of abdominal pain that occur in a 3-month period. Despite recent technologic advances, the diagnosis and treatment of chronic, recurrent abdominal pain has remained a challenge.
Pain is a subjective sensation that patients often find difficult to describe. In contrast to other areas of the body, the abdominal and pelvic organs have a poorly developed sensory system, which contributes to the patients’ difficulty in describing and localizing the pain.
Both pelvic and abdominal pain can be of visceral or somatic etiology.
Visceral pain results from activation of visceral nociceptors. Visceral structures are highly sensitive to stretch, distension, ischemia, and inflammation but are relatively insensitive to other stimuli such as cutting or burning. Visceral pain is diffuse, poorly localized, often referred to other structures, and associated with autonomic and somatosensory reflexes and strong negative affective symptoms.
Visceral abdominal pain is transmitted from nociceptors found on the walls of the abdominal viscera via sympathetic (thoracic branches and lumbar splanchnic nerves synapsing in subsidiary plexuses: celiac, splenic, hepatic, aorticorenal, superior mesenteric, adrenal) and parasympathetic (vagus and nervi erigentes S2–4; motor and sensory) pathways. Visceral nociceptors are polymodal—activated by mechanical, thermal, and chemical stimuli—and sensitize after tissue insult. Some visceral nociceptors are silent, which can be recruited in certain disease states like inflammation. Visceral pain is nonspecific because of wide divergence and a relatively small number of afferent fibers innervating a large area with extensive ramifications. Patients usually have difficulty localizing the source of pain and will describe it as aching, cramping, or burning that fluctuates in intensity. Visceral pain usually is paroxysmal, colicky, deep, squeezing, and diffuse, and it may be referred to other structures. Functional visceral disorders like irritable bowel disorders and functional dyspepsia are characterized by hypersensitivity, often in the absence of pathological explanation for the discomfort and pain.
Viscero-somatic convergence and viscero-visceral convergence of sensory pathways play an important role in the manifestation of acute and chronic visceral pain syndromes.
The phenomenon of referred pain is secondary to viscero-somatic convergence, which is the convergence of visceral afferent nerve fibers entering the spinal cord at the same level as the superficial, somatic structures entering the spinal cord.
Visceral pain syndromes affecting different organ systems often coexist due to viscero-visceral convergence—that is, a visceral afferent from different organs converging on the same spinal segments. Cross-organ sensitization between the lower gut and pelvic gynecologic and urinary organs leads to a major challenge in the diagnosis and clinical management of abdominal and pelvic pain. Patients with functional bowel disorders often also complain of pelvic pain or symptoms consistent with interstitial cystitis. Conversely, many patients with interstitial cystitis also suffer from functional bowel disorders. Both peripheral and central mechanisms are involved in the generation and maintenance of cross-organ sensitization.
CLASSIFICATION OF PELVIC PAIN
Pelvic pain has a number of classifications (Table 44-1).
Classifications of Pelvic Pain
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Classifications of Pelvic Pain
Approximately 9 million women in the United States have pelvic pain: 10% of all gynecologic office visits are for pelvic pain; 44% of all gynecologic laparoscopies and 10% to 15% of hysterectomies are for chronic pelvic pain; 30% of women presenting to a pain clinic have already undergone hysterectomy. The male pelvic pain syndrome comprises 8% of all urologic visits and 1% of all visits to primary care physicians.
The economic impact is enormous, with medical costs of $1.2 billion per year and missed work and productivity totaling more than $15 billion per year.1,2
Any discussion of pelvic pain requires an appreciation of the spatial relations of the pelvic viscera, along with their vascular supply and innervations.
The bony pelvis serves as the wall of the pelvis, and the pelvic diaphragm acts as its floor. The pelvis is lined by an intricate vascular tree and traversed by sympathetic and parasympathetic afferent, visceral afferent, and efferent nerves from the lumbar and sacral plexus.
The bony pelvis includes two hip bones formed from the fusion of the ischium, ilium and pubis, sacrum, and coccyx. The two innominate bones form the sides of the pelvis. They are joined in front at the symphysis pubis and articulate with the sacrum and coccyx in back.
The pelvis is divided into a major pelvis and a minor pelvis and is separated by the pelvic brim, which also serves as the boundary between the abdominal and pelvic cavities (Fig. 44-1). The pelvis contains the bladder and the paravesical fossae anteriorly, the rectum and the para-rectal fossae posteriorly, and the internal genital organs in the middle (Fig. 44-2).
Anatomy of the bony pelvis.
Peritoneal relationships in the female. (Reproduced with permission from Hinman F Jr. Atlas of Urosurgical Anatomy. Philadelphia, Pa: WB Saunders, 1993.)
The pelvic diaphragm, or floor of the pelvis, arises anteriorly from the body of the pubis and continues posteriorly to the coccyx. It includes the levator ani muscles and the coccygeus muscles, holds the lower part of the rectum, and supports the bladder and vagina or prostate by maintaining sufficient intraabdominal pressure. Beneath the diaphragm is the perineum, with the external genitalia.
The pelvic vasculature resembles a woven lining composed of large, thin-walled veins through which the arteries thread their way.
The veins are divided into vesicle, uterine and vaginal or prostatic, and rectal venous plexuses, which drain into the internal iliac vein and into the inferior mesenteric veins via the superior rectal (hemorrhoidal) vein, eventually reaching the portal vein. The middle rectal vein emerges from the lower part of the side of the rectum, passes to the internal iliac vein, and anastomoses with the superior and inferior rectal veins and with the other plexuses of pelvic veins (Fig. 44-3).
Veins of female pelvis. (Reproduced with permission from Hinman F Jr. Atlas of Urosurgical Anatomy. Philadelphia, Pa: WB Saunders, 1993.)
The arteries of the pelvis arise from the internal iliac artery, which runs retroperitoneally, is posterior to the ureter, and is divided into anterior and posterior divisions. The anterior division has seven branches, and the posterior division has three. Collateral circulation is abundant (Fig. 44-4).
Internal iliac (hypogastric) artery branches into anterior and posterior division. Superior gluteal artery passes through superior portion of greater sciatic foramen. Inferior gluteal artery enters foramen below piriformis muscle. Inferior gluteal artery gives off superior and inferior vesical arteries and obturator artery before entering foramen. (Two unpaired arteries in the pelvis, the median sacral and superior rectal, are not shown.) All these arteries enter the pelvis extraperitoneally and may be ligated with impunity. (Modified from Skandalakis LJ, Gadacz TR, Mansberger AR Jr, Mitchell WE Jr, Colborn GL, Skandalakis JE. Modern Hernia Repair. Pearl River, NY: Parthenon, 1996; with permission.)
The major afferent pathways for nociception from the female pelvic organs travel with the sympathetic nerve bundles and have cell bodies in the thoracolumbar distribution.
The suprapubic region is innervated by the iliohypogastric nerve (L1, L2). The inguinal area and the base of scrotum or labia are supplied by the ilioinguinal nerve (L1, L2). The skin of the penis is supplied by the two dorsal nerves of the penis, which are branches of pudendal nerves. The skin of the scrotum and perineal skin are supplied by the posterior scrotal nerves (S2, S3, and S4). The skin between the anus and coccyx is innervated by the lower sacral and coccygeal plexus. The lower third of the vagina is supplied by the pudendal nerve. The genital branch of the genitofemoral nerve supplies the lateral side of the scrotum, the vulva, and the cremasteric muscles (Fig. 44-5).
Formation of lumbosacral trunk and further formation of sciatic and pudendal nerves (highly diagrammatic).
There are sympathetic, parasympathetic, and visceral somatic afferent nerves to the pelvic viscera. The sympathetic nerves cause muscular contraction and vasoconstriction, whereas the parasympathetic nerves cause relaxation and vasodilation.
Most of the autonomic fibers enter the pelvis through the superior hypogastric plexus, which is located bilaterally at the lower third of the fifth vertebral body and the upper third of the first sacral vertebra at the sacral promontory. This plexus is primarily sympathetic and is formed by the confluence of lumbar sympathetic chains and branches of the aortic plexus containing fibers that traverse the celiac and inferior mesenteric plexus. The superior hypogastric plexus divides into the right and the left hypogastric nerves, which descend laterally to the sigmoid colon to reach the inferior hypogastric plexus.
The inferior hypogastric plexus is located against the inside of the pelvis, lateral to the uterovaginal junction and the rectum. It is the major neuronal integrative center in the pelvis. It innervates multiple pelvic organs, including the urinary bladder, proximal urethra, distal ureter, rectum, and internal anal sphincter, as well as genital and reproductive structures via communication through the uterovaginal plexus and the vesical and the inferior rectal plexus.
The parasympathetic nerves, which are branches of anterior rami of the S2, S3, and S4 nerve roots, traverse the inferior hypogastric plexus, in contrast to the superior hypogastric plexus, which is situated predominantly in the extending tissue postero-anteriorly and parallel to the pelvic floor. The location and configuration of the inferior hypogastric plexus does not lend itself to surgical or chemical extirpation (Fig. 44-6).
Neuroanatomy of visceral pelvic pain. (Reproduced with permission from Boscher H. Blockade of the superior hypogastric plexus block for pelvic pain. Pain Practice 2001; 1:165.)
