Ying T. Sia, MD, MSc, FRCRC

• Associate Professor
• Department of Medicine
• University of Montreal
• Attending
• Department of Medicine, Service of Cardiology
• Centre Hospitalier de l?niversity of Montreal
• Montreal, Quebec, Canada

Some clinicians will use photography to document the markings for later comparison and to aid in information transfer to other interested parties antibiotics for uti how many days cheap flagyl 400mg. However antibiotics prescribed for kidney infection buy flagyl 500 mg with amex, the pain diagram suggested a lesion of the lateral femoral cutaneous nerve of the thigh (meralgia paresthetica) due to the appearance of an oval patch at the anterolateral thigh inconsistent with that of the L2 dermatome virus rash cheap flagyl 250 mg without prescription. Sensory abnormalities were limited to that specific area treatment for upper uti cheap flagyl 400mg mastercard, while further testing revealed that light brush sensation was reduced (brush hypoesthesia) antimicrobial fogger cheap flagyl 250 mg line, pinprick was more painful than anticipated (pinprick hyperalgesia) antibiotic guide pdf purchase flagyl 400 mg visa, and temperature sensations were described as delayed but normal in intensity. The remainder of the neurological exam confirmed a normal motor exam, normoreflexia (including at the left knee jerk) and unremarkable straight leg testing. Also, if a topical treatment was planned, the clinician may not want to attempt this should the affected area be significantly large. Bedside method for quantitative sensory pain testing Improving outcomes involves understanding disease risk factors and mechanisms, determining which are relevant, developing accurate and standardized measurements, and then developing and evaluating treatment interventions that address as many of the relevant contributing factors as possible. The evolution of assessment and treatment of hypertension is a model of this paradigm. One of the earliest developments that facilitated this evolution was the ability to accurately measure blood pressure. It began with the introduction of a standardized tool, the sphygmomanometer blood pressure cuff. Accurate and reproducible blood pressure measurement then allowed the development of standardized normal values. From there, deviations from normal could be quantified and tracked over time and as research developed new therapeutic interventions measuring treatment success became quantifiable. The ability to reliably reproduce these measurements was a crucial link between understanding disease mechanisms and improving treatment outcomes. In chronic pain states, the degree of peripheral damage or inflammation does not correlate well with pain severity. This initially led to a focus on the psychosocial aspects of pain to explain a discrepancy but over the last few years research has also focused on identifying the many different biological mechanisms that may contribute to chronic pain. For instance, a patient with osteoarthritis of the knee may also have some evidence of neuropathic pain and central sensitization. This is important information as it will potentially change the entire treatment paradigm for any individual. In the past, if central nervous system symptoms were present (such as fatigue, poor sleep, and pressure allodynia) clinicians tended to relate them to psychological mechanisms. Quantitative sensory testing is one tool that can help to determine the presence of different mechanisms in any given pain state. How it is used is evolving but like measuring blood pressure, its successful introduction as a clinical tool will require attention to detail to ensure the most accurate and reproducible results. The clinical role of bedside pain sensory testing in the diagnosis of neuropathic pain the Neuropathic Pain Special Interest Group of the International Association for the Study of Pain recently published guidelines on the assessment of neuropathic pain [20]. The article stated "A careful bedside examination of somatosensory functions is recommended, including touch/vibration, cold, warmth and pain sensibility" for patients presenting with possible neuropathic pain. Sensory testing alone cannot determine the neuroaxial level of pathology, but documentation of sensory abnormalities will help to confirm or deny the presence of neuropathic pain. It also seeks to provide indirect information used to evaluate underlying sensory function abnormalities using only small, portable tools and with less time requirement than protocols developed by the German Neuropathic Research Network [23, 24]. Both protocols are psychophysical methods utilizing specific physical stimuli (pinprick, touch, vibration, heat, cold) to activate sensory receptors. Both protocols also require active participation and directed attention on behalf of the patient. Feedback to the authors is encouraged to improve the face validity of the procedures. Establish a control site where the patient does not describe any sensory abnormalities or pain and briefly examine to confirm the expected findings. If there are areas where sensation seems reduced or lost and others where there is hypersensitivity, ensure that you test at least one area that represents sensory deficit and one area that represents hypersensitivity. Begin a basic screening examination by testing touch (to evaluate the large A beta fibers) and then pinprick (to evaluate the small A delta fibers) to avoid sensitizing the skin. If these are normal, then vibration (which is also A beta) and temperature sensation (which is a mix of A delta and C fibers depending on the temperature tested) should be tested before you declare the sensory examination is normal. For instance, if the patient rates the stimulus to brush in the right hand as normal but reduced in the left hand, brush the normal right hand again and say, "If this is worth a dollar, (then brush the abnormal left hand) how much is this worth Likewise, a patient who reports a pinprick stimulus as 30/100 in the normal side and 80/100 on the affected side is also providing more information than "I feel it more. These include temperature differences between affected and unaffected areas which can be documented with a laser temperature probe. There may be differences in sweating in an affected body part or trophic changes such as with loss of hair, thinning skin, cracked dry skin, or altered nails. Secondary changes associated with chronic denervation, such as with Charcot neuropathic foot destruction with necrotic arthropathy and chronic ulcers on the plantar surface, should also be documented. The role of neural plasticity Injury to the nervous system results in maladaptive plasticity which can alter function at multiple levels of the somatosensory system including the peripheral 9 Section 1: the Clinical Presentation of Neuropathic Pain Table 1. Peripheral nerve injury can lead to increased neuronal activity throughout the central nervous system, resulting in increased responses to noxious and non-noxious stimuli. Sunburned shoulders are an example of normal, adaptive central sensitization not due to direct nerve injury, and anyone experiencing this will recall features of warm and pressure allodynia as they stood in a shower, for example. Under normal circumstances, this is a temporary phenomenon that may resolve as tissues heal. In some circumstances, however, either affected tissues fail to heal or the mechanisms evolve and, despite tissue healing, neuronal hyperexcitability persists, thus pain is no longer coupled to ongoing tissue damage. Documentation of this phenomenon is clinically important to provide (to patients, their family, insurance companies, and the courts), in the differential diagnosis, a physiological basis that may explain some of their symptoms. Diagnosis of peripheral sensitization relies on a history that has features consistent with neuropathic pain. Research has demonstrated some clinical findings that characterize plasticity at different levels or by different mechanisms but it can be difficult to impossible to separate peripheral from central mechanisms. In some cases this is because both mechanisms contribute to a particular clinical finding. For example, abnormally increased pain following a noxious cold stimulus (cold hyperalgesia) is mediated by peripheral sensitization in addition to reduced inhibition and central sensitization. In other cases peripheral input may be driving central sensitization so both will be present. Clinically, especially in the setting of a brief bedside examination, it can be difficult to document findings that would allow distinction between these two mechanisms. The bedside examination should focus on simply documenting signs consistent with the presence of sensitization. Interpretation of these signs must take into account caveats described at the end of this chapter. Repeated brush strokes (tested as one per second for 10 seconds) that produce increasing pain with each stroke is a simple test to perform. Repeated brush strokes or pinpricks (tested as 1 per second for 10 seconds) that produce increasing pain with each stroke is a simple test to perform. Have the patient rate the pain intensity at the beginning and end of the ten strokes/pinpricks and compare to the normal side. Repeated painful stimuli, like a pinprick, normally results in a progressively facilitated discharge by neurons in the spinal cord and results in an augmented pain response so that following repetitive pinpricks the intensity of the pain rating at the end is graded higher than a single stimulus. An exaggerated response to this test, compared to the normal side, is consistent with