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Kim Y order meclizine medicine kit for babies, Ko M buy meclizine online now medicine plus, Na S discount 25mg meclizine otc medicine song, et al: Effects of single-dose methylphenidate Neuroimage 14:1004–1012 meclizine 25mg without a prescription medicine bg, 2001 on cognitive performance in patients with traumatic brain McDowell S, Whyte J, D’Esposito M: Differential effect of a dopa- injury: a double-blind placebo-controlled study. Clin Reha- minergic agonist on prefrontal function in traumatic brain in- bil 20:24–30, 2006 jury patients. Hum Psychopharmacol Nickels J, Schneider W, Dombovy M, et al: Clinical use of amanta- 20:97–104, 2005 dine in brain injury rehabilitation. J Neurol Sci 103(suppl):S39–S42, 1991 fects of lamotrigine in traumatic brain injury. Neurology Ponsford J: Rehabilitation of attention following traumatic brain in- 70:771–778, 2008 jury, in Cognitive Neurorehabilitation: Evidence and Applica- Lezak M, Howieson D, Loring D: Neuropsychological Assess- tion, 2nd Edition. J Neurol loading on verbal, spatial and affective working memory Neurosurg Psychiatry 60:416–421, 1996 functions in healthy adults. Cogn Behav Neurol Rankin K: Social cognition in frontal injury, in The Human Fron- 18:18–27, 2005 tal Lobes. New York, Guil- Masanic C, Bayley M, VanReekum R, et al: Open-label study of ford, 2007, pp 345–360 donepezil in traumatic brain injury. Scheid R, Walther K, Guthke T, et al: Cognitive sequelae of diffuse J Head Trauma Rehabil 1:424–427, 1999 axonal injury. Arch Neurol 63:418–424, 2006 Whyte J, Hart T, Schuster K, et al: Effects of methylphenidate on Schneider W, Drew-Cates J, Wong T, et al: Cognitive and behav- attentional function after traumatic brain injury: a random- ioral efficacy of amantadine in acute traumatic brain injury: ized, placebo-controlled trial. Am J Phys Med Rehabil 87:85–99, 2008 vastigmine capsules in patients with traumatic brain injury. Nat Rev Neurosci 4:637–648, 2003 Willmott C, Ponsford J: Efficacy of methylphenidate in the reha- Soeda A, Nakashima T, Okumura A, et al: Cognitive impairment bilitation of attention following traumatic brain injury: a ran- after traumatic brain injury: a functional magnetic resonance domized, crossover, double blind, placebo controlled inpa- imaging study using the Stroop task. Exp Neurol 66:136– ogy 71:812–818, 2008 152, 2000 Vakil E: The effect of moderate to severe traumatic brain injury on Zoccolotti P, Matano A, Deloche G, et al: Patterns of attentional different aspects of memory: a selective review. J Clin Exp impairment following closed head injury: a collaborative Eu- Neuropsychol 27:977–1021, 2005 ropean study. Motivation is an ever- is sustained, is directed, is stopped and what kind of sub- present, essential determinant of behavior and adaptation. Psychologically and biologically, motivation is a complex of capacities, and the neural systems that subserve it are themselves Disorders of Motivation both delimited and distributed, integrated and interde- pendent. Disorders of motivation may be and descriptions of their assessment and management that classified by an increase, decrease, or dysregulation of are based on a biopsychosocial approach to the causes of motivation, as well as anergias typified by Lyme disease, motivational loss. We then discuss the neural mechanisms chronic fatigue, and psychomotor retardation. Readers should expect toms of interictal personality in temporal lobe epilepsy the clinical material to be familiar in some ways-because and by appetitive disorders such as aggression and hyper- neuropsychiatric assessment of motivation builds on ev- phagia. Dysregulation of motivation is exemplified by im- eryday clinical skills and experiences-and unfamiliar in pulse control disorders, obsessive-compulsive disorder, others-because most clinicians are not in the habit of and attention-deficit/hyperactivity disorder. Disorders of making explicit their intuitive understanding of motiva- diminished motivation include akinetic mutism, abulia, tion in clinical practice. Literature (Marin 1997) sion and dementia as well as for frontal-subcortical syn- places them on a continuum of motivational loss, with ap- dromes that affect personality and executive cognitive athy at the minor pole and akinetic mutism at the major dysfunction. Patients with diminished motivation all show dimin- Cases of akinetic mutism follow bilateral lesions of the ished activity. Inactivity-whether motor, cognitive, or anterior cingulate cortex that form from the cognitive re- emotional-may result from changes in virtually any do- gion posteriorly to the skeletomotor division of the cingu- main of mental status. Akinetic mutism is with coma, stupor, or mild delirium suggest diminished characterized by profound apathy; a wakeful state with no motivation because they are