Alder Hey Children? Hospital, NHS Foundation Trust,
Liverpool, United Kingdom
Several guidelines are available (with variability related to where they were devised); most include a third- or fourth-generation cephalosporin such as cefotaxime or ceftriaxone blood pressure 75 over 55 buy telmisartan 80mg on line, plus ampicillin for infants and elderly patients and vancomycin for patients whose meningitis may have spread from the skin or scalp (where staphylococcal infection is common and is often methicillin-resistant) wykladzina arteria 95 discount 80 mg telmisartan otc. Splenectomy or functional hyposplenism contribute to rapid demise in infection with encapsulated organisms such as N meningitidis and S pneumoniae prehypertension heart attack cheap telmisartan 20mg on line. Morbidity hypertension pathophysiology buy telmisartan 80 mg low cost, including permanent neurologic deficit, is found in 14% of children who recover from meningitis but is as high as 39% at one year in resource-poor areas, mostly due to hearing loss or hemiparesis (11%) and epilepsy (5%). Despite dexamethasone use, clinically relevant sensorineural hearing loss persists at 1-year follow-up when carefully screened by audiogram. Fifty percent of neonates surviving group B streptococcal meningitis have permanent sequelae. Although 31% of patients with bacterial meningitis have seizures during the acute phase, most do not develop epilepsy, especially without a structural lesion resulting from abscess or stroke. Although protein elevation, hypoglycorrhachia, and pleocytosis may remain abnormal at 48 hours, the culture should become negative if a successful choice of antibiotic was initiated. Extremely ill-appearing patients should receive antiviral coverage for herpes encephalitis in addition to antibacterial therapy when the diagnosis of bacterial meningitis is in doubt. To ensure adequate treatment of Listeria meningitis, gentamicin should be given with a -lactam antibiotic such as amoxicillin or ampicillin. The treatment of choice for the most common adult cause of meningitis, S pneumoniae, is penicillin, with increasing doses in patients with more resistant strains (present in up to 34% of pathogens in the United States). For the most resistant strains, meropenem with a third- or fourth-generation cephalosporin, plus vancomycin or a fluoroquinolone can be substituted. Penicillin resistance can cross over to cephalosporins (14% of S pneumoniae are resistant to ceftriaxone) and carbapenems; thus, timely sensitivity reporting is necessary for all bacterial cultures. Childhood cases have been successfully treated with shorter courses of antibiotics. Rifampin is used in meningococcal infection to eliminate nasopharyngeal carrier status or reduce risk of meningitis in close contacts of the patient. Patients with meningococcal meningitis are the only ones requiring respiratory isolation for 24 hours. Drugs such as ertapenem, gemifloxacin or moxifloxacin, and daptomycin (an oxazolidinone) also show promise for treating meningitis. Because they are frequently used, fluoroquinolones have the highest propensity to develop resistance. However, some guidelines recommend higher doses of vancomycin and other antibiotics toward the end of the course of treatment. Repeat lumbar puncture at the end of therapy is no longer standard practice, although in patients with pneumococcal B. Controversy exists, as patients without definite diagnosis sometimes have increased mortality. Beneficial effects are limited to organisms with a polysaccharide capsule (ie, gram positive), especially S pneumoniae. Confirmation of the benefits of steroids by meta-analysis have been limited to preservation of hearing. Transtentorial herniation-Although an infrequent complication, transtentorial herniation can be fatal. Fluid management can be difficult; the clinician must balance the need for adequate blood pressure with that of avoiding increased intracranial pressure. Glycerol use in less severely ill patients led to paradoxical increases in mortality, as did induced hypothermia. Prophylactic anticonvulsants are not indicated when monitoring (close clinical observation or electrophysiologic) is available. Suppurative thrombophlebitis-This complication can be treated with anticoagulation, especially if the sagittal sinus is thrombosed or there are no other drainage channels. Antibiotic-related complications-Delirium has been reported in 391 cases, from 12 classes of antibiotics. Psychosis with hallucinations was most common with sulfonamides, quinolones, macrolides, and penicillin. If dose and frequency are not corrected for weight and creatinine