sensitization. Patients with nociceptive pain will also report brush and warm allodynia and heat hyperalgesia, such as is described with sunburn. Pressure allodynia, in particular, is common in both nociceptive and neuropathic pain. Allodynia to brush, cold and heat and temporal summation to tactile stimuli, although not pathognomonic, are observed in a much higher frequency in patients with neuropathic pain [5,27]. Bilateral sensory changes can occur in neuropathic pain conditions regarded as unilateral. Conclusion the careful clinical evaluation of patients with possible neuropathic pain is extremely important. Although many neurological diagnoses now rely on sophisticated imaging or testing these modalities have a limited role in determining the presence of neuropathic pain. The tests may determine dysfunction but no test can demonstrate the presence or absence of pain. Improving neuropathy scores in type 2 diabetic patients using micronutrients supplementation. The prevalence and impact of chronic pain with neuropathic pain symptoms in the general population. Randomized control trial of topical clonidine for treatment of painful diabetic neuropathy. New proposals for the international classification of diseases-11 revision of pain diagnoses. Quantitative sensory testing and mapping: a review of nonautomated quantitative methods for examination of the patient with neuropathic pain. Painful traumatic peripheral partial nerve injury-sensory dysfunction profiles comparing outcomes of bedside examination and quantitative sensory testing. Neurophysiology of pruritus: interaction of itch and 12 Name Date Please color the areas where you experience pain. Then circle with a pen all areas of pain and starting with the worst, number the areas in order of severity. In concert, these processes, amongst others, constitute the development of central sensitization. Increased neuronal excitability is often associated with voltage-gated sodium channels (NaVs). In these 50 m sections, epidermal nerve fibers (shown with thick arrows) appear green after immunohistochemical labeling. In diabetic peripheral neuropathy, numbers of epidermal nerve fibers diminish with extension of disease, contributing to sensory dysfunction. Skin lesions soon after rash healing surrounded by an area of anesthesia to punctate touch [solid line] and pin with wider area of pain on moving touch of cotton or tissue [interrupted line]. Disease refers to an identifiable disease process, such as inflammatory, autoimmune, or channelopathy [2]. Restriction to the "somatosensory system" allows the exclusion of motor nerve disease, which can produce pain indirectly by muscle spasticity, for example. This distinction has also streamlined the diagnostic testing required for the identification of etiologies of neuropathic pain, as outlined in this chapter. Neuropathic pain is not a single disease, but a composite of pain and other sensory symptoms with multiple potential underlying etiologies [2]. The diagnosis involves history and clinical examination, using conventional bedside neurological assessment to demonstrate positive or negative sensory, motor, and autonomic function. A diagnosis of "possible" neuropathic pain requires that the history conforms to a pain that fits the character and location of a neuropathic pain. Additional criteria are required to make the diagnosis of "probable" or "definite" neuropathic pain. Probable requires either the demonstration of a neural deficit or gain, or diagnostic tests which document a specific nerve disease process or nerve lesion. History and clinical examination Good clinical practice requires that the clinician takes a good history and performs an appropriate clinical examination in order to establish the diagnosis of neuropathic pain as possible or probable (outlined in Chapter 1). Further diagnostic investigations may be required to confirm the diagnosis and etiology, or to narrow down the differential list of possible causes. Blood tests may be indicated to diagnose treatable causes of painful neuropathy, such as those secondary to vitamin B12 or folate deficiency, or alcoholinduced neuropathy. It cannot locate the site of lesion, as an abnormal result may signal dysfunction anywhere along the sensory pathway between the receptor apparatus, the primary sensory cortex, and the associated sensory cortex. It is also used in drug research, to assess treatment efficacy on different neuropathic pain components (spontaneous or evoked pain) [8]. In particular, it cannot be used for the purpose of resolving medico-legal matters. It has been used to predict the outcome of treatment such as epidural steroid injection for impaired cold sensation in patients with sciatica [13]. Then, test for mechanical allodynia and hyperalgesia by stimulating the most painful area with a brush and pinprick respectively [Table 2. Quantitative sensory testing: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurophysiological testing Neurophysiological testing is used to diagnose disorders of large motor and sensory fibers in the peripheral nervous system. Nerve conduction studies assess activity in only the largest (20%) diameter myelinated fast-conducting fibers (A alpha and A beta fibers only account for 20% of nerve fibers), which functionally supply fine touch, vibration, and position sense. In such cases quantitative sensory testing and autonomic testing will be required. Nerve conduction studies provide the most objective non-invasive measure of nerve function.

While there may be no features on a skull radiograph that allow you to differentiate between the possible causes virus on macbook air buy flagyl with amex, it is worth remembering the more distant secondary features and demonstrating this knowledge infection journal generic flagyl 200 mg overnight delivery. You may be presented with a second related film to allow you to clinch the diagnosis antibiotics benefits discount flagyl 250 mg visa. Look at the cervical spine and upper thorax (if included) for any additional abnormalities antibiotics for uti for male buy flagyl 500 mg fast delivery. Distinguish between cleidocranial dysostosis and pyknodysostosis by assessing the bone density and mandible zinc antibiotic resistance buy flagyl cheap online. There is a rounded bacteria from water discount flagyl express, hyperdense, homogeneous mass in the midline of the posterior fossa. The mass extends into the fourth ventricle, which it compresses and displaces to the right. There is associated dilatation of the lateral and third ventricles in keeping with obstructive hydrocephalus. There is no evidence of an associated cystic component, calcification or extension into the basal cisterns. I would inform the local neurosurgical unit with a view to urgent treatment of the obstructive hydrocephalus. Discussion Whereas the most common cause of a posterior fossa mass in the adult is metastatic disease (most commonly from breast or lung carcinoma), in a child the most common cause is a primary malignancy. Typically, it arises from the cerebellar vermis or roof of the fourth ventricle, enhances avidly and homogeneously, and causing compression of the fourth ventricle. In contrast, ependymomas are characterised by expansion of the fourth ventricle and can extend through the foramina of Magendie and Luschka. Ependymomas contain areas of focal calcification and cystic change, and therefore have a heterogeneous appearance. Both medulloblastomas and ependymomas are associated with intradural extramedullary, spinal "drop" metastases. A cystic lesion with a small enhancing nodule indicates juvenile pilocytic astrocytoma. The lesion is centred on the right suprarenal region, displacing the right kidney and right lobe of the liver. The mass crosses the midline and encases the aorta, elevating it anteriorly away from the vertebrae. No liver metastases can be seen and there is no obvious involvement of the spinal canal. In summary, there is a large, retroperitoneal, soft tissue mass, centred on the right suprarenal region, encasing the aorta and displacing the right kidney. To take this further, I would arrange for the patient to be discussed in the next paediatric multidisciplinary meeting. A bone marrow aspiration is indicated for accurate staging of bony metastatic disease prior to treatment. Discussion There are many causes of an abdominal mass in the paediatric age group. In infants, multicystic dysplastic kidney and hydronephrosis are more commonly seen than tumours. It is very important to know their typical features and how they may be distinguished. In this case, the suprarenal location, encasement of the vessels and displacement of the kidney suggests neuroblastoma. In atypical cases, it may be difficult to tell these two pathologies apart, so both should be included in your list of differential diagnoses when there is a large, solid, perirenal/retroperitoneal mass in a young child. The most common location is the adrenal gland, followed by elsewhere in the retroperitoneum (sympathetic chain) and the posterior mediastinum. Extensive local spread may be seen, with encasement of vessels and invasion of the spinal canal via the neural foramina. If you are doing well in a viva case of neuroblastoma, you may be asked about the staging system. In Stage 1 and 2 disease, there is localised disease that does not cross the midline. In Stage 3 disease, the tumour involves the midline, and/or there is contralateral nodal involvement. Stage 4S is a special category seen in children under 18 months old, where there is a localised primary tumour and skin, liver or mild bone marrow involvement. This stage has a relatively good