often associated with dimin- spontaneous movement or verbalization; indifference to ished activity. Memory loss may suggest diminished mo- pain, thirst, or hunger; and lack of response to prompts tivation when there is increased latency of response or and questions. Intact visual tracking is essential for the when patients have poverty of speech because they have diagnosis; its presence excludes more extensive damage poverty of recall. Conditions that may contribute nations, and reduplicative phenomena-may lead to be- to akinetic mutism include cerebrovascular disease, cra- wilderment and preoccupation, which also may bring ap- niopharyngiomas, and tumor. Disorder of (2002) studied the concept of abulia in a group of British thought content and form may be particularly misleading. Thought blocking, circum- of purposeful and spontaneous movements, poverty and stantiality, and impaired coherence of thought may appear latency of speech, and reduced interest in usual pastimes as reduced goal-directedness or drive. Abulia shades into akinetic mut- In light of these factors, the two groups of disorders to ism when it worsens and into apathy when it improves. Diminished activity suggests diminished motivation and sustain behavior; describe their plans, goals, and in- but is actually due to other impairment. In stupor and terests; and react emotionally to significant events and ex- coma, the essential impairment is diminished level of periences. Delirium may involve a diminished extensive, less intense, and shorter in duration than they level of consciousness but is primarily a disorder of at- are in individuals who are not apathetic. Aprosodia is a disorder of emotion Recognition information; diminished motivation is not a feature. Because motivation is the both may be associated with truncated emotional re- psychological domain concerned with goal-directed be- sponses. Diminished activity is associated with diminished behavioral, cognitive, and emotional concomitants of goal- motivation, but both are due to some other disorder. By definition, it is a diminished motivation and thus is a guideline for identi- dysphoric state. However, motivational symptoms are commonplace in depression; it is dysphoria and negative thought content that distinguish depression. Dementia is, by definition, a disorder found impairment in level of consciousness, attention, of intellect. Memory, executive capacity, or other cog- speech, or motor capacity (Celesia 1997). Output is via the motor cortex, basal ganglia, reticulospinal tract, and pedunculopontine nucleus. The flow of information within and through the circuits permits the translation of motivation into action. First, determining tivity with output regions in the basal ganglia and brain stem. If one is unable to per- tional differentiation into limbic-motive and motor-output ceive what is there, one’s appraisal of its motivational sig- regions. Sensorimotor ca- throughout the circuit in response to a motivational stimu- pacity also modifies behavior because motivation depends lus. Dopamine signals the circuit to initiate behavioral re- on the individual’s subjective assessment of the likelihood sponses to the stimulus and facilitates cellular changes that that behavior will lead to goal attainment. If less decrease spontaneous, stimulant-induced, and food-induced severe-either because the initial insult is less severe or motor activity, with commensurate decreases in food- because a patient with severe injury is improving-the pa- seeking behavior as response requirements of the task tient shows apathy. In rat studies of lesions of as pure or affective apathy, because motivation is lost with- frontal cortical areas, lesions or inactivation of the anterior out impairment of extrapyramidal motor or executive cog- cingulate cortex (Schweimer and Hauber 2005), as well as nition. This interpretation of pathogenesis is supported by inactivation of basolateral amygdala (Ghods-Sharifi et al. This presents as havioral effects similar to those produced by accumbens akinesia or motor apathy, depending on whether the ex- dopamine depletion (Farrar et al. Although there has trapyramidal or motivational symptoms predominate, re- been rapid growth in the evolution of our understanding of spectively.