clearance, several -lactam antibiotics such as imipenem cause seizures and myoclonus. Neurologic deficits are seldom seen in meningococcal meningitis but serious morbidity such as limb loss occurs frequently in patients with the Waterhouse-Friderichsen reaction of thrombocytopenia, disseminated intravascular coagulation, and shock. Impact of an evidence-based guideline on the management of community-acquired bacterial meningitis: A prospective cohort study. Complications associated with antibiotic administration: Neurologic adverse events and interference with antiepileptic drugs. Increased risk for meningococcal disease among men who have sex with men in the United States, 2012-2015. Lumbar puncture performed promptly or after neuroimaging in adult bacterial meningitis: A prospective national cohort study evaluating different guidelines. Serogroup B meningococcus outbreaks, prevalence, and the case for standard vaccination. Adjunctive dexamethasone therapy in unconfirmed bacterial meningitis in resource limited settings: Is it a risk worth taking Escherichia coli K1 modulates peroxisome proliferator-activated receptor and glucose transporter 1 at the blood-brain barrier in neonatal meningitis. Prevalence of maternal colonisation with group B streptococcus: A systematic review and meta-analysis. Epidemiology and treatment of the commonest form of listeriosis: Meningitis and bacteraemia. Thioredoxins and methionine sulfoxide reductases in the pathophysiology of pneumococcal meningitis. Cranial imaging before lumbar puncture in adults with community-acquired meningitis: Clinical utility and adherence to the Infectious Diseases Society of America guidelines. Examples, which include matrix metalloproteinase-9 and neutrophil elastase, are not affected by antibiotics or corticosteroids. Fibroblasts form a thick capsule outside the abscess that limits increasing size, but edema surrounding the abscess can magnify its deleterious effect on brain dysfunction. Other than seizures, which are a common presenting problem, symptoms arise gradually from pressure on nearby structures or, rarely, suddenly from arteritis causing stroke or from rupture into a ventricle. The effect of molecular rapid diagnostic testing on clinical outcomes in bloodstream infections: A systematic review and meta-analysis. Extra caution such as changing sterile gloves before placement of drains or intraventricular catheters and their removal at the first sign of bacteremia may prevent the spread of infection from skin or blood to brain. Older patients who did not receive these vaccines as children and immunosuppressed patients remain at risk. In addition, infection in a vaccinated person can occur with an organism of differing serotype than that used in the vaccine. Symptoms and Signs the neurologic manifestations of an abscess reflect its location(s). Cortical signs evolve slowly over days to weeks and include personality change, aphasia, hemiparesis, hemisensory loss, and visual field defects. Infratentorial signs include ataxia, nystagmus, cranial nerve dysfunction, nausea, and vomiting.
Prevention Although the underlying state of migraine is likely to be genetically based heart attack one direction buy cheap telmisartan 80mg on line, the frequency and severity of attacks can often be altered by patient behaviors blood pressure in the morning buy cheap telmisartan 20mg online. Sleep should be regular blood pressure medication that does not cause joint pain generic 80mg telmisartan, even on weekends and vacations blood pressure chart bpm 40mg telmisartan overnight delivery, because oversleeping or undersleeping can increase the likelihood of an attack. Socalled antimigraine diets are occasionally useful, but a diet diary can be helpful even if strict adherence to the diet is not. Maintaining adequate hydration is important, as is avoidance of any known triggers. Patients should be instructed to avoid missing meals and to minimize caffeine intake while keeping amounts consistent throughout the week. Psychiatric comorbidities such as depression, mania, social phobias, and anxiety should be evaluated and appropriately treated. General Considerations Migraine is the most important cause of disabling headaches, and most medical visits for headache are due to migraine. Although the cause of migraine is unknown, it is most commonly a familial and probably a polymorphic genetic condition. Only 50% of these individuals receive the diagnosis of migraine, generally believing that they suffer from tension-type headaches or sinus headaches. Symptoms and Signs Attacks can be bilateral and nonpulsatile; the severity alone does not define a