prognosis with the potential for spontaneous regression. Pearls In neonates, abdominal masses are frequently related to the genitourinary tract, especially hydronephrosis and multicystic dysplastic kidney. An ill-defined retroperitoneal mass with calcification, displacement of the kidney and vascular encasement is likely to be a neuroblastoma. When presented with a suspected neuroblastoma, look on the available images for nodal, hepatic, bony and soft tissue metastases as well as for involvement of the spinal canal. The umbilical clips and absent femoral head ossification centres indicate that this is a neonate. There is no evidence of pneumoperitoneum, peritoneal calcifications or portal venous gas to suggest perforation or bowel necrosis. After discussion with the paediatric surgeons, a contrast enema examination could be performed to assess the cause. There are multiple, small, filling defects in the right colon and terminal ileum outlined by contrast. Discussion the presence of multiple loops of dilated bowel in a neonate indicates a low bowel obstruction. Meconium ileus is a very common case seen in both the viva and long case part of the examination. It is characterised by bowel obstruction secondary to impacted thick meconium at the terminal ileum. On plain radiography, there may be a "soap-bubble" appearance in the right lower abdomen. A contrast enema is essential for diagnosis, showing the typical microcolon and filling defects in the terminal ileum, followed by reflux of contrast into dilated small bowel proximal to the obstruction. In comparison, there will be no reflux of contrast into the dilated small bowel in ileal atresia. The right colon is usually larger than the left, with meconium commonly causing obstruction at the splenic flexure. This causes a functional colonic obstruction and presents as a failure to pass meconium within the first 48 hours of life. At contrast enema, the aganglionic segment of colon is of normal calibre and the more proximal bowel is dilated. Look for an umbilical cord clip and absent humeral or femoral head ossification centres. Always comment on the presence and position of all catheters and tubes (umbilical artery and/or vein, nasogastric, etc. If yes, then meconium ileus and distal small bowel atresia are the differential diagnoses. We provide a free online form and downloadable certificate for your appraisal portfolio. It affects an estimated one in six adults and is associated with greater functional restriction and lower quality of life than standard chronic pain without neuropathic symptoms. Despite being common and important, a study of 1230 physicians revealed that a majority feel that the diagnosis and treatment of various neuropathic pain syndromes is challenging. Indeed, evaluation of patients does require a detailed history of pain and neuropathic features as well as careful physical examination of associated findings. In practice, the diagnosis of neuropathic pain is made on history and physical examination. This chapter will summarize a standard approach to identifying neuropathic pain for the clinician. History A comprehensive history to be elicited from patients with chronic neuropathic pain involves focusing not only on the description of pain, but also the constellation of frequently associated changes in mood, sleep, and functioning. Like many conditions in medicine, the majority of neuropathic pain syndromes are diagnosed on history while examination is used for subsequent confirmation. Patients with chronic pain often feel that their complaint of pain is minimized by healthcare providers and not appreciated or understood by their families. For this reason, it is best to initiate the medical history by permitting the patient to fully describe their pain experience as they understand it. The measure of pain severity, both during the initial history and subsequent follow-up visits, is purely by subjective patient reporting. A further grading system of "definite", "probable," or "possible" neuropathic pain was proposed based on the likelihood of showing a lesion or disease [3]. Note: chronic neuropathic pain-specific symptoms of sensory avoidance such as specific clothing to avoid contact with skin, wearing dark glasses in the examination room, poor oral hygiene in patients with mouth pain, etc. Q: Quality of the pain: descriptors like sharp or dull, burning or cold, intermittent or constant. R: Region where the pain is primarily felt and Radiation, if any, where the pain may seem to spread toward. However, chronic pain may be neuropathic, non-neuropathic (due to tissue injury or inflammation), due to an abnormality of pain processing or a mixture of all of these. These can be modified to permit particular drawing patterns to demonstrate different features of pain as well. Demonstrated is a patient outlining pain experienced with an L2 radiculopathic process producing pain over the right lumbar region and the right anterolateral thigh. Note that a patient with coincidental mechanical back pain and meralgia paresthetica could have a similar pattern. Patients are instructed to color or shade where they have pain, sometimes with simple word descriptors. Unilateral whole body pain diagrams are consistent with post-stroke pain, while entire body pain is seen with fibromyalgia (which can have neuropathic features). In cases of a mononeuropathy, a history of trauma, surgery, or disc disease must be inquired about, with the latter presenting as a radiculopathy pain. A recent history of spinal cord injury, stroke, or multiple sclerosis generally provides the clinician with the cause of pain. Nutrition history Low levels of folate, vitamin B1, vitamin B6, and vitamin B12 can cause peripheral polyneuropathy [6]. Therefore, it is essential to record a family or personal history of possible malabsorption such as that seen in pernicious anemia, celiac disease and short bowel syndrome. Any of these conditions can affect vitamin B12 levels, as can the use of common medications such as proton pump inhibitors and certain antiepileptic drugs. A vegan diet can also be associated with low vitamin B12 levels due to reduced intake. Furthermore, the supplementation with vitamin B12 can reduce polyneuropathy-associated pain. It is important to ask about multivitamin use in general and B vitamin supplementation in particular. Determination of habits such as poor sleep hygiene (using the bedroom as a place of entertainment, eating, as well as sleeping) and afternoon napping can be important to help guide recommendations for proper sleep hygiene. Patients with chronic pain for many years usually experience a gradual decline in overall and daily functioning. Patients may grow accustomed to this, so not all functional limitations may be reported unless specifically inquired for. The constellation of chronic pain syndromes Chronic pain is more than simply pain that persists for a long duration of time. Instead, chronic pain is a syndrome with a constellation of symptoms including depression, insomnia, fatigue, and decreased functioning [7,8]. Each of these comorbidities contributes to a line of questioning that is as important as the pain itself. The comorbidity of depression is high in the chronic pain population [9], necessitating a discussion of mood in all chronic pain patients. In some cases, this can be examined using screening questionnaires while in other cases, a more detailed and directed history may be appropriate. Beyond questionnaires on history, patient mood is often inferred by looking for common themes of anger after an accident, feelings of abandonment by family members and lack of dreams and goals for the future. Pain can interfere with sleep in many ways, from increasing sleep latency to leading to frequent awakenings and decreased slow-wave sleep. It is important to ask specifically about the need for daytime Chronic pain coping mechanisms Finally, no history of patients with chronic pain would be complete without inquiring into both successful and unsuccessful coping mechanisms. The burden of living with pain and associated symptoms is heavy, leading many patients to eventually attempt methods such as alcohol, illicit substances, or unsuccessful coping mechanisms such as denial or escapism. Positive coping mechanisms Deep breathing and relaxation Visualization Meditation Physical activity Increasing social contact Joining a support group Learning acceptance Negative coping mechanisms Denial Dissociation from self Escapism Addictions Self-harm Passivity 3 Section 1: the Clinical Presentation of Neuropathic Pain Neurological exam for pain the examination of a chronic pain patient should start with an appropriate and directed general examination including a neurological examination. The goal of the examination is to determine the presence of other pathological processes capable of causing pain. Most neuropathic pain disorders are characterized by stimulus-evoked positive sensory phenomena. The clinician will need to identify the area of abnormality (hemibody loss suggesting brain or spinal cord localization vs. A small-fiber neuropathy, a common cause of painful diabetic neuropathy, will present with pain and temperature sensory changes with preserved vibration and light touch in a glove and stocking distribution. Definition of terms A sensory threshold is the lowest point at which a stimulus begins to produce a sensation. This is relatively consistent but has some variability depending on age, sex, and body site tested. Pain tolerance is the greatest level of pain that any given person can tolerate at any given time and varies widely from person to person and in one person over time.