Patients should be transferred lying on a rigid board with their neck in a neutral position cheap meclizine master card treatment zone guiseley. This following neck protection policies at the expense approach reduces the risk of entering the vicious of preventing other major causes of mortality such circle of raising the blood pressure cost of meclizine treatment enlarged prostate, restarting bleed- as overt bleeding has probably cost lives buy generic meclizine 25 mg medicine qid. It may of breathing and the C of circulation should take also avoid the marked reduction of mesenteric and precedence in patients with limb injuries and no renal perfusion order discount meclizine online medicine 44390, which is the normal homeostatic evidence of head or neck injuries. Circulation mum also reduces the complications of interstitial fluid overload – heart failure, pulmonary oedema, Almost all patients who have a major injury will be peripheral oedema and paralytic ileus – and pre- in ‘hypovolaemic shock’ as evidenced by the pres- vents the dilution of clotting factors, which may ence of tachycardia, hypotension, pale and clammy ultimately lead to more bleeding problems. The treatment of shock requires resto- Animal experiments suggest that the rapid res- ration of the circulation. Two intravenous cannulae toration of blood volume results in a lower mortal- should be inserted, one in each antecubital fossa. It seems probable tive route for filling the circulation if a peripheral that both approaches may be beneficial in differ- vein cannot be cannulated. Another alternative is to cut down als probably benefit from an early and complete over, expose and insert a catheter directly into the restoration of their blood volume, whereas elderly long saphenous vein at the ankle. Hartmann’s or Ringer’s lactate should be rapidly Fractured limbs should be stabilized by inflat- infused. Fluid infusion should be given if available, especially if the wounds are be slowed when the systolic blood pressure reaches extensive and heavily contaminated. It Before transfer, wounds should be covered (espe- was originally thought that fluid administration cially chest wounds). Pressure dressings or digital should continue to maintain the blood pressure at a pressure may be appropriate. The rationale was that this would enable United Kingdom is the ambulance, which has the patient to better overcome a rapid decompensa- usually been summoned by an eye witness with a tion from further bleeding and reduce the risk of mobile phone. Satellite locating devices now allow developing some of the complications of prolonged a rapid response to a recognized position. The other intensive care consultants The hospital telephone exchange has the respon- sibility of contacting and requesting all the key The nurse in charge of theatres personnel to assemble at the A&E. The key contacts The blood transfusion consultants consultants in are shown in Table 6. A junior doctor The hospital manager on call should record the progress of the resuscitation and The communications department ensure that all the injuries and the clinical course of The specialist services the patient are carefully recorded. All members of plastic the team must be clearly identified by an appropri- ate tabard (a labelled overall or tunic). He/she should have the ability to contact the operating theatres, the blood bank, intensive The portering services care and the wards in order to arrange the transfer The mortuary of major casualties out of A&E as soon as they have been assessed and resuscitated. The doctor in over- all charge should undertake the initial triage of the made at the site of the accident (described above) patients into one of the following categories: and ensures that appropriate priority is given to the patients who require the most urgent treatment. It is also helpful if some surgeons go directly to the operating theatres to help staff prepare for the A sucking wound should be occluded. A chest amputations, laparotomies, fracture fixations and drain may need to be inserted. A pneumothorax should be treated by the inser- tion of a chest drain through the second anterior Initial resuscitation intercostal space or, alternatively, urgent insertion through the fifth intercostal space in the mid-axil- This follows the same system described above for lary line if it is a tension pneumothorax. A simple the scene of the accident, taking note of the valu- hollow needle or other hollow device may be used able information about the extent and cause of the as an alternative to deflate a life-threatening tension injuries provided by the transporting team. This should be repeated by the doctor in charge of Cardiac tamponade is one of the most difficult the triage to confirm initial reports and ensure that clinical diagnoses to make but should be suspected nothing has altered or been missed in the initial if there are congested neck veins, muffled heart survey. It should be treated by needle aspiration C is for catastrophic haemorrhage This must be con- of the pericardial sac using ultrasound guidance. C is for circulation The injured patients will often A is for airway Consideration is given to the cervical have had intravenous catheters inserted before they spine, which should be immobilized in a collar or by reach hospital but, if this has not occurred, two sand bags if there is any hint of a neck injury. A long mouth if this hasn’t already been done by