James Ip

• Clinical Fellow in Anaesthesia, Great Ormond Street Hospital, London, UK

If the septum is deviated and the scope cannot be easily advanced heart attack in the style of demi lovato ameritz top tracks buy hyzaar uk, try to pass it between the inferior and middle turbinates (laterally) and the septum (medially) blood pressure medication sleepy order 50 mg hyzaar with amex. With the postnasal space in view blood pressure medication for diabetics buy genuine hyzaar line, ask the patient to breathe in through their nose heart attack demi lovato mp3 cheap generic hyzaar uk. Use the control toggle to flex the distal end of the scope inferiorly and gently advance demi lovato heart attack mp3 order 50mg hyzaar with mastercard. The following is a guide: tongue base arteria x veia discount 50 mg hyzaar fast delivery, valleculae, epiglottis (lingual and laryngeal surfaces), supraglottis, interarytenoid bar, vocal cords (appearance and mobility), subglottis, pyriform fossae and posterior Flexible nasolaryngoscopy Explain the procedure to the patient and ask the patient which side of their nose is the easier to breathe through, selecting this side for examination. Spray the chosen side with local anaesthetic or insert a cotton wool pledget soaked in local anaesthetic. The larynx may be difficult to view in those patients with an infantile epiglottis or prominent tongue base. Where this is encountered, ask the patient to point their chin up to the ceiling to draw the tongue base forward and bring the larynx into view. To assess the pyriform fossae, ask the patient to blow their cheeks out while you pinch their nose. Remove the scope gently and supply patients with tissues to use after completing the examination. The first pass of the endoscope should pass along the floor of the nose, the second into the middle meatus and the third into the superior meatus and olfactory niche. The first pass provides an overall view of the anterior nasal cavity, the septum and the floor of the nasal cavity to the posterior choana. The second is into the middle meatus and allows identification of the uncinate process, middle meatal ostium and ethmoidal bulla. The third examines the superior meatus and olfactory niche; the sphenoid ostium may be identified during this pass. Using the head mirror or headlight, begin by examining the lips and face of the patient. Begin by asking the patient to open their mouth and insert one tongue depressor onto the buccal surface of each cheek and ask the patient to clench their teeth. Gently pulling laterally, withdraw the blades examining the buccal mucosa, gingivae, teeth, parotid duct orifices and buccal sulci. Anteriorly, draw the blades superiorly to examine beneath the upper lip and repeat with the lower lip. The openings of the submandibular ducts are found just lateral to the frenulum of the tongue. Using both tongue blades again, examine the retromolar regions and lateral borders of the tongue. Gently depress the anterior half of the tongue, avoiding the posterior third as this can make patients gag. Submucosal tumours in these structures can often be palpated before they are seen. Where the history is suggestive of an abnormality of the submandibular gland or duct, bimanual palpation should be used. Ensure adequate exposure of the patient by removing neck ties and unfasten the upper shirt buttons so that both clavicles are visualized. Inspect the neck, noting scars, sinuses, masses or tattoos (these were previously used to mark radiotherapy fields). Start with the submental then submandibular triangles (level 1), followed by the jugulodigastric and jugular lymph nodes (levels 2, 3, 4) by palpating along the anterior border of each sternocleidomastoid muscle and the paratracheal region. Working posteriorly, palpate the parotid gland and postaural and occipital lymph nodes. Note the site, size and appearance of any mass and whether it is tethered to the skin or underlying muscles. Assess whether the mass moves with swallowing (give the patient a glass of water to drink) or tongue protrusion. Auscultate for a bruit and, in the case of a thyroid mass with retrosternal extension, percuss from superior to inferior along the sternum. All patients must have their facial weakness graded so that any changes can be monitored. Note that there is complete eye closure in a grade 3 and incomplete eye closure in a grade 4 facial palsy. When faced with a true lower motor neuron palsy, look for a cause by examining the remaining cranial nerves, perform otoscopy to exclude middle ear pathology and palpate the parotid glands. Audiology is required with tympanometry, a pure tone audiogram and, occasionally, stapedial reflexes. Accuracy of the Weber and Rinne tuning fork tests in evaluation of children with otitis media with effusion. Examination of facial nerve function Sitting level with the patient, examine their general appearance and for any scars or masses. Remember that there is crossover in the innervation of this region so that a patient is still able to wrinkle their forehead in a unilateral upper motor neuron palsy. Ask the patient to shut their eyes tightly, flare their nostrils, blow out their cheeks and bare their teeth. Where facial weakness is observed, blinking repeatedly may reveal synkinesis where reinnervation has occurred along incorrect pathways; contraction of obicularis oris muscle may result in contraction of the angle of the mouth. It is common, extremely painful and often precipitated by irritants such as cotton buds. There may be an infective component, commonly bacterial, such as Pseudomonas aeruginosa, Staphylococcus aureus and Proteus, or less frequently fungal, such as Aspergillus species or Candida albicans. The external auditory canal is often swollen and filled with debris that requires microsuction. Treatment generally consists of one week of ear drops containing a combination of steroid and antibiotic. An ear swab is useful in directing antibiotic selection where the infection does not resolve with the initial treatment. When the external ear