It is based on the condition that weak opioids can treat mild pain antimicrobial dog shampoo purchase flagyl in india, while strong opioids can treat moderate to severe pain antibiotics obesity order cheap flagyl on-line. It also implies that weak opioids have less abuse potential and therefore would be preferred as a step before using a strong opioid [2] bacteria lqp-79 discount 200mg flagyl otc. Weak opioids consist of codeine antibiotics for uti and breastfeeding order flagyl 250 mg without prescription, dextropropoxyphene antibiotic koi food discount flagyl 200 mg fast delivery, dihydrocodeine opportunistic infection order flagyl 250mg fast delivery, and tramadol while strong opioids consist of buprenorphine, fentanyl, hydromorphone, levorphanol, meperidine, methadone, morphine, oxycodone, and tapentadol. It should be noted that if a weak opioid is given in adequate amounts, it can provide the same analgesic effect as a strong opioid [2]. Another useful way to classify opioids is by their intrinsic activity to the opioid receptors because it can predict the clinical effects. A pure opioid agonist has affinity for binding sites as well as efficacy (ability to produce the effect). A pure antagonist (naloxone and naltrexone) has affinity for binding, however does not produce analgesia. A partial agonist (buprenoprhine) has affinity for binding only with low efficacy, and exhibits a ceiling effect because at high doses the antagonist effect is more pronounced [5]. Tramadol is a very weak -opioid receptor agonist, induces serotonin release, and inhibits the reuptake of norepinephrine in the dorsal horns of the spinal cord [6]. Tapentadol is a centrally acting analgesic with a dual mode of action as an agonist at the -opioid receptor and as a norepinephrine reuptake inhibitor [7]. It also has excellent oral bioavailability and long duration of action of at least 8 hours with repetitive dosing. Neuropathic pain can vary in severity, but usually leads to poor functioning and quality of life, and disturbed sleep and mood [6,8,9]. Neuropathic pain symptoms include numbness, weakness, spontaneous pain (burning, shooting, or electrical shock-like), and stimulus-evoked pain (allodynia and hyperalgesia) [10]. Systematic reviews and meta-analyses of opioids for neuropathic pain the Cochrane review of opioids for neuropathic pain included 14 trials of short duration (less than 24 hours) and nine trials with intermediate duration between 8 and 70 days. Among the short-duration trials there were contradictory results, but among the intermediate duration trials there was consistent evidence that spontaneous pain intensity was 13 points lower (scale from 0 to 100) with opioid than with placebo. The review also found improvement of evoked pain with oxycodone compared with placebo. There were inconsistent findings regarding secondary outcomes such as function, mood, and sleep [30]. In 2010, a systematic review of randomized, double-blind, placebo-controlled trials on neuropathic pain treatments included 174 studies [31]. The authors found the best evidence for a clinically relevant effect for the following drugs: tricyclic antidepressants, serotonin-noradrenaline reuptake inhibitors, gabapentin, pregabalin, and opioids. A recent meta-analysis of opioids for chronic noncancer pain included 62 randomized trials; of these 16 were for chronic neuropathic pain [32]. The oral opioids included: dihydrocodeine, tramadol, oxycodone, morphine, and tapentadol. Be mindful that the duration of trials is short (less than 3 months) in most trials, and that evidence is lacking regarding longterm effectiveness of opioids for neuropathic pain. Reference Population Interventions (1) dihydrocodeine maximum 240 mg/ day for 14 wks. Both groups improved over the 6 wk treatment period Tramadol was significantly more effective than placebo (average dose 210 mg/day) Tramadol group had better results on pain, paresthesia, touch-evoked pain, and allodynia Tramadol group had lower mean pain intensity. In 2011, the American Academy of Neurology, the American Association of Neuromuscular and Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation released an evidence-based guideline for the treatment of painful diabetic neuropathy. According to the authors of this guideline, there is "Level A" recommendation for pregabalin, and "Level B" recommendation for venlafaxine, duloxetine, amitriptyline, gabapentin, valproate, opioids (morphine sulfate, tramadol, and oxycodone controlled-release), and capsaicin. Other treatments were considered to have less robust evidence or the evidence was negative [34]. Adverse effects In a meta-analysis of 62 randomized trials, the most common adverse effects with opioids included nausea (28%), constipation (25%), somnolence (24%), dizziness (18%), dry skin (15%), and vomiting (15%) [32]. Opioid-induced bowel dysfunction consists of constipation, bloating, gastroesophageal reflux, and hard stools [35]. These are very subjective symptoms 243 Section 6: the Management of Neuropathic Pain with variation in the general normal population. For example, normal bowel movement frequency can vary from three times daily to once every 3 days. Prevention of opioid-induced bowel dysfunction can be achieved with high-fiber dietary intake and fluids. The first line of pharmacological interventions includes: stool softeners (docusate sodium) and bulking agents (psyllium). These medications can be used individually or in conjunction, and the dose can be titrated every 2 days until there is a sufficient bowel movement. If there is no bowel movement despite all previously mentioned options in place, or if there is stool impaction, stronger pharmacological interventions should be used, for example bisacodyl (tablets, suppository), glycerin suppositories, or enemas. It should be noted that while most adverse effects of opioids subside with time because of the development of tolerance, tolerance does not develop with constipation. Some patients, actually, may need treatment with metoclopramide for depressed gastric motility. Risk of overdose the risk of opioid overdose is higher in patients with the following conditions: 1. Elderly patients: despite the high prevalence of chronic pain in the elderly, opioids remain underused in this age group, partly because the use of opioids in the elderly has been associated with falls, fractures [40], and delirium [41]. Cognitive impairment: opioids should be avoided in cognitively impaired patients living alone (unless ongoing medication supervision is available) [42]. Sedating substances (benzodiazepines and alcohol): the risk of death from intentional or accidental overdose is increased when opioids are prescribed with other sedating drugs. Unfortunately, many patients with chronic noncancer pain are prescribed sedating drugs to help with their sleeping problems. Renal impairment: fentanyl, alfentanil, and methadone are the least likely to cause harm when used appropriately [43]. Liver impairment: opioids are metabolized in the liver and excreted through the renal system, therefore caution is advised in hepatic impaired patients. Sleep disorders including insomnia and daytime sleepiness: these also cause sedation and are very common among patients with chronic pain [48]. It is characterized by hyperalgesia (increased sensitivity to pain stimuli), worsening