migraine. Neck pain, often unilateral, is common with migraine and often leads to an erroneous diagnosis of tension-type headache. Associated lacrimation and rhinorrhea, due to the activation of cranial parasympathetic nerves, often lead to the erroneous diagnosis of sinus headache or a trigeminal autonomic cephalgia. The attack frequency and degree of disability is higher in migraine without aura than in migraine with aura. Migraine, with its variants, accounts for 94% of primary care visits for the complaint of recurrent disabling headache. Tension-type headaches are the most common headache type, but these headaches are rarely disabling and therefore generally are self-treated. Pathogenesis the so-called vascular theory of migraine, which had widespread acceptance until the 1970s, held that migraine symptoms were a function of hyperemia and ischemia. This perspective led to the development of potent vasoconstrictors, which, in retrospect, were less safe and less effective than most of the current therapies. Biologically, migraineurs have a hyperexcitable cerebral cortex, which probably underlies migraine auras and the frequent comorbid depression, mania, and anxiety. Pain appears to be related to sensitization of peripheral perivascular nerve terminals, possibly a consequence of distended meningeal blood vessels, leading to activation and sensitization of the central trigeminal system. Neuropeptide release results in neurogenic inflammation of meningeal vessels and to further activation of trigeminal sensory fibers. A self-sustaining process of further pain, inflammation, and sensitization of central trigeminal neurons occurs, with sensitization of glial cells in the periaqueductal gray, for which there appears to be a central generator, located in the rostral brainstem. By the time these central structures become sensitized, they are activated independently of peripheral stimuli. This explains why triptans, which do not enter the central nervous system, are ineffective at this stage. Diagnostic Studies Individuals with a normal neurologic examination and a stable pattern of periodic attacks that fulfill criteria for migraine rarely benefit from additional testing. They are nonsedating and do not increase nausea, which, along with decreased gastric motility, can complicate migraine therapy. Risks of gastrointestinal bleeding and hepatic disease, as well as risk of enhancing the development of cardiovascular disease, limit their frequent use. Frequent use has also been associated with an increased risk of cardiovascular and cerebrovascular disease. Triptans-Most migraineurs presenting for management of their headaches are experiencing disabling attacks, for which triptans are the preferred therapy. Nasal sprays (sumatriptan and zolmitriptan) or injections (sumatriptan) are preferred in attacks with a rapid onset of nausea and head pain where gastric stasis may delay the absorption of pills. Orally dissolving tablets are not sublingual and are no faster than their regular tablet counterparts, although they are convenient and therefore may encourage early intervention. Triptans with longer half-lives (naratriptan and frovatriptan) appear to be somewhat less effective than the other products in terminating migraines. They are often used "off label" for short-term prophylaxis of predictable forms of migraine. Recurrences refer to situations in which the headache is relieved but returns within 24 hours. A longer half-life does not ensure a longer duration of action or a lower risk of Typical migraine auras without subsequent headache Auras with dysarthria, vertigo, diplopia, and decreased consciousness with bilateral numbness Paroxysmal vertigo, periodic abdominal migraine, and cyclic vomiting Migraines without aura for at least half of the days, present for at least 2 months, in the absence of medication overuse Familial and sporadic cases with reversible aura of hemiplegia Repeated attacks of monocular visual disturbance, including scintillations, scotomata, or blindness, associated with headache Debilitating migraine attacks lasting >72 h Typical migraines with accompanying vertigo Hemiplegic Retinal Status migrainosus Vestibular Differential Diagnosis "Migraine" is a biologic state, and individuals with migraine who develop additional medical problems (eg, infections, neoplasms) often manifest them by a change in the character and frequency of their preexisting migraines. Therefore, if attacks do not fulfill the criteria for the diagnosis of migraine, if the neurologic examination is abnormal, or if the attack frequency and character of a preexisting headache syndrome are clearly