canal is very swollen, a wick is inserted to splint the meatus open to allow penetration of the topical treatment. The infection may progress to involve the pinna and peri-auricular soft tissues (cellulitis), necessitating hospital admission for intravenous antibiotics. An important differential diagnosis of otitis externa is malignant otitis externa. This is an osteomyelitis of the ear canal and lateral skull base, which occurs more frequently in diabetics and immunocompromised patients presenting with severe pain. Pseudomonas aeruginosa is the most common cause and the typical otoscopic appearance is granulation tissue or exposed bone on the floor of the ear canal. Treatment is a prolonged course of intravenous antibiotics followed by further oral antibiotics (twelve week), regular microsuction, topical antibiotic-steroid ear drops, good glycaemic control and analgesia. A biopsy is often needed to exclude malignancy and determine microbiological sensitivities. Although often asymptomatic, it may cause a conductive hearing loss and discomfort. Impacted wax needs to be removed to facilitate examination of the tympanic membrane. In primary care, removal is facilitated by the use of ceruminolytic agents (2) or ear syringing. Syringing is, however, contraindicated in those who have a tympanic membrane perforation or who have developed otitis externa from previous syringing. The use of cotton buds by the patient should be discouraged as this impacts wax and traumatises the ear canal causing otitis externa. Causative organisms include viruses and bacteria, such as Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. Examination reveals a bulging erythematous tympanic membrane, which may perforate and discharge pus. If symptoms persist, oral antibiotics such as amoxicillin or clarithromycin are indicated (3). Recurrent otitis media may be treated by insertion of grommets or a prolonged course of low dose antibiotics. The typical audiological finding is a mild to moderate conductive hearing loss, associated with a flat (type B) tympanogram. Children with cleft palate can be offered grommets as an alternative to hearing aids. There is a postauricular abscess with lateral and anterior displacement of the pinna and tenderness over the mastoid bone. Early cases may respond to medical treatment with intravenous antibiotics, analgesia and hydration (5). If there is failure to improve, where there is an established postaural abscess, or if the suspicion of complications demands surgical intervention a cortical mastoidectomy and grommet insertion with placement of a corrugated drain within the postauricular wound is undertaken. Needle aspiration of a pinna haematoma followed by a compression bandage is rarely effective. A small incision through the overlying skin under local anaesthetic allows continued drainage and is a more definitive treatment (6). The incision should be placed where the scar will be least visible, ideally along the rim of the conchal bowl, under the helical rim or approached from the cranial surface of the pinna (with a small window of cartilage excised). Through-and-through sutures can be placed to secure silastic splints or dental rolls, to achieve more reliable pressure and to prevent haematoma recurrence under the head bandage. All patients should receive co-amoxiclav or an equivalent antibiotic to prevent perichondritis and should be reviewed after 7 days for suture removal. It commonly occurs as a result of bacterial infection following trauma to the pinna from piercing, insect bite or skin abrasion, although can also be secondary to otitis externa. Previous episodes of perichondritis or inflammation of other cartilaginous structures should be looked into in order to exclude relapsing perichondritis. Perichondritis and pinna cellulitis require a combination of intravenous and oral antibiotics as cartilage compromise can lead to marked disfigurement of the pinna. Rarely, surgery is required to drain a collection or debride necrotic soft tissue (7). In 88% of cases, no obvious cause is found, but a careful history and examination should consider potential infective, autoimmune, vascular, traumatic, neoplastic and neurological causes (8). Competing theories for idiopathic cases include viral and vascular insults to the inner ear and rupture of the cochlear membrane. Standard treatment is with prednisolone (oral for one week first line and or injected into the middle ear if there is no imporvement) (9). Lower motor neurone lesions are distinguished from upper motor neurone lesions by the absence of forehead movement (forehead movement is spared in upper motor neurone lesions as a result of the bilateral upper motor neurone distribution supplying this area). Lower motor neurone pathology can occur anywhere along the path of the affected nerve. An assessment of the cranial nerves, ear, parotid gland, oral cavity and neck examination is mandatory. Although there is inconclusive evidence to support the use of antivirals, acyclovir (800 mg five times a day for 10 days) is also often prescribed (13) along with one week of oral prednisolone. The facial palsy is accompanied by painful vesicles on the pinna or external auditory canal, and occasionally the soft palate. The onset is rapid, and the 8th nerve may become involved with concurrent hearing loss and vertigo. Although described as idiopathic, there is evidence to suggest that the palsy occurs due to herpes reactivation. Initial treatment is with oral prednisolone (1 mg per kg, typically 60 mg for an adult) for seven days. Trauma Every patient undergoing middle ear surgery must have their facial nerve function recorded pre- and post-operatively. Children will need to be held by a parent or nurse, and the first attempt at removal is often the only chance. If the foreign body cannot be removed, a short general anaesthetic in the following few days is indicated to allow removal. The use of crocodile forceps can result in medial displacement of the foreign bodies and their use should be restricted to objects that can be grasped.