the para- saphenous vein cut-down or bone marrow infusion medics. Endotracheal intubation of the airway is car- can be life-saving if these approaches fail. Blood should be sent for blood grouping and if B is for breathing This is assessed once a clear airway a transfusion is likely to be needed, cross-matching. If the patient is breathing sponta- All known wounds should be inspected for overt neously, has a good colour and is talking no further bleeding. All other major laboured or ineffective or if the oxygen saturation bleeding is likely to be covert rather than overt and is low poor while the patient is being given oxygen. Overloading with crystalloid is not help- systems briefly assessed, a secondary survey is care- ful. Blood and blood products should be given as fully carried out to ensure that important injuries soon as possible, especially if there is evidence of have not been missed during the early drama and continuing haemorrhage. Urine respiration, oxygen saturation, Glasgow score and output is a reliable indication of rehydration and urine output should be monitored continuously. Its value has now from the patient, if conscious, focusing on their been firmly established. Pericardiocentesis be ‘log-rolled’ by several staff to inspect their back can be life-saving. D is for disability Primarily disability can be caused The rest of the secondary survey can be per- by any associated brain injury. A alert V responding to verbal stimuli Head and neck P responding to painful stimuli The scalp should be inspected and palpated for U unresponsive. A deeply This can be used to provide a rapid assessment depressed area, especially if there is an overlying of cerebral function until, as soon as possible, a scalp wound, suggests there may be a depressed or full Glasgow Coma Scale has been calculated (see compound fracture of the skull. Battle’s sign and racoon eyes suggest the pres- ence of a fracture of the base of the skull (see E is for exposure All clothing should be removed or Symptoms and Signs). The presence of diplopia on upward gaze suggests there may be a blow-out fracture of the orbital floor. Anaesthesia over the cheek with bruising and enophthalmos suggests the presence of a fractured zygoma. The cornea and conjuctiva of both eyes should be inspected and the visual acuity checked with a Snellen’s chart. The mouth should be opened and the stability of the upper jaw checked by putting a finger and thumb inside the mouth and pulling it backwards and (A) forwards. All wounds in the neck should be carefully assessed to indicate the possibility of damage to major vessels, the airway or, rarely, the gullet. Chest (upper torso) The presence of respiratory distress should have been detected in the primary survey, but it is worthwhile rechecking that the chest movement is equal and full and that there is no evidence of any stridor. The chest wall should be carefully inspected for bruising, asymmetry and possible penetrating lacerations. Look for the presence of a flail segment, a condi- tion in which an area of chest wall is sucked inwards (B) as the chest expands during inspiration (Fig 6. The lungs should be percussed to together with the presence of pulsus paradoxus and check for dullness (a haemothorax or ruptured muffled or inaudible heart sounds is one of the diaphragm) or excessive resonance (a pneumo- main signs of cardiac tamponade.
Iodinated tyrosine residues that are close together in the thyroglobulin precursor molecule undergo a coupling reaction buy generic meclizine line in treatment, which forms the iodothyronine structure order meclizine cheap symptoms neck pain. These free radicals undergo addition to produce an iodothyronine residue and a dehydroalanine residue cheap meclizine 25mg otc symptoms xanax withdrawal, both of which remain in peptide linkage in the Tg structure purchase generic meclizine on-line chi infra treatment. When the thyroid gland is stimulated to secrete thyroid hormones, vigorous pinocytosis occurs at the apical membrane of follicular cells. Pseudopods from the apical membrane reach into the lumen of the follicle, engulfing bits of the colloid (see Fig. Endocytotic vesicles formed by this pinocytotic activity migrate toward the basal region of the follicular cell. Lysosomes mainly located in the basal region of resting follicular cells migrate toward the apical region of the stimulated cells. The lysosomes fuse with the Tg-containing droplet and hydrolyze the Tg to its constituent amino acids. As a result, T, T,4 3 and the other iodinated amino acids are released into the cytosol. The T and T formed from the4 3 hydrolysis of Tg are released from the follicular cell and enter the nearby capillary circulation. Less than 1% of the blood T and This in the free form, which is in equilibrium with the large protein-bound fraction. It is this small4 3 amount of