pain despite increasing doses of opioids, pain that becomes more diffuse, and pain that extends beyond the distribution of pre-existing pain [37]. Opioid-induced endocrinopathy results from the chronic use of opioids which may affect the production of growth hormone, cortisol, and sex hormones [38,39]. Clinically, the most important consequence is hypogonadism in men (decreased libido, sexual dysfunction, fatigue, and increased osteopenia risk) and women (amenorrhea, altered menstrual flow, probable reduced fertility, and possible contributions to opioid-associated depression, osteoporosis, and hyperalgesia). However, these figures are very variable depending on the definition of the diagnosis, the use of screening tests, and drop-outs. The most important risk factor for the development of opioid addiction is previous or current history of addiction. The Opioid Risk Tool includes items of family and personal history of substance abuse, age, history of preadolescent sexual abuse, psychological and psychiatric diagnoses. Patients in the "low risk" category had a 6% risk of exhibiting aberrant drug-related behaviors, compared with 91% in the "high risk" category [50]. This instrument, however, is semi-validated and may not be applicable to all types of neuropathic pain patients. A treatment agreement between the prescribing physician and the patient is intended to improve adherence and minimize misuse, abuse, addiction, and diversion. It is an opportunity for open communication about the potential benefits and risks, and also to reinforce the message that the decision to take the opioid should be taken seriously and responsibly. Opioid treatment agreements are particularly relevant for patients not well known to the physician or at higher risk for opioid misuse [44]. An example of a treatment agreement can be obtained at the website of the National Pain Centre nationalpaincentre. The views about the utility of urine drug screens vary among primary care physicians, pain specialists, and addiction specialists. There is no evidence to support a universal approach (where all patients are tested with urine drug screens in all visits), or a selective approach where (randomly or high-risk) patients are subjected to urine drug screens [52]. Urine drug screens can be used to assess baseline risk before the first opioid prescription is given, and as a monitoring tool for adherence to treatment [44]. The physician ordering the test should be familiar with the various types of tests (point-of-care, laboratory, immunoassay, and chromatography, etc. This n-of-1 trial (not randomized, not double-blinded) has the objective to determine if an opioid is a good option for this patient and if there is emergence of any unacceptable adverse effects, complications, or risks. The baseline assessment should include the therapeutic goals, the pain diagnosis and date of onset, assessment for overdose and addiction risks, and information provided to the patient. During the trial, it is important to monitor the daily dose in morphine equivalents, whether the goals have been achieved, the pain intensity and functional status, any adverse event, emergence of complications, aberrant behaviors, and other medications for pain [53]. The optimal dose can be achieved when there is balance among these three factors: the opioid has been shown to be effective, the benefits plateau, and the adverse events/complications are manageable [44]. Opioids are effective when there is improved function or at least 30% reduction in pain intensity. For chronic non-cancer pain, a daily morphine equivalent of 200 mg is considered a "watchful dose"; above this a careful reassessment of the pain and of risk for misuse is recommended, together with frequent monitoring with evidence of improved patient outcomes [44]. This includes all other physicians involved in the care of this patient and the pharmacist who is 245 Section 6: the Management of Neuropathic Pain dispensing the opioid. Pharmacists can be helpful to reinforce education, to observe aberrant drug-related behaviors, and to alert physicians about potential misuse and overdose [44]. Key points Five actions should always be done when prescribing opioids for chronic non-cancer pain, including neuropathic pain: 1. Start with a comprehensive assessment to ensure opioids are a reasonable choice and to identify risk/benefit balance for the patient. Set effectiveness goals with the patient and inform patient of their role in safe use and monitoring effectiveness. Watch for any emerging risks/complications to prevent unwanted outcomes including misuse and addiction. Results from clinical trials show that opioids are better than placebo for pain and function for certain neuropathic pain conditions. There is some preliminary evidence to suggest more effectiveness when combining opioids with the anticonvulsant gabapentin, but not with the antidepressant nortriptyline, or the anticonvulsant pregabalin. The doses used to achieve benefit in these trials were usually below the watchful dose of 200 mg of morphine equivalent a day suggested by the Canadian Guideline for safe and effective use of opioids [44]. Opioids may carry serious risks of overdose and abuse, while many of their common side effects can usually be appropriately managed. Comparison of analgesic effects and patient tolerability of nabilone and dihydrocodeine for chronic neuropathic pain: randomised, crossover, double blind study. The response of neuropathic pain and pain in complex regional pain syndrome I to carbamazepine and sustained-release morphine in patients pretreated with spinal cord stimulation: a doubleblinded randomized study. The specific disease burden of neuropathic pain: results of a French nationwide survey. Efficacy of oxycodone in neuropathic pain: a randomized trial in postherpetic neuralgia. Results of an open, parallel pilot study vs clomipramine with and without levomepromazine. Opioids versus antidepressants in postherpetic neuralgia: a randomized, placebo-controlled trial. Tramadol in postherpetic neuralgia: a randomized, double-blind, placebo-controlled trial. Controlled-release oxycodone for pain in diabetic neuropathy: a randomized controlled trial. Fentanyl buccal tablet for the relief of breakthrough pain in opioid-tolerant adult patients with chronic neuropathic pain: a multicenter, randomized, doubleblind, placebo-controlled study. Morphine versus mexiletine for treatment of postamputation pain: a randomized, placebo-controlled, crossover trial. A randomized, controlled trial of oxycodone versus placebo in patients with postherpetic neuralgia and painful diabetic neuropathy treated with pregabalin. A comparison between enriched and nonenriched enrollment randomized withdrawal trials of opioids for chronic noncancer pain. Evidence-based guideline: treatment of painful diabetic neuropathy: report of the American Academy of Neurology, the American Association of Neuromuscular and Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. Efficacy and safety of mu-opioid antagonists in the treatment of opioid-induced bowel dysfunction: systematic review and meta-analysis of randomized controlled trials. Opioid-induced abnormal pain sensitivity: implications in clinical opioid therapy. Pharmacological treatment of opioid-induced hyperalgesia: a review of the evidence.