If the clinician desires to directly enter the skinfold thickness in mm (as it is measured) blood pressure medication recommendations order hyzaar 50mg free shipping, 0 prehypertension the rationale for early drug therapy buy generic hyzaar 50mg. Organic disease is diagnosed in 65% of patients presenting with involuntary weight loss exceeding 5% of their usual weight (most commonly cancer and gastrointestinal disorders pulse blood pressure normal order hyzaar 50mg online, although virtually any chronic disease may cause weight loss) arteria mammaria discount hyzaar generic, and psychiatric disorders are diagnosed in 10% of patients (depression blood pressure medication problems purchase hyzaar online, anorexia nervosa pulse pressure facts order hyzaar no prescription, schizophrenia). In 25% of patients, the cause remains unknown despite at least 1 year of follow-ups. The patient is asked to estimate his or her weight before the illness (W) and the amount of weight lost (E). The observed weight loss (O) is the former weight (W) minus the current measured weight. Nutritional assessment: a comparison of clinical judgment and objective measurements. New norms of upper limb fat and muscle areas for assessment of nutritional status. Relation of anthropometric and dynamometric variables to serious postoperative complications. Hand grip dynamometry as a predictor of postoperative complications reappraisal using age standardized grip strengths. Measurement of grip strength: validity and reliability of the sphygmomanometer and Jamar grip dynamometer. Serum albumin and body weight as predictors of postoperative course in colorectal cancer. Handgrip strength and endurance as a predictor of postoperative morbidity in surgical patients: can it serve as a simple bedside test Comparison of forearm muscle dynamometry with nutritional prognostic index, as a preoperative indicator in cancer patients. Hand grip strength: an indicator of nutritional state and the mix of postoperative complications in patients with oral and maxillofacial cancers. Assessing clinical probability of organic disease in patients with involuntary weight loss: a simple score. These sums are then converted by formulas into estimates of total body fat, which correlate well with more traditional measures (r = 0. It is based on the premise that the most important characteristic of obesity is its distribution, not its quantity. Most authorities measure the waist circumference at the midpoint between the lower costal margin and the iliac crest and the hip circumference at the widest part of the gluteal region. Visceral fat is metabolically active, constantly releasing free fatty acids into the portal circulation, which probably contributes to hyperlipidemia, atherogenesis, and hyperinsulinemia. Abdominal obesity is depicted in the top row; gluteal-femoral obesity in the bottom row. The drawings in this figure are adapted from photographs published by Vague,11 who is credited with first associating adverse health outcomes with abdominal obesity. It has the advantages of being simpler to measure and avoiding any consideration of the hips, which, because they encompass bone and skeletal muscle as well as fat, should have no biologically plausible relationship to diabetes, hypertension, and atherosclerosis. Recommended cutoffs for increased health risk are a waist circumference >102 cm (>40 inches) for men and >88 cm (>35 inches) for women. One proposed measure is the sagittal diameter, which is the total anterior-posterior distance between the anterior abdominal wall of the supine patient and the surface of the examining table. Theoretically, visceral fat maintains the abdominal depth in the supine patient, whereas subcutaneous fat allows the abdominal depth to partially collapse from the force of gravity. A comparison of the skinfold method with extent of "overweight" and various weight-height relationships in the assessment of obesity. Anthropometric correlates of total body fat, abdominal adiposity, and cardiovascular disease risk factors in biracial sample of men and women. Body-mass index and cause-specific mortality in 900,000 adults: collaborative analyses of 57 prospective studies. Abdominal obesity and mortality risk among men in nineteenth-century North America. The degree of masculine differentiation of obesities: a factor determining predisposition to diabetes, atherosclerosis, gout, and uric calculous disease. Harmonizing the metabolic syndrome; a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. The bedside findings of Cushing syndrome were originally described by Harvey Cushing in 1932. Diagnostic standard: For Cushing syndrome, elevated daily cortisol or corticosteroid metabolites, or both, with loss of circadian rhythm and with abnormal dexamethasone suppression tests. Results are overall mean frequency or, if statistically heterogeneous, the range of values. Patients with Cushing syndrome develop central obesity (also known as truncal obesity or centripedal obesity), a term describing accumulation of fat centrally on the neck, chest, and abdomen, which contrasts conspicuously with the muscle atrophy affecting the extremities. There are three definitions of central obesity: (1) Obesity sparing the extremities (a subjective definition and also the most common one). Rounding of cheeks and prominent bitemporal fat produces the characteristic moon facies. Fat also may accumulate bilaterally above the clavicles (supraclavicular collar), in front of the sternum (episternal area, or dewlap), and over the back of the neck (dorsal cervical fat pad, or buffalo hump). In these drawings, the dotted line depicts normal contours of patients without Cushing syndrome. The truncal obesity of Cushing syndrome reflects increased intra-abdominal visceral fat, not subcutaneous fat,20 probably from glucocorticoid-induced reduction in lipolytic activity and activation of lipoprotein lipase, which allows tissues to accumulate triglyceride. Proposed mechanisms are suppressed vasodepressor systems (prostaglandins, kallikreinkinin), exaggerated pressor responses to vasoactive substances, and possible activation of the renin-angiotensin system. Significant thinning of the skin probably arises from corticosteroid-induced inhibition of epidermal cell division and dermal collagen synthesis. Striae are more common in younger patients with Cushing syndrome than in older patients. The severity of striae, acne, and hirsutism correlates poorly with cortisol levels, indicating that other factors-temporal, biochemical, or genetic-play a role in these physical signs. Patients with Cushing syndrome present with crying episodes, insomnia, impaired concentration, difficulty with memory, and suicide attempts. Definition of findings: for hypertension, diastolic blood pressure >105 mm Hg; for central obesity, central obesity index exceeds 113 or there is a subjective appearance of central obesity, sparing the extremities4,12; for thin skinfold, skinfold thickness on the back of the hand <1. Patients who take exogenous corticosteroids have the same frequency of central obesity, moon facies, and bruising as patients with endogenous Cushing, but a significantly lower incidence of hypertension, hirsutism, acne, striae, and buffalo humps. The basophil adenomas of the pituitary body and their clinical manifestations (pituitary basophilism). Problems of prolonged cortisone treatment for rheumatoid arthritis: further investigation. Biochemical criteria differentiating patients from lean and obese normal subjects and from females on oral contraceptives. A body measurement to evaluate the pattern of fat distribution in central obesity. Skin manifestations of Cushing disease in children and adolescents before and after the resolution of hypercortisolemia. Clinical and laboratory findings and results of therapy in 58 patients with adrenocortical tumors admitted to a single medical center (1951 to 1978). Clinical features of adrenocortical carcinoma, prognostic factors, and the effect of mitotane therapy. In patients with significant pericardial effusions, the finding of pulsus paradoxus increases the probability that pericardiocentesis will improve cardiac output; its absence decreases the probability that pericardiocentesis will be beneficial. Counting