free thyroid hormone that interacts with target cells. The protein-bound T and T represent a large reservoir of preformed hormone that can replenish the4 3 small amount of circulating free hormone as it is cleared from the blood. This reservoir provides the body with a buffer against drastic changes in circulating thyroid hormone levels as a result of sudden changes in the rate of T and T secretion. The protein-bound T and T molecules are also protected from metabolic4 3 4 3 inactivation and excretion in the urine; thus, thyroid hormones have long half-lives in the bloodstream. Deiodination reactions in the peripheral tissues both activate and inactivate thyroid hormones. The enzymes that catalyze the various deiodination reactions are regulated, resulting in different thyroid hormone concentrations in various tissues under different physiologic and pathophysiologic conditions. Thyroxine conversion to triiodothyronine As noted earlier, This the major secretory product of the thyroid gland and is the predominant thyroid4 hormone in the blood. About 40% of the T secreted by the thyroid gland is converted to T by enzymatic4 3 removal of the iodine atom at position 5′ of the thyronine ring structure in a reaction termed outer-ring deiodination (Fig. Deiodinase type 1 (D1) located in the liver, kidneys, and thyroid gland catalyzes this reaction. D2 is believed to function primarily to maintain intracellular T in target3 tissues, but it may also contribute to the generation of circulating T. A third 3 deiodinase (type 3 or D3) catalyzes inner-ring deiodination reactions during degradation of thyroid hormones as discussed below. This rare amino acid has properties that make it ideal for catalysis of oxidoreductive reactions. Deiodinase type 1 (D1) deiodinates thyroxine (T ) at the 5′4 position to form triiodothyronine (T ), the physiologically active thyroid hormone. Deiodinase type 33 (D3) also enzymatically deiodinates some T at the 5′ position to form the inactive metabolite, reverse T. A3 3 small amount of This also decarboxylated and deaminated to form the metabolite, tetraiodoacetic acid4 (tetrac), which may then be deiodinated before being excreted. Thyroxine and triiodothyronine inactivation Whereas the 5′-deiodination of T to produce T can be viewed as a metabolic activation process, both T4 3 4 and T undergo enzymatic deiodinations, particularly in the liver and kidneys, which inactivate them (see3 Fig. About 40% of the T secreted by the human thyroid gland is deiodinated at the fifth position on4 the thyronine ring structure by D3 to produce reverse T3 (rT3), which has little or no thyroid hormone activity. This deiodination reaction is the major pathway for T metabolic inactivation and disposal. T4 3 and rT also undergo deiodination to yield 3,3′-diiodothyronine, which may be further deiodinated before3 being excreted. Both physiologic and pathologic factors influence the 5′-deiodination reaction, changing the relative amounts of T and rT produced from T. For example, a human fetus produces less T from T than does3 3 4 3 4 a child or adult because the 5′-deiodination reaction is less active in the fetus. During fasting, 5′- deiodination is inhibited, particularly in response to carbohydrate restriction, but it is restored to normal when the person is fed again. Trauma and acute and chronic illnesses also suppress the 5′-deiodination reaction. Under all of these circumstances, the amount of T produced from This reduced and its blood3 4 concentration falls. The amount of rT rises in the circulation, not because its conversion from T is3 4 increased, as originally believed, but rather because its clearance from the blood is reduced. Note that during fasting or in the disease states mentioned above, the secretion of This usually not4 increased, despite the decrease of T in the circulation. Thyroxine glucuronidation, decarboxylation, and deamination T and to a lesser extent T are catabolized by conjugation with glucuronic acid in the liver. The4 3 conjugated hormones are secreted into the bile and eliminated in the feces. Many tissues also catabolize thyroid hormones by modifying the three-carbon side chain of the iodothyronine structure via decarboxylation and deamination. The derivatives formed from T, such as 4 tetraiodoacetic acid (tetrac), may also undergo deiodination before being excreted (see Fig. If the diet is severely deficient in4 3 iodide, as in some parts of the world, the amount of iodide available to the thyroid gland limits T and T4 3 synthesis. Enlargement of the thyroid gland increases its capacity to accumulate iodide from the blood and to synthesize T and T. However, the degree to which the4 3 enlarged gland can produce thyroid hormones to compensate for their deficiency in the blood depends on the severity of the deficiency of iodide in the diet. To prevent iodide deficiency