worsening, further testing is appropriate. Complications Some migraineurs experience a progressive frequency and severity of attacks. Many, but not all, cases of chronic migraine result from the overuse of concomitant medications. Whether aggressive symptomatic and prophylactic treatment of attacks in those with pervasive migraines will alter this natural history remains to be seen. Acute Attacks the goal of therapy for patients experiencing acute attacks is to fully terminate the head pain and its associated symptoms of light and sound sensitivity and nausea, without causing additional disability. It is preferable to avoid sedation, a common disabling side effect of some medications, thereby allowing the individual to return to normal functioning. For this reason, migraineurs should be instructed to identify and aggressively treat their attacks at the earliest stages. As noted, if nausea occurs early in an attack, the absorption of oral medications may be impaired. If nausea occurs later in the attack, triptan tablets are usually satisfactory, because they relieve the nausea, vomiting, photophobia, and phonophobia in parallel with the headache. All triptans are contraindicated in patients with coronary artery disease, although the chance of a triptan actually triggering a cardiac event is exceedingly rare. So-called triptan sensations (chest and neck tightness and pressure) are not due to cardiac ischemia; these effects are probably caused by esophageal constriction, pulmonary arterial constriction, or abnormalities in the energy metabolism of chest wall muscles. Because cerebral ischemic events are commonly associated with headache, cases of migraine with aura can be confused with stroke. Injectable sumatriptan, when administered during an aura, does not prolong the aura but is less effective in treating the subsequent headache. This association has not been investigated with other forms of sumatriptan or other triptan products, but in patients with this response, treatment can be appropriately withheld until the pain actually begins. Therefore, although there is no safety concern of treating during an aura, it is recommended that treatment begin at the earliest stages of head pain. Caution is recommended when coprescribing triptans and selective serotonin reuptake inhibitors or selective norepinephrine reuptake inhibitors, because cases of a serotonin syndrome with hyperthermia, confusion, muscle stiffness, and sweating have been reported. Ergots-Ergot medications are generally less effective than triptans in relieving all migraine symptoms. Triptans and ergots cannot be used concomitantly or within 24 hours of each other. Analgesics-Analgesics containing butalbital are often satisfactory for treatment when they are not overused. Despite a short duration of action, the half-life of butalbital is long, and even modest use can result in the accumulation of the barbiturate.
Late Responses Routine nerve conduction studies can evaluate only distal segments of the nerve xylitol hypertension discount telmisartan 80mg fast delivery. In the leg hypertension patho buy telmisartan 80 mg on line, conduction studies evaluate the peroneal and tibial nerves up to the knee blood pressure herbs order 80 mg telmisartan visa. Therefore hypertension from stress proven telmisartan 40 mg, late responses such as F waves and H-reflex are used to evaluate the less-assessable proximal portions of the nerve. F Waves F waves are low-amplitude responses produced by antidromic stimulation of a small number of motor neurons during motor conduction studies. Because each electrical stimulation activates a different subpopulation of motor neurons, consecutively recorded F waves vary in latency, amplitude, and duration. The F-wave latency is the time between the stimulus and onset of an F wave, and the minimal F-wave latency is the most commonly recorded parameter. Prolonged or absent F-wave latency can reflect a proximal lesion when distal nerve conduction is normal. F-wave study is especially useful if there is suspicion of demyelinating neuropathy in proximal segments. If the motor nerve conduction study is slowed distally due to underlying peripheral or entrapment neuropathy, F-wave latency can also be prolonged. In addition, because of technical limitations, the studies evaluate more proximal portions of the sensory nerve and not the most distal segments. For example, sensory studies of digital nerves supplied by median nerve assess the response in the fingers but not in the fingertips. Often in patients with focal or unilateral lesions, the contralateral limb is used as an internal control. When to Order Motor and