the pulse for 30 seconds and doubling the result is more accurate than 15 seconds of observation. A pulse deficit has traditionally been associated with atrial fibrillation, although it is a common finding with extrasystoles and all fast heart rates and by itself has little diagnostic significance. In patients with myocardial infarction, the increased risk of adverse outcome is a continuum, being greater for patients with higher heart rates and persisting whether or not the patient has a low ejection fraction, takes -blocker medications, or receives thrombolytic therapy. The pulse must be absolutely regular to diagnose pulsus alternans and distinguish it from the bigeminal pulse, which also has beats of alternating strength, although the rhythm is irregular (see Chapter 16). When using the blood pressure cuff, the clinician should stop deflating the cuff at the first appearance of Korotkoff sounds and hold the cuff pressure for several beats just below systolic blood pressure. In patients with pulsus alternans, only the Korotkoff sounds belonging to the strong beats are heard. Further deflation of the cuff allows cuff pressure to fall below the systolic pressure of the weaker beats, causing the cadence of Korotkoff sounds to suddenly double. The usual difference in systolic pressure between the strong and weak beats is only 15 to 20 mm Hg. Typically, the pause is caused by a premature beat or the abrupt termination of a paroxysmal tachycardia. If systole lengthens for any reason, the subsequent diastole must be shorter; if systole shortens for any reason, the subsequent diastole must be longer. In patients with left ventricular dysfunction, a sudden increase in ventricular filling (such as that induced by a postextrasystolic pause) causes the subsequent systole to produce a strong beat, although it takes A. The normal pulse tracing (top row) is displayed with six tracings of abnormal pulse contours (bottom rows). Pulsus alternans (second row) is a regular pulse that has alternating strong and weak beats. Both pulsus bisferiens (third row) and the dicrotic pulse (fourth row) have two beats per cardiac cycle: in pulsus bisferiens both beats are systolic, whereas in the dicrotic pulse one is systolic and the other diastolic. Pulsus paradoxus (fifth row) is a pulse whose systolic blood pressure falls more than 10 to 12 mm Hg during inspiration. Pulsus parvus et tardus (sixth row) is a pulse that has a small volume and rises slowly. The hyperkinetic pulse (last row) is a pulse with unusually abrupt and strong force; it may have a normal diastolic blood pressure. These tracings are facsimiles of actual pulse tracings made more than 100 years ago. By prolonging systole, the strong beat thus shortens the next diastole, which reduces filling of the heart and causes the next beat to be weaker. The weaker beat is ejected more quickly, shortening systole and causing the next diastole to be longer, thus perpetuating the alternating pulse. Most experts now believe that alternation of intrinsic contractility is the fundamental problem in pulsus alternans, because alternation can even be demonstrated in vitro in isolated muscles at constant length and resting tension. Because of the Venturi effect, the rapidly moving bloodstream temporarily draws the walls of the aorta together, reducing flow momentarily and producing a notch with two systolic peaks in the waveform. The term is unfortunate, because the finding is nothing more than an exaggeration of normal physiologic change. When checking for pulsus paradoxus, the clinician should have the patient breathe quietly and regularly, because even normal persons can induce a pulsus paradoxus with vigorous respirations. Pulsus paradoxus is detected by palpating the pulse or using the blood pressure cuff, although only paradoxical pulses exceeding 15 to 20 mm Hg are palpable. Because it is one of three key findings of tamponade-the others being elevated neck veins (sensitivity = 100%) and tachycardia (sensitivity = 81% to 100%)-the clinician should consider tamponade and check for pulsus paradoxus in any patient suspected of having pericardial disease, such as those with elevated neck veins, unexplained dyspnea, pericardial rub, or known pericardial effusion. These patients usually have one of five disorders: (1) atrial septal defect, (2) severe left ventricular dysfunction (especially those with uremic pericarditis),49 (3) regional tamponade (tamponade affecting only one or two heart chambers, a complication of cardiac surgery),50 (4) severe hypotension,51-53 or (5) aortic regurgitation. Knowing that aortic regurgitation may eliminate pulsus paradoxus is especially significant, because patients with proximal (type A) aortic dissection and hemopericardium usually lack the paradoxical pulse despite significant tamponade, and the unaware clinician may exclude the possibility of tamponade to the harm of the patient. The pulse tracing shows the fall in systolic pressure during inspiration, which is characteristic of pulsus paradoxus. To detect and measure the paradoxical pulse, the clinician begins by checking the blood pressure in the usual way but slowly deflates the cuff to precisely identify the cuff pressure at three points: First, the moment Korotkoff sounds first appear (top tracing). In patients with pulsus paradoxus, cuff pressure will fall below the systolic pressure of just the expiratory beats, and the Korotkoff sounds will repeatedly come and go during quiet respiration, disappearing with inspiration and reappearing with expiration. Second, the moment when Korotkoff sounds persist throughout the respiratory cycle (middle tracing). At this point, cuff pressure has fallen below systolic blood pressure of all beats. In this patient, only expiratory Korotkoff sounds are heard between cuff pressures of 140 mm Hg and 120 mm Hg, but Korotkoff sounds are heard throughout the respiratory cycle between pressures of 120 mm Hg and 80 mm Hg. The section on pathogenesis explains why pulsus paradoxus is absent in these clinical disorders. In a busy emergency department with an anxious and dyspneic patient, it is much more convenient to measure peak flow rates using handheld flow meters than trying to interpret the coming and going of Korotkoff sounds. It has been described in three clinical disorders: (1) hypertrophic cardiomyopathy; (2) isorhythmic dissociation. Once this occurs, the diastolic pressure in the heart chambers, reflected in the neck veins, becomes a measurement of the force acting to compress the heart. The four chambers, now smaller in size, begin to compete for space, and an increase in the size of one comes at the expense of the size of another. Inspiration increases, filling to the right side of the heart, and shifts the interventricular septum to the left and posteriorly, thus obliterating the left ventricular chamber and causing the cardiac output to fall. During expiration, the filling of the right side of the heart is less, which increases left ventricular size, and both cardiac output and blood pressure increase. Inspiratory movement of the interventricular septum is prevented when the right ventricle does not fill more during inspiration (atrial septal defect; see Chapter 40), when the left ventricular pressures are very high (severe left ventricular dysfunction), or when the left ventricle fills from some source other than the left atrium (aortic insufficiency). Regional tamponade, by definition, compresses only one or two chambers, enough to impair cardiac output but too confined to cause the heart chambers to compete for space. Difficulty breathing causes wide swings of intrapleural pressure, which then are transmitted directly to the aorta, contributing to the paradoxical pulse. This is not a complete explanation, however, because the amount of pulsus paradoxus in asthma often exceeds the pressure shifts of these respiratory excursions. Other proposed mechanisms are an inspiratory reduction in pulmonary venous return to the left heart41,57,65,66 and the compressive action of the hyperinflated chest, which, like tamponade, may reduce the size of the heart chambers and cause them to compete for space. Pulsus tardus depends on both obstruction to flow and the compliance of the vessel distal to the obstruction.