and consequent goiter formation, iodide is added to table salt (iodized salt) in most developed countries. The sensitivity or responsiveness of a particular cell to thyroid hormones correlates to some degree with the number of receptors for these hormones. In the adult, however, brain cells show little responsiveness to the metabolic regulatory action of thyroid hormones, although they have numerous receptors for these hormones. Once inside the cell, This deiodinated to T, which enters the nucleus of the cell and4 3 binds to its receptor in the chromatin. T can influence cell differentiation by regulating the kinds of proteins produced by3 its target cells and can influence growth and metabolism by changing the amounts of structural and enzymatic proteins present in the cells (Clinical Focus 32. Alternatively, patients may present with hyperthyroidism if the hypothalamic–pituitary axis is more severely affected-a condition termed pituitary resistance to thyroid hormone.
Rigors and loin pain suggest the presence of Further treatment is discussed in Chapter 20 generic meclizine 25mg without a prescription treatment 5 alpha reductase deficiency. The majority can be excluded by a careful history In a few patients it becomes apparent that they and clinical examination purchase meclizine us medicine pouch. The urine should be tested for porphyrins and Many of the latter conditions that are described the blood and urine tested for sugar and ketones meclizine 25 mg on-line medications like xanax. This page intentionally left blank 18 Abdominal symptoms purchase meclizine 25 mg on-line medications beginning with z, masses, the spleen and obesity surgery William E. Burnand Chapter 17 covers the investigation and management High dysphagia, affecting the oral or pharyn- of conditions that present with acute abdominal geal phase, tends to be functional and caused by a pain. This chapter complements that by describ- neuromuscular disorder such as a stroke, multiple ing the investigation and management of the other sclerosis or Parkinson’s disease. Inevitably there is some Low dysphagia, affecting the oesophageal phase, overlap as many conditions are responsible for a tends to be structural or obstructive such as a neo- variety of problems. Its aetiology is not known but it is common and occasionally The term dysphagia is defined as an impairment of responds to anxiolytic and antidepressant drugs. The of functional dysphagia resulting from the ageing act of swallowing may be divided into three phases: process, which can prove difficult to manage. Odynophagia (pain on swallowing) may be The oral phase involves formation of the bolus caused by infections such as candidiasis but can also by means of mastication, tongue movement and occur with neoplasia. Once a bolus is formed, it is Unfortunately the level at which a patient feels delivered posteriorly by pressure of the tongue on that their food is stuck often correlates poorly with the the hard palate, thus delivering it through the pha- actual level of the obstructing lesion. The pharyngeal phase is involuntary and involves delivery of the bolus to the upper oesopha- Investigation geal sphincter while sealing the nasopharynx and Clinical diagnostic indicators protecting the airway. The pharyngeal constric- An accurate history is vital and will assist in target- tor muscles propel the bolus through the upper ing the investigations. The following features give oesophageal sphincter (cricopharyngeus), which an indication of the diagnosis. Speed of onset A sudden onset suggests an obstructed The oesophageal phase is also involuntary. Peristaltic waves propagated in the proximal Duration of symptoms A short history with associated oesophagus deliver the bolus to the lower oesopha- weight loss suggests malignancy, whereas symptoms geal sphincter, which is under vagal control and that have been present for several years suggest a provides a barrier to gastro-oesophageal reflux. Long-standing Dysphagia may therefore be functional or struc- intermittent dysphagia dependent on the nature of tural, high or low (see Table 18. A patient with malignant disease may be cachec- tic (Chapter 4, p59) and have a palpable epigastric Recent weight loss This suggests malignancy. Heartburn or regurgitation soon after eating This sug- Any patient with a possible neurological condi- gests gastro-oesophageal reflux and/or stricture tion should have a full neurological examination. Chest symptoms An associated cough may indicate In many cases the clinical examination is less aspiration. Dysphagia 423 Blood tests Transnasal endoscopy may allow assessment of Iron deficiency anaemia may be associated with a the pharyngeal phase of swallowing using liquids or pharyngeal web, while patients with long-standing solids with or without dye. It It also allows peritoneal washings for cytological is