The sensory nerves from the uterus accompany the sympathetic nerves and enter the spinal cord at the T11 and T12 level, and refer pain to the abdomen. The S2, S3, and S4 afferents from the cervix are referred to the lower back and lumbosacral area.1,2
The ganglion impar (also known as the ganglion of Walther) is a solitary retroperitoneal structure located at the level of the sacrococcygeal junction that marks the termination of the paired paravertebral chains. It receives fibers from the lumbar and sacral portions of the sympathetic and parasympathetic nervous system and provides sympathetic innervation to portions of the perineum, rectum, and genitalia.
Acute pelvic pain refers to pelvic pain that has been present for less than 6 months. It is caused by structural disruption or physiologic dysfunction. The etiology of acute pelvic pain is presented in Table 44-2.
Differential Diagnosis of Acute Pelvic Pain
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Differential Diagnosis of Acute Pelvic Pain
Complications of pregnancy
Ovarian and adnexal torsion
Pelvic inflammatory diseases
Ninety-eight percent of women with ectopic pregnancy experience unilateral pain, which may be accompanied by light or missed menses. Symptoms of pregnancy such as nausea and breast tenderness may be present.3
The pain of ovarian cysts may be dull and aching, localized to the side of the abscess, and accompanied by pelvic tenderness. An ovarian cyst with a twisted pedicle can cause acute pain, which becomes intermittent when the pedicle untwists. Other symptoms include nausea and vomiting, diarrhea or constipation, and leukocytosis.
Symptoms of a palpable mass, delayed menses, and pelvic tenderness also occur with corpus luteum cysts, which can bleed into the peritoneum and mimic pelvic inflammatory disease.
Pelvic inflammatory disease (PID) is defined as a spectrum of upper genital tract inflammatory disorders that may include endometritis, salpingitis, tubo-overian abscess, and pelvic peritonitis. The diagnosis should not be considered conclusive without a positive cervical culture. The primary pathogens are Neisseria gonorrhea and Chlamydia trachomatis. Cervical cultures for Chlamydia can detect up to 80% of cervical infections, and antibody testing, enzyme-linked immunosorbent assay, and DNA probe testing can detect 60% to 90% of infections. Because of this wide range in positive findings, specimen cultures from the urethra and anus should also be considered.
Tubo-ovarian abscesses may occur as a complication of PID, in postpartum and postoperative patients, and in women with implanted intrauterine devices. Bacteria present in tubo-ovarian abscesses occur in the lower genital tract and may not be the same agents involved in PID.4
Pelvic pain is considered chronic when it has been present for at least six months. It may initially be an acute episode, transition into episodic pain, and then persist for 6 months or longer. Several causes for chronic pelvic pain exist on both female and male patients.
Female Chronic Pelvic Pain
Differential Diagnosis of Female Chronic Pelvic Pain
Ovarian remnant syndrome
Primary and secondary dysmenorrhea
Pelvic congestion syndrome
Sympathetic pelvic syndrome
Irritable bowel syndrome
Inflammatory bowel disease
Interstitial cystitis/painful bladder syndrome
Musculoskeletal and myofascial pain
Chronic pelvic pain without obvious pathology
Psychogenic pelvic pain
Endometriosis is the presence of ectopic endometrial glands and stroma outside the uterine cavity. In addition to persistent pelvic pain, patients with endometriosis may have dysmenorrhea, dyspareunia, back pain, and rectal discomfort. The symptoms are related to the site of the endometrial implant. However, the intensity of the pain may not correlate with the size of the implant.5 The incidence of endometriosis is 1% to 2% of the general female population and 15% to 25% of infertile women. Some patients may remain asymptomatic until they are evaluated for infertility. Definitive diagnosis can only be made by gynecologic laparoscopy, although elevated serum CA-125 levels correlate with severity and reflect the course of the disease. Treatment includes medical and surgical options. Medical options include oral contraceptives, Medroxy-progesterone acetate, danazol, and gonadotrophin-releasing analogues. The goals of surgery are to restore normal pelvic anatomy and to resect, coagulate, or vaporize all endometrial implants.
Adenomyosis is a benign invasion of the wall of the uterus by endometrial tissue. Most patients are 35 to 50 years of age and have had a prior pregnancy. Additional presenting symptoms include dysmenorrhea and menorrhagia.
Uterine leiomyomas (fibroids) are painful when they press on, or become entangled in, other structures and cause discomfort when they grow. Dyspareunia, dysmenorrhea, and pelvic pressure are frequent symptoms, along with intermenstrual, postmenstrual, and heavy menstrual bleeding. A degenerating leiomyoma may cause only episodic pain in the initial phase and then cause fever, increased pain, and leukocytosis with a left shift in the later phase. Leaking purulent material can cause peritonitis. Leiomyomas undergo malignant transformation in 2 to 3 per 100,000 women, but grow slowly. Surgical intervention is typically utilized in the management of heavy bleeding, growths of large size, and additional symptoms.6
Cervical cancer may be a cause of pelvic pain as it metastasizes. Ovarian cancer may be asymptomatic until later stages, after which it causes vague and nonspecific symptoms. In 90% of cases, endometrial cancer presents with vaginal bleeding or discharge. Pelvic pressure or discomfort occurs from uterine enlargement and then spread of the tumor into extrauterine structures. Any tumor that compresses the bladder or rectum can cause pressure, pain, or dyspareunia.7
Women with ovarian remnant syndrome present with unilateral constant or cyclical pain, postcoital ache, postmicturition pain, or postdefecation pain. Patients may have a history of removal of one or both residual ovaries for pain associated with pelvic adhesions or endometriosis. Although localized abdominal pain is a constant feature of the syndrome, no mass is often found on pelvic examination. Ultrasound examination is usually diagnostic, revealing a mass that must be distinguished from accessory ovaries, an embryologic variant of normal development. Treatment is surgical removal of the remnant.8
Primary and Secondary Dysmenorrhea
Women with major gynecologic diseases can have pelvic pain in the form of dysmenorrhea. This term is applied to severe cramping in the lower abdomen, lower back, and upper thighs that occurs during menstruation. Primary dysmenorrhea is the most prevalent source of chronic episodic pain in premenopausal women. It is primarily caused by prostaglandin release from the endometrium at menses, in particular prostaglandins F2 alpha and E2. Cramping pelvic pain is often accompanied by nausea, vomiting, headache, diarrhea, and fatigue. Secondary dysmenorrhea and atypical cyclic pain are caused by underlying intrauterine or extrauterine pathology, such as endometriosis, adenomyosis, and other pathology that alters blood flow, increases pressure, or causes irritation of the pelvic organs.
The treatment of primary dysmenorrhea includes nonsteroidal anti-inflammatory drugs (NSAIDs) and oral contraceptive pills. NSAIDs are effective in up to 80% of cases. Other modes of menstrual hormonal suppression are recommended for patients who obtain no relief with NSAIDs and oral contraceptives. Secondary dysmenorrhea requires a thorough evaluation and treatment of the underlying cause.
Premenstrual syndrome (PMS) includes mood, behavioral, and physical changes that occur during the luteal phase of most menstrual cycles. Studies suggest that about one-third of premenopausal women experience some degree of PMS. As in the treatment of dysmenorrhea, underlying illnesses, such as endometriosis and leiomyomas, should be ruled out. Treatment includes NSAIDs for pain, diuretics such as spironolactone for fluid retention, and antidepressants for dysphoria.
Pelvic Congestion Syndrome
Pelvic congestion syndrome is usually seen in premenopausal women, thus suggesting that there are hormonal factors involved in pelvic venous dilation.9 The capacity of pelvic veins to increase in size 60-fold by the end of pregnancy makes them, in the nonpregnant state, vulnerable to chronic dilation and stasis. Weakened fascial support during parturition and the vasodilating effects of cyclically fluctuating hormones augment the tendency to dilation.10 The most common symptom is a dull, aching pain in the pelvic area that worsens on standing, walking, and lifting and is relieved by lying down. Deep dyspareunia is one of the most consistent symptoms of pelvic congestion syndrome, with an incidence ranging from 71% to 78%. The severity of the pain is determined by the extent of the venous stasis, which leads to hypoxemia and local tissue damage followed by the release of pain-producing substances. The presence of dilated veins in the infundibulo pelvic ligament, ovarian hilum, or broad ligament—combined with polycystic changes in the ovary, which may be apparent only on close inspection—is diagnostic of pelvic congestion. Imaging via ultrasound and computed tomography is important for identifying polycystic changes in the ovaries and dilated veins in the broad ligament and uterus. Medical therapy consists of oral contraceptives to suppress ovarian function and intermittent courses of anti-inflammatory agents and antibiotics when inflammation occurs secondary to local infection.11 Surgical management includes hysterectomy and ligation of the ovarian vein. Radiologic transcatheter embolization of the ovarian veins has been used with varying success.
Sympathetic Pelvic Syndrome
Sympathetic pelvic syndrome is assumed to be secondary to visceral illness being transmitted to a corresponding cutaneous region. The area of innervation includes the cervix and vagina (with innervation from the pudendal nerves, having derivation from S2 through S4), along with the uterus, fallopian tubes, and ovaries (with innervation from the sympathetic pelvic branches of T10 through T12). Repeat local anesthetic sympathetic nerve blocks are recommended in addition to the medications used in patients with chronic pain.