The corticospinal (or pyramidal) tracts the corticospinal system enables intricate prehypertension 120 80 buy hyzaar once a day, strong and organized movements arrhythmia 2 hyzaar 50mg online. The upper motor neurone the corticospinal tracts originate from neurones of the motor cortex and terminate on the motor nuclei of the cranial nerves and the anterior spinal horn cells arrhythmia effects cheap 50mg hyzaar mastercard. Tetraparesis (quadriplegic blood pressure chart american medical association cheap hyzaar online master card, weakness of the arms and legs) indicates high cervical cord damage blood pressure effects purchase hyzaar 50 mg mastercard, most commonly resulting from trauma hypertension questions nclex order hyzaar toronto. Muscle disease may give a similar clinical picture, but reflexes are usually preserved. Elevation of plasma muscle enzymes such as creatine kinase is highly suggestive of muscle diseases. Numbness the sensory system the peripheral nerves carry all the modalities of sensation from nerve endings to the dorsal root ganglia and thence to the cord. Axons from the second-order neurones cross the midline to form the medial lemniscus and pass to the thalamus. These fibres synapse in the dorsal horn of the cord, cross the midline and ascend as the spinothalamic tracts to the thalamus. Paraesthesiae (pins and needles), numbness and pain are the principal symptoms of lesions of the sensory pathways below the level of the thalamus. Peripheral nerve lesions Symptoms are felt in the distribution of the affected peripheral nerve. Polyneuropathy is a subset of the peripheral nerve disorders characterized by bilateral symmetrical, distal sensory loss and burning (p. A lesion at the spinal level of the pathway for proprioception will result in loss of these senses ipsilaterally below the level of the lesion. Thalamic lesions A thalamic lesion is a rare cause of complete contralateral sensory loss. Spontaneous pain may also occur, most commonly as the result of a thalamic infarct. Cortical lesions Sensory loss, neglect of one side of the body and subtle disorders of sensation may occur with lesions of the parietal cortex. Tremor Tremor is a rhythmic involuntary muscular contraction characterized by oscillations of a part of the body. Unlike essential tremor, Parkinsonian tremor is generally unilateral for the first few years. Postural tremor occurs when a patient attempts to maintain a posture such as holding the arms outstretched. Causes include physiological (due to any increase in sympathetic activity), essential tremor (p. Intention tremor occurs during voluntary movement and gets worse when approaching the target. In many cases the cause of a tremor will be apparent from the history and examination. Disorders of these systems will not produce muscular weakness but may produce incoordination. The cerebellum the cerebellum and its connections have a role in coordinating movement, initiated by the pyramidal system, and in posture and balance control. Each lateral lobe of the cerebellum is responsible for coordinating movement of the ipsilateral limb. The midline vermis is concerned with maintenance of axial (midline) balance and posture. A lesion within one cerebellar lobe causes one or all of the following: An ataxic gait with a broad base; the patient falters to the side of the lesion. The olfactory nerve (first cranial nerve) the olfactory nerve subserves the sense of smell. The most common cause of anosmia (loss of the sense of smell) is simply nasal congestion. Neurological causes include tumours on the floor of the anterior fossa and head injury. The optic nerve (second cranial nerve) and the visual system the optic nerves enter the cranial cavity through the optic foramina and unite to form the optic chiasm, beyond which they are continued as the optic tracts. In addition, the pupillary responses, mediated by both the optic and the oculomotor nerve (third cranial nerve), must be tested. Optic nerve lesions Unilateral visual loss, starting as a central or paracentral scotoma (an area of depressed vision within the visual field), is characteristic of optic nerve lesions. Complete destruction of one optic nerve results in blindness in that eye and loss of the pupillary light reflex (direct and consensual). At the optic chiasm (3), fibres derived from the nasal half of the retina (the temporal visual field) decussate, whereas the fibres from the temporal half of the retina remain uncrossed. Lesions of the retina (1) produce scotoma (small areas of visual loss) or quadrantanopia. Afferent pathway (1) A retinal image generates action potentials in the optic nerve. Convergence centre Defects of the optic chiasm the most common cause of bitemporal hemianopia. Defects of the optic tract and radiation Damage to the tracts or radiation, usually by tumour or a vascular accident, produces a homonymous hemianopia (blindness affecting either the right or the left half of each visual field) in one half of the visual field contralateral to the lesion. The macular region may be spared in ischaemic lesions as a result of the dual blood supply to this area from the middle and posterior cerebral arteries. In contrast, injury to one occipital pole produces a bilateral macular (central) field defect. Optic disc oedema (papilloedema) and optic atrophy the principal pathological appearances of the visible part of the nerve, the disc, are: Swelling (papilloedema) Pallor (optic atrophy). As disc oedema develops, there is enlargement of the blind spot and blurring of vision. Optic atrophy Optic atrophy is the end result of many processes that damage the nerve (see Optic nerve lesions, p. The pupils the pupils constrict in response to bright light and convergence (when the centre of focus shifts from a distant to a near object). They run from the hypothalamus through the brainstem and cervical cord and emerge from the spinal cord at T1. They then ascend in the neck as the cervical sympathetic chain, and travel with the carotid artery into the head. The main causes of persistent pupillary dilatation are: A third cranial nerve palsy (p. It is of no pathological significance and may be associated with absent tendon reflexes. The cranial nerves 733 the main causes of persistent pupillary constriction are: Parasympathomimetic eye drops used in the treatment of glaucoma. There is unilateral pupillary