Other effects require collaboration with the health care provider to address the effects oral antibiotics for acne in india discount 500mg flagyl with mastercard. A patient with nausea and vomiting after receiving a narcotic pain reliever may be comforted by the nurse who provides small frequent meals antibiotic treatment for h pylori order generic flagyl from india, small sips of clear liquids antibiotic basics for clinicians pdf discount 400mg flagyl, or frequent changes of linen infection signs and symptoms purchase 250mg flagyl free shipping. But an antiemetic drug ordered by the health care provider may also be required to limit the effects to manageable levels antimicrobial hand sanitizer flagyl 500mg generic. Therapeutic and adverse drug effects must be documented during the implementation phase can antibiotic resistance kill you order flagyl cheap online. This should include documentation of the appropriate administration of the medication, as well as the effects observed. Patient medication teaching is a vital part of the intervention phase of the nursing process. Deficient knowledge and even noncompliance are directly related to the type and quality of education a patient has received about the medication. State nurse practice acts and regulating bodies such as the Joint Commission consider teaching to be a primary role for nurses, giving it the weight of law and key importance in accreditation standards. Because the goal of pharmacotherapy is the safe and effective administration of medications, teaching is targeted to providing the patient with the information necessary to ensure this occurs. Every interaction a nurse has with the patient presents an opportunity for teaching. Small portions of education given over time are often more effective than large amounts of information given on only one occasion. Discussing the medications each time they are administered is also an effective way to increase the amount of education accomplished. Providing written material also assists the patient to retain the information and review it later. Some medications come Using the Nursing Process in an Outpatient Setting In an outpatient setting, a lack of drug response determined during the evaluation phase may be caused by patient nonadherence to the drug regimen. While conducting a reassessment, the nurse needs to determine if the patient is taking the drug as prescribed. If nonadherence is discovered, the nurse must further assess possible reasons for the nonadherence: Cost issues, unpleasant side or adverse effects caused by the drug, inability to obtain transportation to a pharmacy, or inadequate drug storage options are all reasons for nonadherence. Of particular concern is lack of prior patient teaching regarding the need for the drug, selfadministration strategies, or methods for managing or alleviating side and adverse effects. The reassessment will direct the planning and implementation strategies for increasing adherence. By determining the precise cause for nonadherence, the nurse can work with the patient to ensure safe and effective medication use with the best therapeutic outcome possible. The patient (or the caregiver) must be able to read and understand the material provided. Pharmacies may dispense patient education pamphlets that detail all of the effects of a medication and the monitoring required, but if the reading level is above what the patient can understand or is in a language not used by the patient, they will not be useful. Having the patient "teach" the nurse, or summarize key points after the teaching has been provided, is a safety-check that nurses may use to verify the information has been understood. Older adults and pediatric patients sometimes present special challenges to patient teaching. For the older adult, the use of written or video teaching materials, especially those that may be taken home and reviewed, and teaching that is repeated and provided in small increments may be helpful. For young children, simple explanations accompanied with illustrations, perhaps in the form of a coloring page, may help the child to feel that they are a part of their care. The Nursing Practice Applications throughout this text also supply intervention strategies and teaching points for specific classifications of drugs. Do you know what other medications you should not take while taking this medication Are there any foods or beverages you must not consume while taking this medication Children Use family-centered approaches when providing drug teaching for children and adolescents. Adults Adults learn best when the topic is of immediate value, and new material is connected to previous experiences. Employ multiple methods of delivering information; combinations of verbal and written material are beneficial. Ensure that the patient has the necessary aids (glasses, magnifying glass, hearing aid) to maximize learning experience. The nurse will then evaluate the effectiveness of these interventions in the final step of the nursing process. Providing Culturally Appropriate Teaching Effective teaching requires the nurse to be sensitive and respect ethnic and cultural diversity. The following are some multicultural patient teaching considerations: Evaluation 9. As the final step of the nursing process, evaluation considers the effectiveness of the plan of care and interventions in meeting the established goals and outcomes. The process comes full circle as the nurse reassesses the patient, reviews the nursing diagnoses, uses the goals and outcomes established as the evaluation criteria to judge the effectiveness of the plan, and makes any changes needed. If the patient has met the outcomes identified in the plan of care, the problem has been resolved. If it has not been resolved, the nurse reviews and rewrites goals and outcomes in the plan of care, and carries out further interventions necessary to meet these goals and outcomes. When evaluating the effectiveness of medication administration, the nurse assesses for therapeutic effects and for the occurrence of any side or adverse effects. The nurse also evaluates the effectiveness of teaching provided and notes areas where further teaching is needed. Rather, it is the beginning of another cycle as the nurse continues to strive for safe and effective medication use and active involvement by the patient in his or her care. It is a checkpoint where the nurse Show respect; acknowledge cultural and ethnic differences. Assess for cultural and ethnic self-care practices that may interact with medications or treatment, such as folk or home remedies and dietary practices. Consider possible differences in family structure and decision making for health care concerns. The nursing process acts as the overall framework in medication administration to work toward this success. The nurse knows that furosemide is a potent diuretic that acts in the loop of Henle to prevent reabsorption of sodium and chloride, and because these are being flushed out in the urine, water follows. The nurse also knows that furosemide carries the risk for dehydration, ototoxicity with hearing loss, and allergic reaction. Identify a nursing diagnosis, the goal, evaluation criteria, nursing Mary Richards, who is 70 years old, sees her health care provider later that morning, who diagnoses her with an acute exacerbation of heart failure. The patient is now being prepared for discharge and is to continue taking furosemide 20 mg/day by mouth at home. Identify a nursing diagnosis, the goal, evaluation criteria, nursing interventions, and evaluations to provide drug teaching for this patient. Evaluation What are the two main steps of the planning phase of the nursing process Evaluating for adverse drug effects Which of the following would the nurse evaluate first during the evaluation phase of the nursing process The possibility of nonadherence with drug therapy Which of the following is appropriate information to gather during the assessment phase of the nursing process Adverse effects that have been prevented A nursing diagnosis of Noncompliance may be established for a client who is not taking a drug as prescribed. Before deciding that "noncompliance" is the correct diagnosis, the nurse would assess that what two criteria have been met What elements need to be included in the assessment phase of the nursing process for this patient List three evaluation criteria the nurse will use to evaluate the effectiveness of medication administration for this patient. Describe physiological changes during pregnancy that may affect the absorption, distribution, metabolism, and excretion of drugs. Explain how drugs administered during the different stages of fetal development affect the potential for teratogenic effects. Outline important points in patient and family education regarding drug use during pregnancy and lactation. Pharmacotherapy During Lactation Transfer of Drugs into Breast Milk Adverse Drug Effects During Lactation Administering medications to pregnant women requires special precauplacenta, 127 tions. The nurse must be aware of the pregnancy physiological changes occurring in categories, 127 the pregnant woman along with the teratogen, 129 developmental stage of the