Another chronic pelvic pain syndrome is focal vulvitis, characterized by burning vulvar pain and superficial dyspareunia. One study found that a majority of patients continued to have symptoms of vulvitis after Woodruff perineoplasty. The authors concluded that surgery was not the best treatment. They noted that these women often had insufficient lubrication or hypertonia of the pelvic floor, or both, during sexual intercourse. Thus, an integrated approach was recommended, including protection of the vulvar skin, relaxation of pelvic muscles, and treatment of psychosexual and relational aspects of the disorder.12
One study of women with chronic pelvic pain found that more than 75% had irritable bowel syndrome. Among women referred to a gynecologic clinic for dysmenorrhea, dyspareunia, and abdominal pain, half had significantly more symptoms of irritable bowel syndrome than did those referred for symptoms other than pain. Irritable bowel syndrome is a functional bowel disorder of uncertain etiology characterized by a chronic relapsing pattern of abdomino pelvic pain and bowel dysfunction with constipation or diarrhea, or both. It affects 10% to 15% of the population. Symptoms include abdominal pain, bloating, belching, excessive flatus, diarrhea and constipation, passage of mucus, and painful defecation with a sense of incomplete evacuation. Symptoms are often worse during periods of increased stress—and the premenstrual phase of the cycle—and may accompany anxiety and depression.
The pathophysiology of irritable bowel syndrome is multifactorial, involving altered bowel motility, visceral hypersensitivity, intestinal inflammation, alteration in gut flora, and genetic and psychosocial factors. Other contributing factors include diet and prior infection. Therapeutic options range from education, reassurance, dietary modifications, psychotherapy, and hypnotherapy to adjunctive pharmacological agents, which include antidepressants, antispasmodics, 5 hydroxytryptamine (serotonin) receptor 4 agonists for constipation, 5 hydroxytryptamine (serotonin) receptor 3 antagonists for diarrhea-prone irritable bowel syndrome, and probiotics.13 The diagnosis of irritable bowel syndrome is made by taking a careful history and by use of colonoscopy or barium enema to exclude other conditions.
Inflammatory Bowel Disease
Inflammatory bowel disease may manifest the same symptoms as irritable bowel syndrome. More than 50% of patients with Crohn's disease and ulcerative colitis present with abdominal and/or pelvic pain. Ulcerative colitis is a chronic inflammatory condition characterized by relapsing and remitting episodes of inflammation of the colonic mucosa, which invariably involves the rectum and extends proximally to the other portions of the colon. Crohn's disease is characterized by transmural inflammation and by skip lesions. About 90% of patients with Crohn's disease have bloody diarrhea, whereas patients with ulcerative colitis have moderate cramping that resolves with defecation. In one study, chronic pelvic pain was reported in 35% of patients with irritable bowel syndrome and in 13.8% of those with inflammatory bowel disease.14 Although the pathogenesis of inflammatory bowel disease remains unclear, a number of risk factors—including age, racial ethnicity, genetic susceptibility, smoking, dietary allergens, and infections of the gut with antibiotic use—have been identified.
At present, available therapies mainly rely on the control of inflammation and alleviation of abdominal pain. Pharmacotherapy is used in remission and exacerbations and the surgical options are used in severe cases. Pharmacotherapy includes aminosalicylates, corticosteroids, immunosuppressants, antibiotics, and biological agents targeted against certain inflammatory markers.15
Interstitial Cystitis/Painful Bladder Syndrome
Interstitial cystitis/painful bladder syndrome is a chronic, progressive, severely debilitating, heterogeneous syndrome that affects the urinary bladder. It is characterized by urgency, frequency, and pain. Its etiology is poorly understood; current hypotheses focus on occult or resistant microorganisms, urothelial hyper-permeability from a defective glycosaminoglycan mucus layer, neurogenic or hormonal dysfunction, mast cell activation, and genetic susceptibility as possible causative factors. The diagnosis is made clinically, by cystoscopy with hydro-distention, and sometimes by biopsy when other pathology has been excluded.16 This condition is underdiagnosed in women with pelvic pain. Symptoms of urinary frequency and urgency, dysuria, hematuria, and nocturia occur along with the pelvic pain. Patients have often been treated for recurrent urinary tract infections. Urinalysis results may be normal, but microscopic hematuria without white blood cells is sometimes noted. Patients must have at least two of the following symptoms: pain in the suprapubic, perineal, and urethral region; pain on bladder filling that is relieved by emptying; decreased compliance on cystometrogram; and glomerulations on endoscopy. When these criteria are not met, patients are considered to have urgency-frequency syndrome.
Treatment approaches include use of systemic agents, instillation therapy, and surgical management. Trials of systemic agents—including antihistamines, azathioprine, corticosteroids, Heparin, pentosan polysulfate, and tricyclic compounds—have shown inconsistent results. Dimethyl sulfoxide (DMSO) has been used for intravesical therapy, with varying response rates. Surgical treatments include urinary diversion procedures and augmentation cystoplasty. Denervation procedures are reserved for patients with severe, intractable disease. Hypogastric plexus blocks and neuromodulatory procedures have been used with some success.
Infectious cystitis manifests with symptoms of suprapubic pain, dysuria, and frequency and urgency, along with pyuria and a positive urine culture. These symptoms respond to antibiotics. In about 25% of women with irritant urinary symptoms and pyuria, C. trachomatis is found in the urethra. Urethral syndrome occurs when the urinary bacterial count is low, urinalysis is negative, and Chlamydia is negative. The etiology of this syndrome is unclear, but it may be caused by chronic inflammation of the peri-urethral glands or urethral spasticity with peri-urethral muscle fatigue. Treatment is similar to that of interstitial cystitis and urgency-frequency syndrome and consists of a combination of medication, biofeedback, and reeducation of voiding habits.17
Musculoskeletal and Myofascial Pain
Evolving lumbar disk disease and intradural neoplasms in the upper lumbar spine produce symptoms that may be interpreted as pelvic pain. Symptoms consistent with radiculopathy occur late in the course of these diseases. Musculoskeletal pain can be the result of decreased abdominal and pelvic muscle strength, decreased range of motion of the hip, and limb-length discrepancy. Trigger points for this pain may be near surgical incisions.
Surgical procedures can lead to significant postoperative pain that develops months to years afterward. An example is the Pfannenstiel incision, a horizontal incision across the lower pelvis, which can lead to pulling along the pathway of the ilioinguinal and iliohypogastric nerves. The stretching and trauma arising from labor and delivery also can lead to pelvic pain from the lower pelvis, although it may be experienced as visceral in origin.18 Pelvic pain during pregnancy has been associated with pubic symphyseal distention. However, the degree of pain is not proportional to the degree of distention. Studies of pain in pregnancy have attempted to correlate pain with elevated hormones, such as serum concentrations of relaxin and the propeptide of Type III Pro-collagen measured in early pregnancy.19,20
Similar pain symptoms may occur with adhesions, which may be responsible for pelvic pain as sequelae of past infection, chronic active inflammatory state, endometriosis, and postoperative adhesions. Colposcopy is the key diagnostic procedure after history taking and physical examination. There is no systematic relation between the clinical picture and anatomic findings. A diagnosis of chronic pelvic pain is recommended in the absence of any macroscopic, histologic, and bacteriologic lesions.21
In laparoscopic studies, about 25% of cases of acute pain and 35% of cases of chronic pain have been attributed to adhesions. The primary sources for the adhesions are in the bowel and omentum. It has been suggested that this pain develops when adhesions fix the pelvic organs in place, hampering their motility. The pain of adhesions can be aggravated by activity. Lysis of adhesions can reduce symptoms of pain, but the duration of relief cannot be predicted. There is no strong scientific evidence that using crystalloids, macromolecular solutions, intraperitoneal heparin, corticosteroids, mechanical barriers such as intercede and Gore-Tex, or biodegradable barriers to reduce adhesions.22
A study of laxity of the posterior ligament support of the uterus suggests that concurrent pelvic pain is attributable to parasympathetic pain at the T12 to L1 level. The pain may result from gravitational pull on nerves that are not being supported by the lax uterosacral ligaments.23
Vulvar vestibulitis refers to pain that occurs during sexual intercourse. The diagnosis is based on the presence of dyspareunia that lasts for at least 6 months and red areas in the vestibulum that are extremely sensitive to touch. The etiology is multifactorial and includes repeated use of antibiotics, local treatment of Candida and human papillomavirus infections, use of hormonal contraceptives, frequent use of local substances that may be irritative, lack of arousal, vaginismus, and tense pelvic floor muscles. There is increased intraepithelial innervation and no inflammation. Treatment includes biofeedback, tricyclic antidepressants, psychotherapy, and surgery.24
Pudendal nerve entrapment should be considered as a differential diagnosis in patients with anoperineal pain. The idea that pudendal nerve entrapment is the cause of some pelvic pain syndromes has gained momentum in the past 15 years.25,26 The pudendal nerve navigates along a tortuous path, supplying sensation to virtually the entire pelvic area, including the penis, scrotum, perineum, and rectum, as well as motor function to the pelvic floor musculature and urethral sphincter. The two major areas of entrapment include the junction of the sacrotuberous and sacrospinous ligaments and the pudendal canal of Alcock. Also, scar tissue from previous trauma or surgery in the surrounding structures can be a cause of entrapment. Evaluation includes reproduction of pain on application of rectal digital pressure at the ischial spine. In addition, rectal stimulation of the pudendal nerve trunk and a recording response in the bulbospongiosus muscle with distal motor latency longer than 5.0 msec is suggestive of pudendal neuropathy. Treatment includes fluoroscopic, computed tomography-guided, or ultrasound-guided local anesthetic and corticosteroid injections at the ischial spine27 or the canal of Alcock; physical therapy; and neuropathic agents. Other modalities include surgical pudendal nerve decompression, radiofrequency stimulation, and spinal cord stimulation.