sensory conduction studies can be used to identify focal lesions and to distinguish peripheral neuropathy from myopathy and motor neuron diseases. They can also detect subclinical lesions (eg, Charcot-Marie-Tooth disease, carpal tunnel syndrome) and differentiate among inherited and acquired, axonal, and demyelinating polyneuropathy. Axonal neuropathy-In axonal neuropathy, motor and sensory action potentials show low amplitudes, with conduction velocity either preserved or only mildly slowed. H-Reflex the H-reflex is the electrophysiologic equivalent of the Achilles tendon reflex. By early childhood it is present only in gastrocnemius-soleus and flexor carpi radialis muscles. It is a motor-evoked response that is elicited by stimulating sensory fibers in a peripheral nerve, usually the tibial nerve. The action potential then propagates to the dorsal root ganglion and subsequently into the dorsal horn of the spinal cord, and through a monosynaptic pathway, anterior horn cells are activated, in turn activating the corresponding muscle (the soleus). Because the H-reflex is mediated primarily through the S1 root, asymmetry of latency between sides is often used to support a diagnosis of S1 radiculopathy or a proximal tibial nerve lesion. In normal subjects, persistent stimulation at rates less than 5 Hz cause progressive decline in release of acetylcholine vesicles into the synaptic cleft. Normally, because there is a large excess of vesicles and neurotransmitters compared with the number of receptors, the decline does not result in reduced numbers of activated muscle fibers. In individuals with myasthenia gravis, reduced number of functional acetylcholine receptors results in failure of neuromuscular transmission with repetitive stimulation. In myasthenia gravis, the drop in amplitude is progressive from the first to the fourth response, which is usually the nadir response, and more than 10% decline in amplitude is considered abnormal. Repetitive stimulation immediately after brief (15-second) exercise at maximal effort has the opposite effect and reverses the decrement that is seen at baseline before exercise (post-exercise facilitation). In normal subjects, postexercise facilitation never causes increased response (increment) greater than 50% of baseline. However, in patients with Lambert-Eaton myasthenic syndrome, a presynaptic disorder, the increment increase from post-exercise facilitation can be more than two- to threefold. This amplitude increase can also be seen with repetitive stimulation at a high rate (50 Hz). A: Baseline repetitive stimulation: (1) Stabilize limb and obtain supramaximal response in distal nerve-muscle pain (eg, median-thenar or ulnar-hypothenar); (2) deliver 10 supramaximal stimuli at 3 Hz; (3) calculate % decrement between first and fourth potentials (shown here, 30% decrement). B: Post-exercise facilitation: (1) Perform voluntary maximal contraction of muscle being tested for 15 seconds; (2) deliver 10 stimuli at 3 Hz immediately after exercise; (3) calculate % decrement (here 2%) and look for increment. C: Post-exercise exhaustion: (1) Exercise using maximal force for 1 minute; (2) repeat train of stimulation at 3 Hz at 1, 2, 3, and 4 minutes after exercise; (3) calculate % decrement (here 45%) and, if no decrement, repeat study in the proximal system (accessorytrapezius or facial-nasalis). Almost any muscle can be examined, although to do so is not always practical or useful. Spontaneous Activity At rest, a normal muscle is electrically silent except in the region of the neuromuscular junctions, where spontaneous endplate potentials result from spontaneous continuous release of vesicles containing acetylcholine. Fibrillations and positive sharp waves are spontaneous discharges of individual muscle fibers and have characteristic configurations. They are present in both neurogenic denervation and myopathic diseases, and they have similar pathologic significance. Fibrillations and positive sharp waves are seen about 2 weeks after nerve injury, indicating muscle denervation. In chronic neurogenic diseases such as peripheral neuropathy or motor neuron disease, these potentials can be persistent. Fibrillations and positive sharp waves are also present in myopathic conditions, especially inflammatory myopathies and muscular dystrophy, in which muscle necrosis can separate remaining muscle fibers from their nerve axons and effectively denervate them. Thus these abnormal spontaneous potentials by themselves cannot distinguish neuropathic from myopathic processes, and information from nerve conduction studies as well as motor unit and recruitment analysis are