fetus. The nurse must also be able to identify potential adverse drug events occurring in both the mother and the fetus. This chapter describes the pharmacokinetic changes that occur during pregnancy, and explains the importance of carefully monitoring the pharmacotherapy of pregnant and lactating women. Emphasis is placed on drugs to avoid or use cautiously, efforts to prevent adverse effects, and the importance of patient and family education. In other cases, a medication may need to be discontinued, changed to a lower dose, or replaced with a safer drug. In all pregnant patients, health care providers must carefully consider the therapeutic value of a given medication against its potential adverse effects. Some physiological activities speed up while others slow down, altering the pharmacokinetic responses to drugs. Absorption: During pregnancy, increased levels of progesterone cause a decrease in gastric tone and intestinal motility, resulting in delayed gastric emptying. High estrogen levels in the pregnant woman cause increased hydrochloric acid production in the stomach, which may affect the absorption of certain acid labile drugs. Furthermore, as the enlarging uterus rises into the abdomen it presses up against the stomach, leading to slower gastric emptying. Medications may take a longer time to be absorbed and distributed, thus prolonging their onset and durations of action. Some women experience nausea and vomiting and are unable to take oral medications during early pregnancy. Progesterone also increases pulmonary blood flow, respiratory tidal volume, and minute volume by 40%. As a result, respiratory agents such as cromolyn (Intal) are absorbed in larger quantities, leading to higher serum drug levels. Distribution: Distribution of drugs during pregnancy is affected by changes in total body water, which may increase by over 50%. The nurse caring for the pregnant or lactating woman faces the challenge of concurrently being responsible for the health and safety of two persons, knowing that most medications cross the placenta and are secreted in breast milk. Despite potential risks to the fetus, first-trimester use of prescription drugs has increased by more than 60% in the past 30 years (Mitchell et al. By 2008, approximately 50% of pregnant women reported taking at least one medication, with a large increase observed in antidepressant use. In addition, more than 9% of pregnant women take an herbal supplement (Broussard, Louik, Honein, & Mitchell, 2010). Health care providers always exercise great caution when initiating pharmacotherapy during pregnancy or lactation. Drug therapy is often postponed until after delivery and lactation, and if that is not possible, safer nonpharmacologic alternatives may be implemented. Certain acute and chronic conditions, however, must be managed with medications during pregnancy. If the patient has preexisting epilepsy, asthma, hypertension, or a psychiatric disorder, it would be unwise to discontinue pharmacotherapy during pregnancy or lactation. Thromboembolic disorders, gestational diabetes, and gestational hypertension may occur during pregnancy, and must be treated for the safety of both the mother and growing fetus. Acute urinary tract infections and sexually transmitted infections have the potential to harm the mother or fetus if undetected or inadequately treated. The goal of pharmacotherapy in pregnant patients is to treat the mother without causing ill effects for the fetus. Because the plasma proteins are diluted, fewer are available to bind with drugs, thus causing a higher concentration of "free" drug in the plasma. This results in more drug molecules being available for transfer across the placenta or to be secreted in breast milk. Highly lipophilic drugs are distributed into the lipid-rich breast milk and are ultimately passed to the lactating infant. Metabolism: Of the pharmacokinetic variables, metabolism is least affected by pregnancy. Because the placenta and fetal liver contribute to overall drug metabolism, the metabolism of certain drugs may increase during pregnancy. Drugs such as nicotine can increase the amounts of placental metabolic enzymes, possibly affecting drug metabolism. Excretion: Excretion of drugs during pregnancy is enhanced by renal plasma flow, which can increase 50% to 70% during the first two trimesters. Because these changes result in the increased renal elimination of drugs, doses of many medications must be adjusted. In general, the higher the dose taken by the mother, the greater the amount of drug available to cross the placenta and affect the fetus. This is the rationale for prescribing the lowest effective doses of drugs during pregnancy. Highly lipid-soluble drugs will cross the placental barrier more easily than water-soluble drugs. Thus drugs that are highly protein bound are more likely to cross the placenta more slowly and in lower doses compared to nonbound drugs. Upon reaching the relatively acidic environment of the fetus, drugs that are weak bases become ionized. This effectively traps them on the fetal side of the placenta, because ionized drugs cannot recross the placental membrane back to the mother (ion trapping). An example is nicotine (a weak base), which can appear in higher concentrations in the fetus than in the mother due to ion trapping. Decreased uterine blood flow may cause drugs to remain trapped in the fetus for extended periods, resulting in fetal adverse effects. During labor the patient is usually instructed to remain in the lateral position during active uterine contractions to prevent pressure on the aorta and vena cava. Pressure on these vessels will obstruct uterine blood flow and may cause drug accumulation in the fetus. The placenta is a temporary organ that allows for nutrition and gas exchange between the mother and fetus. Although the blood of the mother does not circulate through the fetus, capillary-like structures in the placenta allow an extensive exchange of substances.

No evidence of underlying inflammatory or demyelinating disease was found in clinical work-up how long do you take antibiotics for sinus infection purchase flagyl 400mg fast delivery, and enhancement resolved antibiotic klebsiella buy flagyl 500 mg fast delivery. Intravenous gadolinium should be routinely administered antibiotics for uti uk purchase 200 mg flagyl with mastercard, as it helps in the differentiation of recurrent disc herniation from postoperative scarring virus 368 purchase flagyl canada. Moreover antibiotics for acne dry skin discount flagyl online master card, it may assist with diagnosis of postoperative arachnoiditis and spinal infection antibiotics for acne from dermatologist cheap flagyl 500 mg without prescription. Sagittal as well as axial images should be routinely obtained in postoperative spine without and with intravenous gadolinium. This is because of accompanying postsurgical alterations and edema, as well as frequent co-incidence of scar and herniated disc. One may be able to identify a thin band of very low signal surrounding the disc, suggestive of fibers of annulus. Recurrent disc herniation generally does not enhance with intravenous contrast other than at its periphery [1]. However, it is imperative that the imaging should begin promptly after contrast administration. The disc may enhance homogeneously on delayed enhanced images and may therefore be inseparable from scar. Postsurgical scar is generally ill-defined, demonstrates low T1 as well as T2 signal, and enhances with contrast administration. The scar is infiltrative and does not exert mass effect on the nerve root of the thecal sac. However, scar often coexists with recurrent disc, and it may not always be possible to differentiate reliably between the two. Differential diagnosis Recurrent disc and scar demonstrate similar signal intensities on unenhanced T1-weighted sequence. The disc has a globular or polypoid appearance, and it is usually contiguous with the parent disc unless sequestrated. An overlying, peripheral rim of dark signal may outline the disc, enhancing after contrast administration. Mass effect on the nerve or thecal sac points to the disc, whereas retraction of the thecal sac toward a soft tissue lesion is suggestive of scar. An examination with gadolinium contrast allows the differentiation between postoperative scar and recurrent disc herniation with a very high accuracy. If postoperative scar is the predominant pathology, the issue of reoperation should be considered very carefully. Importance Accurate differentiation of recurrent disc herniation from scar formation may allow improved treatment choices and references 1. Note a postoperative collection (curved arrow) and diffuse epidural soft tissue anterior to the thecal sac. The peripheral band of low intensity and maintained connection to the disc differentiate the disc from adjacent postoperative soft tissue thickening. A small extruded disc fragment in the left lateral recess is marked with an arrow on enhanced T1-weighted axial image. Peripheral rim of enhancement and presence of mass effect on adjacent L4 nerve root on T2-weighted image differentiate this from the more extensive and laterally located scar (curved arrow). Diffuse