Coccygodynia is a common problem, characterized by pain and tenderness at the tip of the spine or in the coccyx. The pain frequently radiates to the perineal, gluteal, and posterior sacral areas; worsens on sitting; and is eased on standing. The common causes are trauma, abnormal mobility of coccyx, disc degeneration at the sacrococcygeal and intercoccygeal segments, coccygeal spicules, osteomyelitis, and tumors. Treatment includes conservative methods such as physical therapy, local heat, anti-inflammatory agents, use of cushion, injection of the sacrococcygeal joint with local anesthetic and corticosteroid, and radiofrequency ablation. Some patients—especially those with abnormal mobility of coccyx and who are refractory to conservative treatment—may benefit from coccygectomy.
Tension myalgia refers to spasm of the involved muscles, which can be the levator ani, the piriformis, or the coccygeus muscle groups. Treatment includes heat and massage, local anesthetic injection of the muscles, and follow-up exercises.28
Pelvic joint instability and persistent pelvic pain can occur in instances of precocious puberty and use of oral contraceptives prior to the age of reproduction. Diagnosis is based on a history of early onset of menarche. Osteoporotic sacral fractures are associated with pelvic pain.
Sports-related injuries leading to pelvic pain include pyramidal muscle hematoma, osteitis pubis, and adductor tendonitis.
Pyramidal hematomas can cause impingement of the sciatic, inferior gluteal, and pudendal nerves when the nerves are compressed between the muscle and the iliac spine.
Osteitis pubis, considered to be the most common inflammatory disease of the pubic symphysis, is a self-limiting inflammation secondary to trauma, pelvic surgery, childbirth, or overuse. It occurs more often in men during the third and fourth decades of life, causing pain in the pubic area, in one or both groins, and in the lower rectus abdominis muscle. The pain may be exacerbated by exercise or by specific movements, such as running, kicking, or pivoting on one leg, and is relieved with rest. During physical examination, pain can be elicited by resisted long and flexed adductor contraction. A waddling antalgic gait and symphysis tenderness also can occur. Initial therapy should focus on decreasing inflammation with active rest, ice, nonsteroidal anti-inflammatory agents, and physical therapy. In selected cases, local injections with steroids are helpful. In refractory cases, surgical options are sometimes considered to excise the inflamed tissue with or without fusion of the joint.
Chronic Pelvic Pain Without Obvious Pathology
Studies indicate that between 10% and 50% of chronic pelvic pain patients experience pelvic pain without pathology. The wide incidence range cited suggests there may be some ambiguity in the definition of chronic pain and in the procedures used to evaluate patients with pelvic symptoms.29,30
For a group of chronic pelvic pain patients, no physiologic mechanisms have been elucidated. Some of these patients have pelvic pain that is considered a somatoform disorder similar to irritable bowel syndrome, the prevalence of which is comparable to that of asthma and back pain.31
A syndrome of chronic pelvic pain without obvious pathology (CPPWOP) has been described, but it is unclear whether it exists because pathology that may be present has been overlooked or the pathology typically found in specific diseases is not present, thus possibly excluding damage to ligaments and smooth and striated muscle. Patients with CPPWOP have a constellation of symptoms that include intermittent pain that can vary with the menstrual cycle and is localized to the low abdomen and back and dyspareunia. Patients are typically aged 20 to 30 years of age and usually have a history of childhood sexual abuse or abuse in their present relationships.32
Treatment of CPPWOP is similar to that of other chronic pelvic pain syndromes and includes NSAIDs and antidepressants. Psychological intervention also plays a major role in the treatment of patients with these syndromes and may include cognitive behavioral therapy.
Psychobiological factors, including anxiety, depression, and possible history of sexual trauma, may play a role in patients presenting with chronic pelvic pain, particularly in patients with no obvious pathology. Studies of patients with chronic pelvic pain syndrome and chronic vulvar pain syndrome have shown a significantly higher incidence of sexual abuse compared with women who do not have a history of abuse. In addition to physical and emotional trauma, there is a significant association between sexual victimization before age 15 years and chronic pelvic pain. Sexual abuse and somatization are highly predictive factors for chronic pain. There is a higher incidence of depressive symptoms in this group of patients as well.
The association of sexual abuse and pelvic pain was the basis for psychoanalytic studies of personality development throughout the past century. The first case studies were women with the diagnosis of hysteria. The term hysterus is Greek for uterus, and the concept of hysteria, derived from a theory of a “wandering womb” as the root of inexplicable symptoms in women, was the basis for treatments that reflected sociocultural values about the status of women. Hysteria is no longer considered a valid diagnosis; it has been replaced in current practice by the diagnoses of conversion and somatoform disorders, which may affect both men and women. Nevertheless, the legacy of hysteria as a medical condition persists.
Hysterical conversion has been defined as somatization in which physical symptoms express a psychological conflict (often sexual) that includes affects that were not sufficiently expressed at the time of the incident and are now represented symbolically. In classical psychotherapy, after elucidating the traumatic precipitant, the next step was to clarify how affects were not expressed directly and were converted into physical symptoms. Patients were said to be using the defenses of repression, denial, and somatization to deal with their feelings. Because women were under social pressure to limit their direct expression of aggression and their vulnerability to sexual abuse, it was postulated that they were more likely to have chronic pain and to express themselves somatically.33,34
An alternative explanation has been sought for pelvic pain that occurs in the absence of confirmed laparoscopic and imaging findings—because not all women with chronic pelvic pain have been previously abused. The bio-psycho-social model attempts to integrate physiologic and psychological causes of pain, suggesting the existence of a mind–body dualism between psychological factors and physical symptoms. However, given newer theories on central pain mechanisms focusing on neurotransmitters and neural networks that express affective and cognitive functions, a major deconstruction of studies for chronic pelvic pain needs to be carried out before the diagnosis of hysteria can be considered obsolete.
Evaluation and treatment of male chronic pelvic pain is complicated by the lack of objective diagnostic criteria (Table 44-3).
Differential Diagnosis of Chronic Pelvic Pain in Men
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Differential Diagnosis of Chronic Pelvic Pain in Men
Pelvic floor tension myalgia
Seminal vesicle dystrophy
Irritable bowel syndrome
Inflammatory bowel disease
Chronic prostatitis is poorly understood. The diagnosis is based on symptoms, with no measurable parameter to define the presence of the disease, its severity, or etiology. A National Institutes of Health (NIH) classification system indicates that 38% of men with chronic prostatitis have chronic bacterial prostatitis, with 7% of cases resulting from inflammatory chronic pain syndrome and 55% from noninflammatory chronic pelvic pain syndrome.35
The objectives of current studies include refining and standardizing the evaluation of symptoms of chronic prostatitis. Some men have elevated levels of tumor necrosis factor-α and interleukin-1β proinflammatory cytokines. Seminal cytokine levels may provide an objective measure of disease in these patients and suggest specific therapeutic strategies.36 Patients with prostatitis report more perineal, lower abdominal, testicular, penile, and ejaculatory pain than patients with benign prostatic hypertrophy and sexual dysfunction.
Another attempt at determining objective criteria is to look for evidence of T-cell reactivity with normal prostatic proteins in autoimmune prostatitis. In one study, the CD4 T-cell proliferative response to seminal plasma was found to be statistically significant in men with a history of chronic prostatitis and chronic pelvic pain syndrome, but it was not statistically significant in normal men.37 In studies using color Doppler ultrasonography, chronic prostatitis was associated with abnormal prostate blood flow in men with and without inflammation in comparison with controls.38
In a study of men with pelvic pain, the reported locations of the pain were the prostate or perineal region, or both, in 45.6% of cases; the scrotum or bladder in 38.8% of cases; the penis in 5.8%; the bladder in 5.8%; and the lower abdomen and back in 1.9%.39 Regardless of the location, most subjects had increased urethral sensitivity, suggesting an apparent association of pelvic floor dysfunction with pelvic pain. Treatment was aimed at modulating the pelvic floor with biofeedback, medication like alpha blockers, antibiotics, 5 alpha reductase inhibitors, and sacral anterior root stimulation.40
Pelvic Floor Tension Myalgia
Pelvic floor tension myalgia may also contribute to the symptoms in men with chronic pelvic pain syndrome. The presence of detrusor instability, hypersensitivity to filling, or bladder-sphincter pseudodyssynergia on pretreatment urodynamic studies is not predictive of treatment results. Treatment recommendations include a formalized program of neuromuscular reeducation of the pelvic floor muscles plus interval bladder training to improve objective measures of pain, urgency, and frequency in patients with chronic pelvic pain syndrome.41
Pelvic Varicocele and Seminal Vesicle Dystrophy
Pelvic varicocele and seminal vesicle dystrophy are other causes of pelvic pain. In men, diagnosis of varicocele is based on clinical findings (in contrast with women, in whom instrument evaluation is needed to identify causes such as incontinence of ovarian veins or development of adnexal varicosities). Treatment of male varicocele involves percutaneous sclerotization, surgical excision, or therapeutic embolization.42
NSAIDs have been studied extensively in the treatment of primary dysmennorrhea and have proven efficacy in various causes of pelvic pain. Combination estrogen-progestin oral contraceptives, danazol, and gonadotropin-releasing hormone agonist are used in a stepwise sequence in the management of pelvic pain secondary to endometriosis. Other adjuvant medications, such as tricyclic antidepressants, have a role in some chronic pelvic pain conditions.