crucial for diagnosis. Their firing pattern is slow and irregular, and although their configuration may be identical to an activated motor unit, they are not under voluntary control. A fasciculation represents a motor unit (all the muscle fibers innervated by a motor neuron); its configuration is therefore larger in amplitude and more complex than a fibrillation or a positive sharp wave. Often visible on skin surface as small muscle movements that are insufficient to move the joint, fasciculations are characteristic of motor neuron diseases such as amyotrophic lateral sclerosis. They can also occur in chronic neurogenic conditions such as peripheral neuropathy or radiculopathy, and they can be a normal finding in small foot muscles and in patients with benign fasciculation syndrome. In addition to documenting the presence of abnormal spontaneous activity, it is important to note the frequency and abundance of these activities. Myotonic discharges are high-frequency repetitive discharges that wax and wane in amplitude to produce a sound similar to revving up of a motorcycle engine. Myotonic discharges are seen in myotonic dystrophy, myotonia congenita, paramyotonia, familial periodic paralysis, and acid maltase deficiency. Complex repetitive discharges are highfrequency discharges that begin and end abruptly without the waxing and waning quality of myotonic discharges. Myokymia are grouped discharges occurring in a semi-rhythmic manner separated by periods of silence. Corresponding to continuous rippling or quivering in the muscle, they are often seen in facial muscles, especially in patients with multiple sclerosis, brainstem tumors, hypocalcemia, or post-radiation treatment. Cramps can be benign (eg, nocturnal or post-exercise cramps), but they are also associated with neuropathic and metabolic abnormalities. Its amplitude varies with the size of the motor unit and its proximity to the recording needle. The number of fibers in each motor unit varies, from very few in muscles requiring fine control (eg, eye muscles) to hundreds in large muscles, such as calf muscles. When a nerve impulse travels down a motor axon, all the muscle fibers in that motor unit fire almost simultaneously, producing the characteristic triphasic waveform. In initial voluntary contraction at low effort, small motor units are activated first, with an initial increase in power from higher firing frequency.
Symptoms Depend on underlying disorder but include dyspnea arrhythmia foods to avoid cheap 40 mg telmisartan, cough blood pressure zero gravity generic 80mg telmisartan with mastercard, fatigue heart attack heart attack buy telmisartan 80mg otc, and sputum production (in parenchymal diseases) arteria carotida externa safe 20mg telmisartan. Right-Heart Catheterization Can confirm presence of pulmonary hypertension and exclude left-heart failure as cause. Loop diuretics must also be used with care to prevent significant metabolic alkalosis that blunts respiratory drive. Rare causes of aneurysms are infections (syphilitic, tuberculous, mycotic) and vasculitides. History May be clinically silent, but thoracic aortic aneurysms can result in deep, diffuse chest pain, dysphagia, hoarseness, hemoptysis, dry cough; abdominal aneurysms may result in abdominal pain or thromboemboli to the lower extremities. If clinically suspected, obtain serologic test for syphilis, especially if ascending thoracic aneurysm shows thin shell of calcification. In pts with Marfan syndrome or bicuspid aortic valve, thoracic aortic aneurysms >5 cm usually warrant repair. Less invasive endovascular repair is an option for some pts with descending thoracic or abdominal aortic aneurysms. Alternative classification: Type A-dissection involves ascending aorta; type B-limited to transverse and/or descending aorta. Etiology Ascending aortic dissection is associated with hypertension, cystic medial necrosis, Marfan and Ehlers-Danlos syndromes; descending dissections are commonly associated with atherosclerosis or hypertension. Incidence is increased in pts with coarctation of aorta, bicuspid aortic valve, and rarely in third trimester of pregnancy in otherwise normal women. Asymmetry of carotid or brachial pulses, aortic regurgitation, and neurologic abnormalities associated with interruption of carotid artery flow are possible findings. Aortography is rarely required, as sensitivity of these noninvasive techniques is >90%. Ascending aortic dissection (type A) requires surgical repair emergently or, if pt can be stabilized with medications, semielectively. Symptoms include intermittent claudication of the buttocks and thighs and impotence (Leriche