postoperative epidural fibrosis (scarring) in this patient exists along the right L5 laminectomy, lateral and anterior to the thecal sac on the right (arrow). Note the infiltrative nature of the scar surrounding the nerve root as well as the presence of enlargement and subtle high signal in the S1 nerve root. Discitis is an inflammatory process that is a result of infection that initially seeds in the vertebral endplate. With progressive destruction of the disc, fluid starts to accumulate and there is developing paravertebral and/or epidural inflammatory change. Destruction and erosive changes of the endplate are a hallmark of discitis/ osteomyelitis. In discitis, the disc is hyperintense on T2-weighted studies and demonstrates enhancement, but in degenerative disease it is hypointense, although in rare cases there can be T2 hyperintensity within the disc space in the setting of degenerative disease. The enhancement is intense in discitis/osteomyelitis but fairly subtle in denenerative endplate change. Additionally, paraspinal inflammatory changes are a hallmark of discitis but not appreciated in degenerative disease. While these are non-specific, when they are negative they can be used to exclude discitis. Imaging description Disc degeneration is accompanied by loss of hydration in the nucleus pulposus and declining structural integrity of the annulus fibrosus. The nucleus pulposus loses its high signal on T2-weighted images and there is a loss of disc height. Alterations in the adjacent vertebral endplates and vertebral marrow are commonly identified adjacent to the degenerated disc. These changes have been classified based on the pathologic changes in the vertebral endplate. Modic type 1 marrow change signifies vascularized marrow, appearing hypointense on T1-weighted and hyperintense on T2-weighted sequences. Type 2 changes occur with more chronic disc degeneration, with fatty changes in the adjacent marrow. This type of degenerative change demonstrates high signal on T1-weighted and slightly high signal on T2-weighted images. Type 3 changes represent sclerosis and marrow fibrosis, resulting in dark signal on T1- and T2-weighted sequences [1]. There is relatively little evidence that the exact type of marrow changes harbor any clinical significance. However, it is imperative that radiologists be aware of the spectrum of signal abnormalities that can occur in the marrow and not confuse these with more sinister pathologies. Teaching points Although extensive marrow alterations may accompany degenerative disc disease, these can be differentiated from discitis because of sparing of the endplate margins, lack of high T2 signal in the disc, and relatively modest enhancement with contrast. Importance Marrow changes accompanying degenerative disc disease are commonly mistaken for discitis and osteomyelitis. Differentiation between these two processes may, however, occasionally prove to be quite difficult or even impossible. Typical clinical scenario Degenerative endplate changes are mainly identified on studies performed for the evaluation of back pain or radiculopathy. Differential diagnosis Endplate and degenerative marrow alterations are frequently confused with discitis and osteomyelitis. Note symmetric, low-intensity bands that demonstrate high signal edema on T2-weighted study. The endplates remain well defined and the disc has low T2 signal, suggesting degenerative process. Again, note that the endplates are well corticated and there is no paravertebral of epidural edema. Imaging description Spina bifida properly refers to lack of fusion of the posterior bony element of the spinal canal. However, it is commonly confused with spinal dysraphisms, which are malformations of the spinal column and/or spinal cord across previous stages of development. The classification of spinal dysraphism takes into account the clinical, neuroradiological, and embryological features [1]. The neural placode is a segment of flattened, non-neurulated embryonic neural tissue [2]. It can be terminal or segmental, depending on its location with relation to the cord. Clinically, spinal dysraphism can be categorized into open and closed varieties, depending on the location of the neural placode. When discovered in childhood or adulthood, it is important to look for associated abnormalities such as tethered cord, syringomyelia, dermal sinuses, vertebral anomalies, and intraspinal masses. A comprehensive classification of spinal dysraphism, based on embryogenesis, clinical findings, and radiological features, is summarized in Table 97. Differential diagnosis A bifid spine may not be associated with spinal dysraphism. In myelomeningocele, the neural placode protrudes above the cutaneous surface due to expansion of the underlying subarachnoid spaces. However, in myelocele, the placode is at the same level as the surface of the skin. In a terminal myelocystocele the terminal syrinx cavity, including terminal portion of the cord, herniates within a meningocele. All posterior dermal sinuses above the natal crease should be suspected of occult spinal dysraphism and further evaluated. Caudal regression and agenesis may be associated with lower limb abnormalities or anorectal malformations. The accuracy of abnormal lumbar sonography findings in detecting occult spinal dysraphism: a comparison with magnetic resonance imaging. The low-lying spinal cord enters the outpouching (short arrows) and ends in the terminal placode. Note the terminal portion of the low-lying spinal cord within the spinal canal (short white arrow). It attaches to a lipoma (short arrow) outside the anatomic boundary of the spinal canal. It is suggested that the surgical release of tethered cord should be performed on appearance of an upper motor neuron sign. The technical goal of untethering surgery is to remove the tension from the spinal cord, while the therapeutic goal is to stabilize symptomatology and cord function [1]. Imaging description In a radiological study, termination of conus medullaris below L2 vertebral level is considered tethering of the cord. Closed spinal dysraphisms such as lipomyelomeningocele, diastematomyelia, neurenteric cyst, lumbosacral lipoma. Almost all children born with open spinal dysraphisms such as spinal meningoceles. With increasing tension on the spinal cord, the blood flow and oxidative metabolism become impaired, with resultant ischemic injury and diminished conduction in both motor and sensory nerve fibers. The epicenter of syringomyelia associated with tethered cord is very close to the tethering site or dysraphism [5]. Ultrasound can be used for determining the conus level in the newborn, but the sonographic window disappears at 2 months of age. Typical clinical scenario the clinical presentation of tethered spinal cord depends on the age group and etiology. Cutaneous stigmata in neonates, such as presence of nevi, posterior midline lipomas, tufts of hair, hemangiomas, and dermal sinuses may be the only sign. There is a high association with a presence of anorectal malformations, scoliosis, and orthopedic lower limb deformity. In childhood and adolescence, gait difficulty, progressive motor dysfunction, sensory deficits, progression of scoliosis, foot drop, pain, and sphincter dysfunction are seen. In a small minority of patients, it is possible to have a low-lying conus medullaris without evidence for filum lipoma or thickening of terminal filum on axial imaging. The low position of the conus in the postoperative setting causes difficulties in interpretation. After repair of spinal dysraphism and untethering of the cord, there is a high incidence of retethering. However, radiologic low position of conus medullaris in the postoperative setting cannot be used to diagnose retethering. Teaching points the classic imaging appearance is conus medullaris terminating below the inferior endplate of L2 vertebra, a tight filum terminale with associated tethering mass. It is seen in a majority of cases with open or closed spinal dysraphism, but can also be seen in completely intradural conditions, scar tissue from prior surgery, trauma, infection, and neoplasm. Terminal syringomyelia can be seen in up to a third of patients with tethered cord. The high incidence of retethering following surgery for spinal dysraphism demands critical evaluation of the postsurgical spine. Importance There are conflicting opinions regarding surgical management of patients with tethered cord. A few studies indicate that reversal of upper motor neuron function is poor even after surgery if there is onset of neurologic deficit. Based on these observations, prophylactic release of tethered cord is advocated [2]. Clinical significance of terminal syringomyelia in association with pediatric tethered cord syndrome. Preuntethering and postuntethering courses of syringomyelia associated with tethered spinal cord. The tethered spinal cord is low-lying (black arrow) with presence of a lipoma of filum terminale (white arrow). Imaging description Hans Chiari described Chiari malformations as a congenital condition in the late nineteenth century [1].

Generic flagyl 400 mg mastercard. Swiss TPH: Jakob Zinsstag on One Health and antimicrobial resistance.