Superior Hypogastric Plexus Block This block modulates pain that results from a sympathetic mechanism originating in the pelvic viscera. Several techniques have been described for performing it. Needle placement with fluoroscopy from the posterior approach, using landmarks and coaxial imaging technique, is commonly used. A transdiscal approach through the L5–S1 disk using fluoroscopy or CT guidance has been reported. An anterior approach under CT guidance may be used in selected cases. Neurolytic hypogastric plexus is quite effective in relieving pelvic pain in patients with gynecologic, colorectal, or genitourinary cancer43 (Fig. 44-7).
Superior hypogastric plexus block: transverse section illustrating proper needle placement. Superior hypogastric plexus block: AP radiograph illustrating proper needle placement and contrast spread.
This block is used to evaluate and manage pain of sympathetic origin that has its root in the perineum, rectum, or genitalia. There are various techniques for performing this block. One technique uses fluoroscopic guidance and an approach via the trans-sacrococcygeal with a straight needle.44 Another technique involves entering at the level of the anococcygeal ligament with a curved needle.45 Neurolysis of ganglion impar is used for refractory cases of perineal pain. Neurolysis can be achieved by using chemicals such as phenol or by cryoablation or radiofrequency lesioning (Fig. 44-8).
A 22-gauge, 7-inch spinal needle (passed through a 10-gauge, 5-inch intravenous needle and angiocath) is percutaneously advanced to the anterior border of the sacrococcygeal disc. Diagrammatic lateral view of the proper placement of curved needle for blockade of the ganglion impar.
Pudendal nerve block is an effective diagnostic and/or therapeutic modality for perineal pain. Various approaches such as transperineal, transvaginal, computerized tomography (CT) guided, fluoroscopy guided, and sono guided have been well described.
In women, the block can be performed transvaginally with the patient in the lithotomy position. The needle tip must be advanced through the sacrospinous ligament just past the ischial spine. The transperineal approach is used in men. CT-guided pudendal nerve block has also been reported as a very effective technique in the treatment of pudendal neuralgia.46 The fluoroscopy-guided approach is now one of the most commonly practiced approaches. With the patient in prone position, the C-arm is tilted in the ipsilateral oblique angle to visualize the ischial spine. The needle is then guided toward the ischial spine.47 The ultrasound-guided technique has also been described for blocking the pudendal nerve as it passes between the sacrospinous and sacrotuberous ligaments.
Several different techniques of neuromodulation—including spinal cord stimulation, sacral root stimulation, pudendal nerve stimulation, and even tibial nerve stimulation—have been described for pelvic pain. Sacral neuromodulation, which involves insertion of sacral nerve stimulators, has been performed for patients with voiding disorders, including urinary urge continence, urgency-frequency, and nonobstructive urinary retention; for patients with intractable interstitial cystitis; and for those with chronic intractable pelvic pain.47 This technique is especially beneficial in patients with bladder sphincter dysfunction because it restores balance between the sacral reflexes. Electrical stimulation of the S3 nerve activates the pelvic floor and modulates innervations of the bladder, sphincter, and pelvic floor. Neuromodulation has also been described as beneficial in male chronic pelvic pain syndrome.
Delivery of an analgesic into the epidural or subarachnoid space is used most often in the management of patients with pain secondary to malignancy. Opioids remain the most commonly used drugs for this therapy; however, several other agents, such as local anesthetics and clonidine, can be used in conjunction.
In patients with unilateral pelvic pain secondary to malignancy, cordotomy or rhizotomy can be used in selected patients. The side effects include paresis, ataxia, and bladder dysfunction.
In a review of 1524 gynecologic laparoscopies performed for chronic pelvic pain, endometriosis was the most commonly diagnosed disorder (33%), followed by adhesive disease (24%), chronic PID (5%), ovarian cysts (3%), pelvic varicosities (<1%), leiomyomata (<1%), and a variety of other diagnoses (4%). No visible pathology was detected in 35% of patients.12 Resection and ablation of the endometriotic lesions and lysis of adhesions are the two therapeutic approaches commonly employed laparoscopically.
Laparoscopic uterosacral nerve ablation involves the destruction of the uterine nerve fibers that exit the uterus through the uterosacral ligaments. There seems to be little evidence to support the performance of this procedure.48
Presacral neurectomy is a procedure designed to interrupt the sympathetic innervation of the uterus at the level of superior hypogastric plexus. It is performed by incising the pelvic peritoneum over the sacrum and then identifying and transecting the sacral nerve plexus. This procedure is helpful in the management of patients with persistent midline pelvic pain.
Gonadectomy and Hysterectomy
Bilateral oophorectomy with or without hysterectomy is the most effective procedure for women who have recurrent symptomatic endometriosis and who have no desire to retain reproductive function.
Pelvic floor manual therapy, which involves decreasing the pelvic floor hypertonicity, may ameliorate the symptoms of urgency-frequency syndrome and interstitial cystitis.49 Other physical therapy modalities, including heat, electrical stimulation, deep ultrasound, and massage, may be used depending on the individual need of the patient.
Intra-levator injection of Botulinum toxin type A (Botox) injections for refractory myofascial pelvic pain with short tight pelvic floor may provide significant relief with few self-limiting adverse effects.50,51
The various psychological modalities of treatment should be selected based on individual need, which can vary dramatically among patients. Behavioral therapy, progressive relaxation training, guided imagery, self-hypnosis, breathing exercises, and biofeedback are some of the techniques employed. Other options that may be more useful in the setting of chronic pelvic pain include group therapy, couples therapy, and sex therapy.
Alternative or complementary medicine is receiving greater interest from both patients and health care providers. Yoga, meditation, chiropractic treatment, acupuncture, and magnet therapies are some of the common forms of these modalities.
Pelvic pain is the end result of disease-initiated stimuli and the interpretation of these stimuli by the central nervous system. It is a complex interaction that involves sensory, psychological, and environmental factors. Hence, applying a multidisciplinary approach that involves employing an integrative approach to the psycho-social-mind-body paradigm is the most effective strategy in the management of patients with chronic pain states. This approach integrates medical intervention with identification and management of socioenvironmental problems, cognitive behavioral pain strategies, and treatment of concurrent psychological morbidity. Available evidence suggests that outcomes—including pain severity, general health, and functional status and disability—improve more significantly after this approach than after isolated medical or surgical interventions.
Abdominal pain is one of the most common presenting complaints in the primary care physician's office and is often a diagnostic dilemma for surgeons. Frequently, it is a benign complaint; however, it can also herald serious acute pathology. The prevalence of abdominal pain is consistently high across diverse geographic regions and age groups.
By contrast with other areas of the body, the abdominal organs have poorly developed sensory systems that also may contribute to the patient's difficulty when trying to describe and localize the pain. For a patient to perceive pain, the autonomic nervous system must be intact.51 The abdominal viscera are relatively insensitive to many stimuli compared with a more sensitive organ such as the epidermis. In addition to the relative paucity of sensory nerve endings, the same group of nerves may innervate several viscera. There are a few well-known nociceptive triggers in the abdominal cavity. These include abnormal distention or contraction of hollow organ walls; ischemia of the visceral musculature; direct action of chemical substances on the mucosa; formation of allogenic mediators; and traction or compression of ligaments, vessels, or mesentery.52,53
The location and cause of pain patterns are not well differentiated. Nevertheless, there are some recognizable pain patterns, and a careful history often can lead to the correct diagnosis. The history and physical examination provide diagnosis in approximately two-thirds of clinical presentations. Laboratory and radiologic tests are important adjuncts for investigative workup.54-57 The invasiveness and cost-effectiveness of the proposed tests should always be considered.
CLASSIFICATIONS OF ABDOMINAL PAIN (TABLE 44-4)
Classifications of Abdominal Pain
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Classifications of Abdominal Pain
Nociceptive (visceral or somatic)
Acute < 6 months
Chronic > 6 months
Theories of Abdominal Pain Transduction
There remains only a theoretical explanation for transduction and transmission of visceral pain.58 Central and peripheral theories of pain are widely recognized.
The convergence projection theory states that visceral fibers with nociceptive input converge onto somatosensory spinal neurons and that the viscerosomatic cells project through nociceptive pathways.
The convergence facilitation theory focuses on the fact that visceral activation changes the excitation of multiple spinal units (including pain pathways) without direct activation of spinal neurons.
The peripheral theory proposes that vasoactive substances released into cutaneous and deep tissues lead to hyperalgesia and referred pain from these structures.
Somatic and Referred Pain
Differentiating somatic from referred pain can typically be accomplished by a combination of history and selective blocks.
Somatic pain tends to be more intense or sharp and is aggravated by movement. It is produced by the stimulation of nociceptors in the parietal peritoneum and intraabdominal connective tissues. It is usually well localized and described as constant, aching, gnawing, and throbbing. It can be relieved by opiates and peripheral nerve blocks.