constriction, slight ptosis (sympathetic fibres innervate the levator palpebrae superioris), enophthalmos (backward displacement of the eyeball in the orbit) and loss of sweating on the ipsilateral side of the face. There is a small irregular pupil which is fixed to light but which constricts on convergence. The site of a lesion may be suggested if clinical examination shows the involvement of other cranial nerves at that site. The abducens nerve (sixth cranial nerve) supplies the lateral rectus muscle and the trochlear (fourth cranial nerve) supplies the superior oblique muscle. All the other extraocular muscles, the sphincter pupillae (parasympathetic fibres) and the levator palpebrae superioris are supplied by the oculomotor nerve (third cranial nerve). The lateral rectus muscle moves the eyeball to the temple, away from the midline of the face. The medial rectus muscle moves the eyeball to the nose, toward the midline of the face. The superior rectus muscle moves the eyeball upward, and the inferior rectus muscle moves the eyeball downward. Thus infranuclear (lower motor neurone) lesions of the third, fourth and sixth cranial nerves lead to paralysis of individual muscles or muscle groups. Frequently the lesion is partial, particularly in diabetes mellitus, when parasympathetic fibres are spared and the pupil reacts normally. The unopposed pull of the medial rectus muscle causes the eye to turn inward, thereby producing a squint (squint, or strabismus, is the the cranial nerves 735 appearance of the eyes when the visual axes do not meet at the point of fixation). Patients complain of diplopia or double vision, which worsens when they attempt to gaze to the side of the lesion. The patient complains of torsional diplopia (two objects at an angle) when attempting to look down. Disordered ocular movements may also result from disease of the ocular muscles. In these conditions all the muscles tend to be affected equally, presenting a generalized restriction of eye movements. The trigeminal nerve (fifth cranial nerve) the trigeminal nerve has both motor and sensory functions and enters the brainstem at the level of the pons. The neurones for pain and temperature descend to the upper cervical spine before they synapse with neurones of the descending tract of the fifth nerve. It also supplies the mucous membranes of the sinuses, the nose, mouth, tongue and teeth. The motor root travels with the mandibular division and supplies the muscles of mastication. A complete fifth-nerve lesion on one side causes unilateral sensory loss on the face, tongue and buccal mucosa. A fifth-nerve lesion is due to pathology within the brainstem (tumour, multiple sclerosis, infarction, syringobulbia), at the cerebellopontine angle (acoustic neuroma, other tumour), within the petrous temporal bone (spreading middle ear infection) or within the cavernous sinus (aneurysm of the internal carotid artery, tumour, thrombosis of the cavernous sinus). Trigeminal neuralgia Trigeminal neuralgia (tic douloureux) is of unknown cause, seen most commonly in old age, and is almost always unilateral. If this fails, thermocoagulation of the trigeminal ganglion or section of the sensory division may be necessary. Differential diagnosis Similar pain may occur with structural lesions involving the trigeminal nerve. The facial nerve (seventh cranial nerve) the facial nerve is largely motor in function, supplying the muscles of facial expression. It has, in addition, two major branches: the chorda tympani, which carries taste from the anterior two-thirds of the tongue, and the nerve to the stapedius muscle (this has a damping effect to protect the ear from loud noise). These two branches arise from the facial nerve during its intracranial course through the facial canal of the petrous temporal bone. The face, especially the angle of the mouth, falls and dribbling occurs from the corner of the mouth. There is weakness of frontalis, the eye will not close and the exposed cornea is at risk of ulceration. Peak incidence is between the ages of 65 and 74 years and it is more common in pregnancy. In addition, the facial nerve is the most common cranial nerve lesion in meningitis associated with Lyme disease (erythema migrans on the limbs and trunk in a patient with a history of tick bite) and in sarcoidosis (p. Management the eyelid must be closed to protect the cornea from ulceration (either adhesive tape or, in prolonged cases surgical tarsorrhaphy). Oral prednisolone (60 mg/day for 10 days) given within 72 hours of onset increases the chance of a full recovery. Prognosis Most patients recover completely, although 30% are left with a permanent weakness. Ramsay Hunt syndrome this is herpes zoster (shingles) of the geniculate ganglion (the sensory ganglion for taste fibres) situated in the facial canal. Deafness may occur as a result of involvement of the eighth nerve in the facial canal. Upper facial muscles are spared because of the bilateral cortical innervation of neurones supplying the upper face. The clinical features of a cochlear nerve lesion are sensorineural deafness and tinnitus. Causes of a cochlear nerve lesion are within the brainstem (tumour, multiple sclerosis, infarction), cerebellopontine angle (acoustic neuroma and other tumours) and petrous temporal bone (trauma, middle-ear infection, tumour). The main symptom of a vestibular nerve lesion is vertigo, which may be accompanied by vomiting. It results from disease of the inner ear, the eighth nerve or its central connections (p. Nystagmus Nystagmus is a rhythmic oscillation of the eyes, which must be sustained for more than a few beats to be significant. It is a sign of disease of either the ocular or the vestibular system and its connections. Pendular nystagmus A pendular movement of the eye occurs; there is no rapid phase. Jerk nystagmus Jerk nystagmus has a fast and a slow component to the rhythmic movement: Horizontal or rotary nystagmus may be either peripheral (middle ear) or central (brainstem and cerebellum) in origin. In peripheral lesions it is usually transient (minutes or hours); in central lesions it is long lasting (weeks, months or more). There is also dysarthria, dysphagia and nasal regurgitation, but the tongue is small and spastic and there is no fasciculation. The jaw jerk is exaggerated, the gag and palatal reflexes are preserved and the patient is emotionally labile.