the investigation of choice for patients in whom examination and the use of laparoscopic ultra- a pharyngeal pouch is suspected as there is a risk of sound to look for previously undetected secondary perforation from endoscopy in these patients. Single-contrast studies are recommended for detecting strictures, diverticula, hiatus hernia and achalasia (‘bird’s beaking’), while double-contrast Biopsy studies, giving an effervescent agent prior to swal- All tumours, mucosal abnormalities (e. Barrett’s lowing the barium, is superior for visualizing oesophagus), or strictures must be biopsied. Gastro-oesophageal reflux can be demon- Functional investigations strated by asking the patient to perform a Valsalva Oesophageal motility disorders require functional manoeuvre. Manometry provides an assessment Video-fluoroscopy is a modification of the of the function, pressure and relaxation of the barium swallow in which the act of swallowing the lower oesophageal sphincter as well as the peri- barium in either liquid, solid or semi-solid form is staltic activity of the body of the oesophagus. All screened and watched by a radiologist and, if avail- medication that may impact on motility must be able, a speech therapist. This provides information stopped before passing a pressure sensor catheter, about transit time, function of the oesophageal either solid state or fluid-perfused, via the nose sphincters, efficacy of peristalsis and the risk of into the stomach. It provides direct visualization Twenty-four-hour pH monitoring is used to of any mucosal lesion and the ability to biopsy and assess gastro-oesophageal reflux, which may be carry out therapeutic measures. It is the first choice responsible for causing dysmotility and ultimately investigation for low dysphagia and is well tolerated a stricture. This may be done in conjunction with and safe, although the perforation rate increases if manometry, but any acid-suppressing medication therapeutic dilatation or stenting is added. A transnasal catheter is passed and the Management pH sensor positioned about 5cm above the lower First-aid is by Heimlich’s manoeuvre. The data are analysed in Endoscopy will be required if first-aid fails to relation to the patient’s activity, e. By convention, a normal study Alternatively it can be pushed onwards into the is accepted as a pH of less than 4 for greater than stomach. Sudden Investigation onset of dysphagia combined with chest pain and retching indicate the diagnosis. Clinical diagnostic indicators This disorder is most common in females (3:2) aged Imaging 30–40 years who present with progressive, often A plain chest X-ray may show a foreign body painful dysphagia for both solids and liquids. Other symptoms can include weight loss and regurgitation, which may cause aspiration pneumonia. Endoscopy Flexible oesophagoscopy should be obtained to Blood tests exclude neoplasia, but cannot diagnose achalasia. Manometry Imaging This should demonstrate a high-pressure, non- A chest X ray may show a widened mediastinum relaxing zone at the lower end of the oesopha- caused by an oesophagus full of food residues gus, which is associated with disordered or absent (Fig 18. At a late stage, a large flaccid dilated oesophagus containing food residues which smoothly tapers at its Management lower end can be seen on barium swallow (Fig 18. This may be expectant at first, but mild to mod- At an early stage, lower oesophageal narrowing can erate symptoms should be treated by balloon be caused by a carcinoma of the oesophagus. This is successful in relieving symp- toms in 80–90 per cent of patients and can be Investigation repeated if symptoms recur. H2 receptor blockers Clinical diagnostic indicators or proton pump inhibitors may be required if dila- This condition usually presents with intermittent tation is followed by reflux. The cardia and lower oesophagus Barium swallow and endoscopy show the appear- are defined and the longitudinal, circular, smooth ance of a corkscrew oesophagus, with distorted muscle of both are divided down to the mucosa. A fundoplication may be car- ried out to cover the myotomy and prevent reflux (see below). Reflux is prevented by fundoplication, which also reduces the risk of perforation and reflux stricture. Prognosis The mortality of balloon dilatation and Heller’s cardiomyotomy is low, less than 1 per cent, and recurrent problems occur in less than 5 per cent of patients after surgery. At times seepage of saliva is a problem Management because of the inability to swallow. Plummer–Vinson syndrome can cause an quence of repeated, forcible peristalsis of unknown oesophageal web. The diagnosis can be confirmed by oesopha- cated by a past history of reflux and heartburn. Tricyclic drugs and biofeedback Investigation can be tried, but are rarely helpful.
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