Referred pain can be explained easily by our knowledge of the segmental distribution of the spinal nerves. The pain can be referred to remote areas of the body if visceral impulses enter the spinal cord at the same level as afferent nerves from another area. These impulses are mistakenly interpreted as pain initiating at the second site. In addition, the pain may spread cranially to adjacent segments. Diaphragmatic irritation as a result of abdominal insufflation during laparoscopy frequently presents as shoulder pain. This is the most frequently used example of referred pain (Fig. 44-9).
Examples of referred pain.
It is important to have an organized approach to the examination of the patient with abdominal pain. Description of current and previous disease (including psychiatric treatment) in conjunction with a social and family history will create a picture of the pain and possibly provide a presumptive diagnosis. A history of allergies and current medications must also be elicited. Knowledge of the pain pattern and character is also important. Following this, the patient should be carefully examined.58,59 A useful algorithm is presented in Figures 44-10 and 44-11.
Clinical approach to abdominal pain.
Diagnosis and treatment of acute abdominal pain.
Frequently, it is easy for the patient to differentiate superficial abdominal pain from deep abdominal pain.
The more common deep abdominal pain is, by definition, either somatic or visceral (autonomic: sympathetic and parasympathetic). Somatic pain originates in the parietal peritoneum, the root of the mesentery, and near the nociceptive source. It is intense, sharp, precisely localized, associated with external stimuli, and represented at the cortical levels. Severity is related to the intensity of the stimulus. Visceral pain is often described as a poorly localized, vague (can be colicky, cramping, squeezing, dull, aching) pain associated with internal factors. Sometimes, the pain can be referred to another part of the body. It can also present as diffuse midabdominal discomfort. The intensity of the stimulus is as essential as its quality (i.e., cutting or coagulating the bowels is painless, but distention will cause pain). This pain is primarily reflexive and can be represented at the cord levels. Sometimes, severe visceral pain can generate a secondary physiologic reaction mediated by the autonomic nervous system and manifested by nausea, vomiting, sweating, lightheadedness, and salivation.
The pain from the stomach, pancreas, and hepatobiliary tree is referred to the epigastrium. Periumbilical localization occurs from the small bowel and right colon; the rest of the colon and the genitourinary organs cause pain that presents in the epigastrium. The common midline pain location is a result of the bilateral innervation of the abdominal organs from both sides of the spinal cord (Fig. 44-12).
Differential diagnosis of abdominal pain based on location.
To determine the source of the pain, it is important to assess its intensity, location, and character. It is also important to note its onset, whether acute or insidious, and its temporal profile. The circumstances that intensify or alleviate the pain are significant. Relief with eating or antacids suggests ulcer disease or gastroesophageal reflux. Postprandial pain—depending on its location, character, and timing—could be biliary, ischemic, or associated with a more benign condition, such as lactose intolerance or irritable bowel syndrome. Seasonal patterns are frequently seen in ulcer disease and, occasionally, with regional enteritis. The pain of inflammatory bowel disease and irritable bowel syndrome may be relieved by defecation, whereas heat usually relieves pain of musculoskeletal origin. Posture, sudden movement, coughing, straining, and sneezing may worsen the pain from peritoneal irritation or of spinal origin. The abdomen is not exempt from psychogenic pain. This may be manifested as a component of irritable bowel syndrome. Although common, psychological pain should and does remain a diagnosis of exclusion.
PHYSIOLOGICAL CAUSES OF ABDOMINAL PAIN
Functional esophageal disorders comprise a group of conditions that present with symptoms presumed to originate from the esophagus (chest pain, heartburn, dysphagia, and globus sensation). The exact etiology is unclear; however, the different proposed underlying mechanisms include esophageal hypersensitivity due to peripheral and/or central sensitization, altered central processing of stimuli, and altered autonomic activity. Primary esophageal motility disorders such as achalasia and diffuse esophageal spasm and gastroesophageal reflux disease have to be ruled out. Heartburn is the most common symptom attributable to the esophagus. It is a burning or warm substernal discomfort that frequently migrates toward the neck. It may also be localized to the epigastrium. Eating, bending, lying down after eating, and, occasionally, vigorous exercise may precipitate it. It is not entirely clear whether heartburn is caused by the chemical irritation of acid or bile, or if secondary muscle spasm plays a role. Occasionally, the pain is described as a heaviness or tightness in the chest, with secondary restricted respiration and subsequent shortness of breath, simulating myocardial ischemia. The shortness of breath may be caused by an intercostal muscle spasm mediated by spinal reflex arcs.
Typically, esophageal pain is felt at the level of the irritation. In some patients, however, pain caused by a lesion in the lower third of the esophagus is felt in the throat or in the superior retrosternal area. The opposite is uncommon. When heartburn is severe, such as that associated with an ulcerating or infiltrating process, esophageal pain can radiate into the back, between the shoulder blades.
Pain modulators such as antidepressants, antiepileptic agents, and adenosine antagonists are often used in the treatment of functional esophageal disorders.
The character of pain from ulcer disease varies widely. Typically, it is located in the epigastrium. It may be a sharply localized burning or gnawing pain or a vague discomfort occurring from ½ to 2 hours after eating. Occasionally, it occurs shortly before meals or on an empty stomach, and it may wake the patient up in the early hours of the morning. Food or antacids tend to relieve it. The pain may, at times, be more localized to the right or left upper quadrant. When the pain bores through into the back, it may indicate a posterior duodenal wall ulcer with secondary irritation of, or penetration into, the pancreas. This pain is typically deep, persistent, poorly localized, and does not respond well to treatment. Unlike heartburn, ulcer pain frequently occurs in clusters; several weeks of daily pain may be followed by variably long pain-free intervals. There may be seasonal variation with the symptoms as well.
Pain from gastritis tends to be more persistent and may be difficult to abolish. The associated nausea and vomiting may be particularly troublesome. As in heartburn, it is not known whether the pain is produced by acid irritation of the nerve endings in the ulcer bed or secondary to a spasm of antral or duodenal smooth muscle.
Epigastric pain occurring soon after eating, unrelieved by antacids, and with lack of periodicity does not necessarily exclude ulcer disease. Pyloric channel ulcers may present in such a manner, and, unless there is associated postprandial vomiting, the diagnosis may not be made until frank gastric outlet obstruction occurs.
As a rule, pain originating in the small intestine is periumbilical in location and crampy or colicky in nature. Jejunal lesions tend to be associated with pain in the left upper quadrant. Ileal pain tends to localize in the right lower quadrant, and it may result from abnormal bowel motility patterns. A low threshold for the pain of bowel distention or contraction can also contribute. A lesion obstructing the lumen of the bowel, such as regional enteritis or a malignant process, may be the precipitating factor.
The pain of irritable bowel syndrome frequently is chronic and, at times, can be incapacitating. The pain is frequently located in the lower abdomen, in either the right or left lower quadrants. Its description ranges from burning, sharp, and stabbing to dull and achy. Most commonly, it is intermittent, but it may be constant, with superimposed acute attacks. The pain may remain localized or may migrate with time. Eating usually precipitates it; defecation or fasting tends to relieve it. Nausea, bloating, and dyspepsia frequently occur and may simulate peptic ulcer or biliary tract disease. A change in bowel habits is not a universal finding, but, classically, diarrhea alternates with constipation. Predominant diarrhea or constipation, however, can be part of the syndrome.
Pain from partial small bowel obstruction also occurs after meals. The closer the lesion is to the stomach, the earlier the pain occurs. Moreover, nausea and vomiting are more likely to occur when the lesion is close to the stomach. The pain is frequently described as crampy and comes in waves. Regional enteritis is suggested by localization of the discomfort to the right lower quadrant and associated diarrhea, fever, weight loss, or extraintestinal manifestations, such as arthritis and mouth ulcers. Significant weight loss and cachexia may suggest an underlying lymphoma or metastatic disease to the bowel. It may be several months before complete obstruction occurs. At this time, the diagnosis becomes more evident. As in appendicitis, the initial pain may be a nonspecific discomfort, but as the underlying process develops and eventually involves the overlying peritoneum, the pain localizes and approximates the site of the underlying disease.
Postoperative adhesions are frequently blamed for chronic or recurrent abdominal pain. Before exploration is considered, definitive evidence of bowel obstruction using plain abdominal x-rays or angulation and proximal dilation of the bowel using a barium study should be documented.
Pain from the colon is typically poorly localized to the lower abdomen. However, an adenocarcinoma of the colon or diverticula of the colon with secondary microperforation and abscess formation may have localized symptoms overlying the area of disease. Pain from the rectosigmoid area, in addition to being in the left lower quadrant, may be located in the sacral region as well.
Pancreas, Liver, and Biliary Tract
Because the pancreas, liver, biliary tract, stomach, and duodenum share some of the same afferent neuropathways, it is easy to understand some of the difficulties involved in the differential diagnosis of chronic epigastric pain. Diseases of the pancreas—in particular, pancreatic cancer—are some of the most difficult to diagnose. Pain resulting from pancreatic cancer usually signifies infiltration of the retroperitoneal region or celiac axis or spread to surrounding organs. Some of the pain may be a result of pancreatic duct obstruction and surrounding pancreatitis. Tumors in the head of the pancreas cause pain that is more localized to the epigastrium or right upper quadrant. Those in the tail tend to cause pain in the left upper quadrant. Lesions in the body of the pancreas can cause the pain to radiate into the back. Back pain, alone, can also be a presenting symptom.