Both co-oximetry and pulse oximetry indicate normal oxygen levels in pseudocyanosis heart attack jack buy hyzaar 50 mg with visa. Typical etiologies are pulmonary edema heart attack grill arizona cheap hyzaar 50mg amex, pneumonia pulse pressure equation order 50 mg hyzaar, and intracardiac right-to-left shunts blood pressure chart pregnant buy hyzaar on line amex. In clinical practice arrhythmia icd 9 codes discount hyzaar 50mg visa, common causes of peripheral cyanosis are low cardiac output arrhythmia recognition posters purchase 50 mg hyzaar with visa, arterial disease or obstruction. Pseudocyanosis may occur after exposure to metals (argyria from topical silver compounds; chrysiasis of gold therapy) or drugs (amiodarone, minocycline, chloroquine, or phenothiazines). In patients with acute blood loss, the abnormal vital signs of hypovolemia are the most prominent physical findings (see Chapter 17), but in chronic anemia (the subject of this chapter), physical findings reflect instead changes in color of the skin and conjunctiva. In patients without anemia (bottom left), there are two zones of color: a reddish color at the rim (due to its prominent vascular supply) and a contrasting paler color nearer to the globe (from prominent lymphoid tissue). In patients with anemia (bottom right), the entire inner surface of the lower lid has a pale color (conjunctival rim pallor). These studies excluded patients with acute bleeding or those who had recently received transfusions. As much as possible, the color of skin and conjunctiva was determined using natural lighting. Importantly, no physical sign convincingly decreases the probability of anemia. Usefulness of physical examination in detecting the presence or absence of anemia. Clinical pallor is useful to detect severe anemia in populations where anemia is prevalent and severe. Taking a medical history and using a colour scale during clinical examination of pallor improves detection of anemia. Diagnosing anaemia in pregnancy in rural clinics: assessing the potential of the haemoglobin colour scale. Accuracy and reliability of pallor for detecting anaemia: a hospital-based diagnostic accuracy study. These studies enlisted mostly elderly patients presenting to emergency departments with vomiting, decreased oral intake, or diarrhea. Testing skin turgor over the thighs, sternum, or subclavicular area was more accurate than testing skin over the forearms. The presence or absence of confusion, weakness, or abnormal speech had little diagnostic value in these studies. Although poor capillary refill time has been advanced as a reliable sign of hypovolemia, it lacked diagnostic value in one study. The Principles and Practice of Medicine (Facsimile by Classics of Medicine Library). The measurement of axillary moisture for the assessment of dehydration among older patients: a pilot study. Instead, hospitalized patients with malnutrition present with decreased muscle mass (evident from limb circumference measurements) and decreased grip strength. Among patients admitted to surgical services in industrialized nations, 9% to 27% exhibit signs of severe malnutrition. In industrialized countries, however, most malnourished patients have less dramatic symptoms and present instead with combinations of low body weight, atrophy of muscle and subcutaneous fat, weakness, and various laboratory abnormalities. Based on the hypothesis that malnutrition influences the outcome of surgical patients and that muscle weakness is an important sign of malnutrition, Klidjian et al. The subsequent sphygmomanometer reading (in mm Hg) is a measure of grip strength; formulas for converting these readings to dynamometer readings (in kilograms or pounds) have been published. Interestingly, the presence of recent weight loss has little diagnostic value in predicting complications, possibly because this finding not only identifies patients with weight loss from malnutrition (which should increase complications) but also overweight patients who voluntarily lose weight before surgery (which should decrease complications). The pulse waveform rises rapidly in stiff vessels but slowly in more compliant vessels that act like low-pass filters and remove the high frequency components of the waveform. The dicrotic wave is felt to represent the rebound of blood against the closed aortic valve. The dicrotic pulse occurs in younger patients with severe myocardial dysfunction, low stroke volumes, and high systemic resistance. The importance of a resilient arterial system may explain why the dicrotic pulse usually occurs in young patients with cardiomyopathy, who have more compliant vessels than older patients. Chapter 45 discusses the significance of the water hammer pulse and large pulse pressure of aortic regurgitation. In patients with mitral stenosis, the pulse is characteristically normal or diminished. Normal sinus heart rate: appropriate rate thresholds for sinus tachycardia and bradycardia. Serial cardiovascular variables in survivors and nonsurvivors of human septic shock: heart rate as an early predictor of prognosis. Does initial and delayed heart rate predict mortality in patients with acute coronary syndromes Differentiation between patients with acute upper gastrointestinal bleeding who need early urgent upper gastrointestinal endoscopy and those who do not. The predictive value of admission heart rate on mortality in patients with acute myocardial infarction. Prognostic significance of the initial electrocardiogram in patients with acute myocardial infarction. Heart rate during myocardial infarction: relationship with one-year global mortality in men and women. Resting heart rate in first year survivors of myocardial infarction and long-term mortality: a community study. The dynamics of pulsus alternans: alternating end-diastolic fiber length as a causative factor. Clinical and hemodynamic characteristics of patients with inducible pulsus alternans. The hemodynamic effects of paroxysmal supraventricular tachycardia in patients with the Wolff-Parkinson-White syndrome. Use of pulse oximetry to recognize severity of airflow obstruction in obstructive airway disease: correlation with pulsus paradoxus. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Inferior vena cava plethora with blunted respiratory response: a sensitive echocardiographic sign of cardiac tamponade. Low pressure cardiac tamponade: diagnosis facilitated by Doppler echocardiography. Vital signs including pulsus paradoxus in the assessment of acute bronchial asthma. Pectus excavatum with inspiratory inferior vena cava compression: a new presentation of pulsus paradoxus. Varying ejection fractions of both ventricles in paradoxical pulses: demonstration by radionuclide study. Echocardiographic study of the paradoxical arterial pulse in chronic obstructive lung disease. Pulsus tardus: its cause and potential limitations in detection of arterial stenosis. Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observation study. Even so, all arrhythmias require electrocardiography for confirmation and monitoring. Nonetheless, bedside diagnosis of arrhythmias is still possible, using principles discovered 100 years ago by Mackenzie, Wenckebach, and Lewis. These principles, based on extensive investigation and many polygraph recordings of the arterial and venous pulse,1-4 allow diagnosis of simple arrhythmias when the electrocardiograph is not immediately nearby. Basic abnormalities include (1) the pause, (2) regular bradycardia, (3) regular tachycardia, (4) irregular rhythm that varies with respiration ("in" depicts inspiration and "out" depicts expiration), and (5) irregularly irregular (or "chaotic") rhythm. Although the clinician must compare the radial pulse with the ventricular pulse to diagnose arrhythmias, the difference in rate between the two by itself indicates no particular diagnosis. After the basic rhythm of the radial pulse is identified, analysis of the jugular venous waveforms, heart tones, and response of the heart rhythm to vagal maneuvers may further distinguish the various causes. When there are three radial pulse beats between each pause, the appropriate term is trigeminal pulse or trigeminal rhythm. The finding of several beats between each pause is usually called group beating, and even longer periods of regular rhythm interrupted by the rare pause are sometimes referred to as pulse intermissions. Because the cadence of these rhythms becomes predictable after short periods of observation, the term regularly irregular is sometimes used. This term, however, inaccurately conveys to others what is actually going on and is best discarded. The two most important questions that distinguish these mechanisms are the following: (1) Is there a premature radial pulse immediately preceding the pause The radial pulse tracing and heart tones are presented, illustrating the three mechanisms for the pause: (1) premature contraction that opens the aortic valve, (2) premature contraction that fails to open the aortic valve, and (3) heart block. This early beat is always evident in the form of a palpable apical impulse or additional heart tones, although it may not be felt in the radial artery. If so, the clinician will feel a quick beat in the radial pulse just preceding the pause, although the quick beat is usually not as strong as a normal sinus beat. When listening to the heart tones, the clinician will hear both the first and second heart sounds of the early beat, which produces the following characteristic cadence: lub dup lub dup lub dup lub dup lub dup (In this and the following two examples, lub is the first heart sound and dup is the second sound; each rhythm begins with three normal beats, i. Listening to the heart, he or she will only hear the first sound of the premature beat (S2 is absent because the aortic valve never opens): lub dup lub dup lub dup lub lub dup B. The cadence of heart tones contrasts with those of the premature beat: lub dup lub dup lub dup lub dup 3. In causes 2 and 3, both beats of the couplet are strong, but cause 2 has evidence of a ventricular contraction during the pause, whereas cause 3 does not. This occurs because the right atrium, still beating under the direction of the uninterrupted sinus impulses, contracts after the ventricular premature contraction has closed the tricuspid valve. Rarely, extremely premature ectopic atrial beats may also produce cannon A waves, but these waves precede the first heart sound of the premature contraction, whereas cannon A waves from ventricular premature contractions always follow the first heart sound of the premature beat. There are three causes of regular bradycardia that are recognizable at the bedside: sinus bradycardia, complete heart block, and halved pulse. Sometimes the atrial and ventricular contractions are contiguous, and sometimes they are far apart. Atrioventricular dissociation causes two important bedside findings: changing intensity of the first heart sound and intermittent cannon A waves in the venous pulse. Intermittently, however, the atrium contracts just before the ventricle contraction, which results in a first heart sound of booming intensity (named bruit de canon because of its explosive quality; see Chapter 40 for the pathophysiology of S1 intensity). If cannon A waves appear intermittently, however, in a patient whose ventricular pulse is regular, the only possible diagnosis is atrioventricular dissociation. All of these findings represent regular atrial contractions that continue during the long ventricular diastoles. A rare sign of complete heart block is an intermittently audible summation gallop (or third heart sound; see Chapter 41). This is usually due to premature contractions that appear every other beat but are too weak to open the aortic valve and reach the radial pulse. Rarely, pulsus alternans may be the cause (total alternans),7 although in these patients, the heart tones at the apex are regular, whereas in premature contractions, they are bigeminal. The regular tachycardias that sometimes are recognizable at the bedside include sinus tachycardia, atrial flutter, paroxysmal supraventricular tachycardia, and ventricular tachycardia. The bedside observations that distinguish these arrhythmias are response to vagal maneuvers, signs of atrioventricular dissociation, and abnormalities of the neck veins. Even so, bedside examination is diagnostic in only the minority of patients with rapid rates, and the careful clinician always relies on electrocardiography for diagnosis. To perform the Valsalva maneuver, the clinician asks the patient to bear down and strain against a closed glottis as if "having a bowel movement. In patients with supraventricular tachycardia, 15 seconds of straining is as effective as 30 seconds. Abrupt termination of the tachycardia indicates paroxysmal supraventricular tachycardia (which occurs with both nodal reentry tachycardias and reciprocating tachycardias from accessory pathways). No response is unhelpful, being characteristic of ventricular tachycardia13 but also occurring with every other regular tachycardia. These findings include the intermittent appearance of cannon A waves in the neck veins, changing intensity of the first heart sound, and changing systolic blood pressure (usually detected with the blood pressure cuff). Other causes of regular tachycardias are less likely to create neck palpitations because the atrial and ventricular contractions occur at slightly different times. Definition of findings: For varying arterial pulse, varying amplitude of radial or carotid pulse by palpation. This term describes a cadence of ventricular and radial beats that is completely irregular and unpredictable. Frequent multifocal premature contractions may sometimes seem chaotic at the bedside, but two findings distinguish this rhythm from atrial fibrillation: (1) Venous pulse. In atrial fibrillation, the venous pulse is simple and consists of only one wave per cardiac cycle. In atrial fibrillation, the interval between ventricular beats is random, and it is quite common to have one pause followed by an even longer pause. Definition of findings: For chaotic pulse, "frequent or continuous irregularity" during 20-second examination of the radial pulse. The irregularly irregular or chaotic rhythm may represent atrial fibrillation (top) or sinus rhythm with multiple extrasystoles (bottom).

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