The pain of chronic pancreatitis, which is often a result of alcohol abuse, can be constant and debilitating and can frequently lead to drug abuse. The persistent inflammation of the pancreas causes some of the pain, as does the ductal distention secondary to ductal obstruction by creation of strictures. The pain may be dull or sharp, burning, and steady. It commonly radiates into the back. Superimposed, more acute attacks last from days to several weeks. Eating, moving, or lying down may aggravate the pain; sitting up or leaning forward may relieve it.
Mechanisms of pain generation in pancreatic cancer and pancreatitis have not been completely understood. In the past, pain in these two conditions was attributed to various causes such as increased intraductal pressure, ductal strictures, and increased parenchymal pressures. It is now widely accepted that pain sensation in both pancreatic cancer and chronic pancreatitis has been identified as neuropathic due to the prominent neuroplastic changes in the form of neural hypertrophy, increased neural density, perineural invasion of inflammatory cells in pancreatitis, and cancer cells in pancreatic cancer.53
In patients who are not surgical candidates, the pain specialist may be asked to intervene. Neurolytic celiac plexus block has been used to treat patients who have not responded to conservative or surgical therapies.
Placement of stents during endoscopic retrograde cholangiopancreatography was used initially to decompress a dilated biliary tree. Recently, however, this technique has been used to decompress the pancreatic duct. Relief may occur if the dilated biliary (or pancreatic) duct was the cause of the pain. Both benign and malignant lesions are amenable to this technique.
Biliary pain may be due to a calculus or biliary tree dilation secondary to an obstruction. Contrary to the commonly used term biliary colic, the pain tends to have a gradual onset. After it peaks, it tends to reach a plateau until again, hours later, it diminishes. An attack can last from several hours to a day or more. The pain is characteristically localized in the right upper quadrant and may radiate to the right shoulder and shoulder blade, but it is also commonly felt in the epigastrium, with radiation into the back. Vomiting occurs in most patients and may provide some relief. After an acute attack, residual soreness may persist for several days to weeks. Commonly, these symptoms occur after eating, but they may become constant if the common bile duct is impacted by a stone or infiltrated by a malignant process. Associated dyspepsia is common and occurs in approximately one-quarter of all patients. It responds to antacids, further confusing its cause. The appearance of complicating cholangitis (with symptoms of fever and jaundice) usually leads quickly to the correct diagnosis.
The liver parenchyma is insensitive to pain, but relatively rapid distention of the liver capsule will initiate well-localized right upper quadrant pain. Acute processes such as viral hepatitis, alcoholic hepatitis, and cardiac decompensation with secondary liver congestion may infrequently present as right upper quadrant pain, but this pain does not evolve into a chronic complaint. Chronic, active hepatitis may follow a course of recurrent attacks of right upper quadrant pain. The pain is frequently well localized and accompanied by worsening liver function tests.
Benign focal nodular hyperplasia or adenomas associated with the use of birth control pills may cause recurrent right upper quadrant discomfort or, occasionally, a dramatic crisis of severe abdominal pain and hypotension from a hemorrhage into the capsule or peritoneum. The recurrent warning pains are likely caused by small bleeding episodes into the lesions. Bleeding into or necrosis of malignant lesions in the liver causes similar pain, but this usually is accompanied by fever and jaundice. The pain may be well localized, sharp, and steady. Any movement producing friction between the liver surface and the ribs may exacerbate this pain. When sought, a bruit over the lesion may be identified in approximately 25% of patients.
VASCULAR DISEASES OF THE BOWEL
Although mainly asymptomatic, occlusive vascular disease may be associated with chronic, recurrent, dull periumbilical, or epigastric pain. The pain of intestinal angina begins approximately 1½ hours after eating and lasts throughout digestion and absorption of the meal. Typically, at least two of the three major splanchnic vessels are affected by significant obstruction from atherosclerotic changes. It is postulated that the collateral supply is insufficient to meet the increased need during digestion, and this state of relative ischemia creates subsequent pain. Classically, this recurrent pain may create a fear of eating and can lead to severe weight loss. When patients with acute ischemia are questioned carefully, they often will report postprandial abdominal discomfort preceding the acute event by weeks to months.
Superior mesenteric artery syndrome and celiac compression syndrome are frequently mentioned in the differential diagnosis of chronic abdominal pain, but their validity is controversial. Superior mesenteric artery syndrome is described as occurring in so-called asthenic patients or patients with significant weight loss. The postprandial epigastric pain, vomiting, and distention are believed to be caused by compression of the duodenum by the superior mesenteric artery. The pain of celiac compression syndrome is not necessarily related to meals. The celiac axis frequently has a high take-off and may be compressed by the median arcuate ligament of the diaphragm or by the tissue of the celiac ganglion. Whether bowel ischemia is the cause of the pain or whether the pain originates from the celiac ganglion is also unclear.
An abdominal aortic aneurysm usually presents more acutely, but a slowly expanding or leaking aneurysm may be associated with recurrent, dull midepigastric or back pain over several months. As with pancreatic pain, sitting up or leaning forward may occasionally relieve this pain. The pulsating, sometimes tender, mass can be palpated, and a bruit may be heard.
The parietal peritoneum is well innervated by the branches of the spinal nerves, and, consequently, the pain perceived is well localized. Such pain is frequently associated with secondary muscle spasm of the overlying abdominal wall. The visceral peritoneum, however, has no pain receptors, and any pain that is generated is poorly defined. A malignant process most often causes chronic pain originating in the peritoneal cavity. Metastatic bowel or ovarian tumors and lymphoma are common. Mesothelioma is the most common primary tumor. Teratoma, carcinoid, or sarcoma is much less common. The abdominal discomfort is often compounded by the presence of ascites, which distends the peritoneum further and causes more pain.
In young patients of Mediterranean descent who have chronic recurrent attacks of sudden diffuse or localized peritoneal pain, familial Mediterranean fever should be considered. Abdominal tenderness, fever, and arthritis are common. Despite feeling very ill, the patient recovers in several days and is well until the next attack.
Recurrent localized or generalized abdominal pain in an older patient associated with the displacement of the stomach or bowel on x-ray studies should suggest a mesenteric or omental lesion. Fever, weight loss, nausea, vomiting, and a palpable tender mass may be associated with mesenteric panniculitis or retractile mesenteritis. Metastatic tumors to the mesentery are more common than primary lesions. The latter usually are fibromas, myomas, histiocytic, or lipomatous tumors. Leiomyomas and leiomyosarcomas tend to involve the omentum.
The acute pain of renal colic or pyelonephritis is classic. The triad of hematuria, flank pain, and a palpable mass suggests renal cell carcinoma, but this triad occurs infrequently. The tumor is often diagnosed as a result of systemic complaints (dull upper abdominal or flank pain may be included). Perinephric abscess, although uncommon, should be considered in a patient with a history of urinary tract infections or pyelonephritis. Typically, dull upper quadrant or flank discomfort is present, accompanied by malaise and low-grade fevers.
Gynecologic problems usually cause acute pain. Depending on the patient's age, chronic lower abdominal pain, usually more localized to one of the lower quadrants, could be a presenting symptom of chronic pelvic inflammatory disease or uterine or ovarian cancer. The pain can be dull, steady, or crampy. The local irritation by the mass or inflammatory process can cause changes in the urine or bowel patterns.
MUSCULOSKELETAL CAUSES OF ABDOMINAL PAIN
Chronic Abdominal Wall Pain
Chronic abdominal wall pain (CAWP) has been recognized for more than 75 years but remains a frequently overlooked diagnosis. This can lead to extensive diagnostic testing before an accurate diagnosis is achieved.60-63 It occurs in about 10% to 30% of patients with chronic abdominal pain.
A variety of causes such as myofascial pain, thoracic radiculopathy, abdominal wall lesions including nerve entrapment, and referred pain secondary to neural convergence from abdominal or thoracic viscera have been discussed in literature.
Anterior cutaneous nerve entrapment syndrome (ACNES) is the most common cause of abdominal wall pain. This is thought to be caused by entrapment of the anterior branch of the T7 to T11 intercostal nerves as they pass through the lateral border of the rectus abdominis.64,65 The diagnosis can typically be established via history and physical examination. The pain is often sharp, and the patient is usually able to point with one or two fingers to the exact location. A positive Carnett's sign with increased pain during muscle tensing is diagnostic. A study by Greenbaum and colleagues showed a sensitivity of 85% and a specificity of 97%.64 False positives may result from visceral causes of pain that affect the peritoneum. Local injections of anesthetic/steroid under ultrasound guidance are the treatment of choice for patients with moderate to severe pain resulting from the abdominal wall. Pain relief is achieved in anywhere from 60% to 90% of patients and assists in confirming the diagnosis.66-68 In some patients, neurolysis may be a possible option. In refractory cases, surgical explorations and neurectomy may be considered.
Xiphoidalgia is a relatively rare syndrome that presents with localized discomfort and tenderness to palpation over the xiphoid process. This can occasionally cause nausea and vomiting with pressure on the area and can be exacerbated by eating a heavy meal or by bending or twisting movements. Anti-inflammatory medications or injections of anesthetics/steroids into the area often provide a cure for the condition.69,70
Pain syndromes involving the lower ribs have been given many names over the years, including rib-tip syndrome, slipping rib, twelfth rib, and clicking rib. The syndrome itself is characterized by reproducible pain in the lower chest or upper abdomen and a tender area located on the costal margin. In slipping rib syndrome, the rib intermittently slips out of place, causing a stretching of the ligamentous support of the ribs in the front and back. Without muscles to hold the ribs in place, loose ligaments allow extended rib movements that can cause further stretching of the ligaments, manifested as periodic episodes of severe pain and underlying chronic chest, upper abdominal, and/or upper back pain. The mobile ribs may also irritate intercostal nerves, resulting in excruciating pain around the chest into the back. Many practitioners recommend a diagnostic test called the “hooking maneuver,” in which the examiner's curled fingers are hooked under the ribs at the costal margin and then gently pulled forward. A positive test may reproduce pain and may cause a click. The majority of patients with this condition are female, with a mean age of 40.71,72
In mild cases, simple oral analgesics, topical ice packs, and transient reduction of physical activity may be recommended. For moderately severe cases, intercostals block with local anesthetic agents and steroids may provide temporary relief. If conservative management fails or for those cases interfering with regular activities, resection of the anterior end of the rib and costal cartilage may be performed with many reports of successful outcomes.
Ilioinguinal, iliohypogastric, and genitofemoral neuralgias are among the common causes of lower abdominal and pelvic pain. All three nerves overlap in their pattern of innervations, which may lead to confusion in the diagnosis. The most common cause of these neuralgia is injury to the nerve induced by trauma, including direct blunt trauma to the nerve and damage during inguinal or pelvic surgery.
Ilioinguinal neuralgia is caused by compression of the ilioinguinal nerve as it passes through the transverse abdominis muscle at the level of the anterior superior iliac spine. Ilioinguinal neuralgia presents as paresthesias, burning pain, and occasionally numbness over the lower abdomen that radiates into the scrotum or labia and occasionally into the inner upper thigh.
Iliohypogastric neuralgia is caused by compression of the iliohypogastric nerve as it passes through the transverse abdominis muscle. It presents as paresthesias, burning pain, and occasionally numbness of the abdominal skin above the pubis.
Genitofemoral neuralgia presents as paresthesias, burning pain, and occasionally numbness over the lower abdomen, which radiate into the inner thigh in men and women and into the labia majora in women and the bottom of the scrotum and cremasteric muscles in men.
Treatment of these neuralgias includes simple analgesics, neuropathic agents, and nerve blocks with local anesthetic steroids. In some cases, neuromodulatory and neurolytic blocks with radiofrequency and cryoablation may be useful. Advanced therapies include surgical options to relieve entrapment and neuromodulation by using peripheral stimulation.
METABOLIC CAUSES OF ABDOMINAL PAIN
Metabolic causes of chronic abdominal pain are rare but should be considered when the usual diagnostic avenues have been exhausted. The hepatic porphyrias have many features in common, including their clinical presentation. Abdominal pain is the most prominent symptom. It is thought to result from autonomic neuropathy, which causes disturbances in gastrointestinal motility. Spasm and dilation of the bowel can cause severe pain. The frequent association of fever and leukocytosis mimics an inflammatory process. Although vomiting and constipation are frequently present, the abdomen is soft, without marked tenderness. These attacks may last from days to weeks. Fasting, infections, the menstrual cycle, and drugs whose metabolism involves the hemoproteins of cytochrome P-450 are often the precipitating factors. Such drugs include alcohol, barbiturates, anticonvulsants, estrogens, and contraceptives. Knowledge of so-called safe or probably safe drugs may be useful to the clinician treating the pain. Drugs that are considered safe include morphine and related opiates, which may be required to treat the pain in an acute attack.
In the United States, lead poisoning is primarily encountered in children. Although anemia, peripheral neuritis, and encephalopathy complete the picture, the young patient may have only lead colic, sometimes called painter's cramps. Severe, migrating, poorly localized guarding and rigidity of the abdominal wall should raise the suspicion of an acute intraabdominal event that may accompany crampy abdominal pain.
When in a hemolytic crisis, a patient with paroxysmal nocturnal hemoglobinuria may have substernal, lumbar, or abdominal pain, in addition to generalized weakness. The pain may be colicky and last for several days. The abdomen may be tender, with some guarding and even a rebound phenomenon. Venous thrombosis occurs with increased frequency in these patients. It should be considered if a sudden increase in liver size accompanies these attacks, suggesting thrombosis involving the portal system.
Hyperparathyroidism has been called the syndrome of bones, stones, and groans. Associated peptic ulcer disease or pancreatitis usually causes the abdominal pain.
The lightening-sharp abdominal pain of tabes is associated with syphilis, but it may occur with diabetes and meningeal tumors. This is a radicular syndrome resulting from damage to the large posterior lumbosacral roots.
The diagnosis of chronic recurrent abdominal pain can be a challenge to both diagnose and subsequently treat. Unfortunately, many patients with this type of pain undergo multiple surgical procedures without any significant findings. Good knowledge of the underlying anatomy and pain patterns can improve the diagnosis and subsequent treatment (Fig. 44-13).
Classification of pain (pain patterns).
PSYCHOSOMATIC CAUSES OF ABDOMINAL PAIN
The abdomen is the third most common site of pain in psychiatric patients. Diagnosis of psychological pain can be made based on exclusion criteria. There are some signs that can be helpful or supportive. Suspicion is raised when location, timing, quality, and distribution of symptoms do not relate to pathophysiologic patterns. There is often marked discrepancy between reported severity of pain and presented behavior. The patient sometimes reports pain in other parts of the body and may have a history of many negative diagnostic workups for various complaints. The onset of pain may have an obvious relationship to a stressful event.
MANAGEMENT OF ABDOMINAL PAIN
When a treatable disorder is identified, appropriate therapy should be instituted. Unfortunately, in many patients with chronic abdominal pain, a specific diagnosis is not identified despite an extensive workup. In other patients, a condition is diagnosed, but conventional methods fail to treat the disease and pain.
Medical management in most cases of chronic abdominal pain requires a multidisciplinary approach including identification of risk factors associated with disease progression and appropriate modification.
A systematic evaluation of the exact cause of pain and complications followed by appropriate treatments is essential in all patients. Analgesics are typically titrated according to the World Health Organizatin ladder principle, but, in some situations, a top-down approach may be useful to control pain and avoid sensitization of central pain pathways. Also, adjuvant analgesics should be considered at an early stage and combinations of drugs are often used.
Modification of diet, nonencapsulated enzyme therapy, somatostatin-analogues, and antioxidants can be considered as supplements to conventional analgesics in special situations. Nerve blocks can be helpful in treating acute and chronic abdominal pain. Nonspecific methods, such as antidepressants, stress reduction techniques, and behavioral approaches, often are useful in treating these difficult presentations. Nonoperative treatment for functional abdominal pain syndromes includes cognitive, behavioral, physical, occupational, recreational, and medical therapies. Detailed discussion about the role of cognitive and behavioral therapies is beyond the scope of this chapter.
Celiac plexus block and splanchnic nerve block are interventional techniques utilized for diagnostic and therapeutic purposes in the treatment of abdominovisceral pain. The richly innervated celiac plexus provides sensory input about pathologic processes in the liver, pancreas, spleen, omentum, alimentary tract to the mid-transverse colon, adrenal glands, and kidney. Chronic pancreatitis and chronic pain from pancreatic cancer have been treated with celiac plexus block to theoretically decrease the side effects of opioid medications and to enhance analgesia from medications. Fluoroscopy, CT guidance, and endoscopic ultrasound assistance may be utilized to aid the practitioner in performing the blockade of the celiac plexus.
The celiac plexus innervates the abdominal viscera with fibers arising from preganglionic splanchnic nerves, preganglionic parasympathetic vagus nerve fibers, sensory nerve contribution from the phrenic and vagus nerves, and postganglionic sympathetic fibers. Sympathetic innervation is derived from the anterolateral horn of the spinal cord as axons from T5 to T12 leave the spinal cord with ventral nerve roots to join white rami communicans (WRC) en route to the sympathetic chain. The greater, lesser, and least splanchnic nerves provide the major preganglionic contribution to the celiac plexus and transmit the majority of nociceptive information from the viscera. The splanchnic nerves are contained in a narrow compartment made up by the vertebral body and the pleural laterally, the posterior mediastinum ventrally, and the pleural attachment to the vertebra dorsally.
Although celiac and splanchnic nerve blocks share common risks, the rates of pneumothorax, thoracic duct injury, and inadvertent spread of the injected drug to the somatic nerve roots are higher for splanchnic nerve block than for celiac plexus block.
Neurolysis with alcohol, phenol, and radiofrequency techniques have been well described.
Video-assisted thoracoscopic splanchnicectomy has also been used in the treatment of chronic pancreatitis pain and in pancreatic cancer pain.73
Pelvic and abdominal pain remains a diagnostic and therapeutic challenge for the health care provider. Patients presenting with this are best assessed and treated using a multidisciplinary approach. Close collaboration among gynecologists, urologists, proctologists, neurologists, pain specialists, gastroenterologists, psychiatrists, psychologists, physiatrists, and neurologists is needed. Special emphasis should be placed on preventive strategies, such as screening and treatment of avoidable causes.
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