syndrome); femoral and other distal pulses are absent. Catheter-based endovascular treatment or aortic-femoral bypass surgery is required for symptomatic treatment. Pain in buttocks and thighs suggests aortoiliac disease; calf muscle pain implies femoral or popliteal artery disease. More advanced arteriosclerotic obstruction results in pain at rest; painful ulcers of the feet (sometimes painless in diabetics) may result. Some, but not all, pts note symptomatic improvement with drug therapy (cilostazol or pentoxifylline). Pts with severe claudication, rest pain, or gangrene are candidates for revascularization (arterial reconstructive surgery or percutaneous transluminal angioplasty/stent placement). Physical Examination Absent pulse, pallor, and decreased temperature of limb distal to the occlusion. For acute severe ischemia, immediate endovascular or surgical embolectomy is indicated. Atheroembolism A subset of acute arterial occlusion due to embolization of fibrin, platelets, and cholesterol debris from more proximal atheromas or aneurysm; typically occurs after intraarterial instrumentation. Atheroembolism to lower extremities results in blue toe syndrome, which can progress to necrosis and gangrene. Treatment is supportive; for recurrent episodes, surgical intervention in the proximal atherosclerotic vessel or aneurysm may be required. However, suspect an underlying disease (Table 135-1) if tissue necrosis occurs, if disease is unilateral, or if it develops after age 50. Arteriography shows smooth tapering lesions in distal vessels, often without proximal atherosclerotic disease. More serious conditions such as cellulitis or lymphangitis may mimic this, but these are associated with fever, chills, lymphadenopathy, and red superficial streaks along inflamed lymphatic channels. Particularly common in pts on prolonged bed rest, those with chronic debilitating disease, and those with malignancies (Table 135-2). May lead to erythema, hyperpigmentation, and recurrent cellulitis; ulcers may appear at medial and lateral malleoli. Physical Examination Marked pitting edema in early stages; limb becomes indurated with nonpitting edema chronically. Differentiate from chronic venous insufficiency, which displays hyperpigmentation, stasis dermatitis, and superficial venous varicosities. Hypoxemic Lung Disease Chronic obstructive lung disease Interstitial lung disease Sleep-disordered breathing Chronic hypoventilation 4. Chronic Pulmonary Thromboembolic Disease Chronic pulmonary embolism Nonthrombotic pulmonary embolism. Differential Diagnosis Other disorders of heart, lungs, and pulmonary vasculature must be considered. Rarely, pulmonary hypertension is due to parasitic disease (schistosomiasis, filariasis). Cardiovascular disorders to be excluded include pulmonary artery and pulmonic valve stenosis, ventricular and atrial shunts with secondary pulmonary vascular disease (Eisenmenger syndrome), and clinically silent mitral stenosis. All potential etiologies and associated conditions must be investigated in a pt with clinical findings consistent with pulmonary hypertension. If short-acting vasodilators are beneficial during acute testing in catheterization laboratory, pt may benefit from high-dose calcium channel blocker. Bosentan is contraindicated in pts taking cyclosporine (which greatly increases bosentan plasma levels) or glyburide (combination is associated with increased hepatic transaminases). Do not prescribe concurrently with nitrovasodilators; the combination could result in marked hypotension. For selected pts with persistent right heart failure, lung transplantation can be considered. The respiratory system includes not only the lungs but also the chest wall, pulmonary circulation, and central nervous system. There are three key types of respiratory system physiologic disturbances that occur in varying combinations in different lung diseases: ventilatory function, pulmonary circulation, and gas exchange. Disturbances in Ventilatory Function Ventilation involves the delivery of gas to the alveoli. The classification of lung volumes, which are measured with pulmonary function testing, is shown in. Plateau of the inspiratory curve on the flow-volume loop suggests extrathoracic large airway obstruction, while plateau of the expiratory curve suggests intrathoracic large airway obstruction. Lung volumes and flow rates are typically compared with population-based normal values that adjust for the age, height, sex, and race of the pt. There are two major patterns of abnormal ventilatory function detected by pulmonary function testing: restrictive and obstructive (Tables 137-1 and 137-2). Weakness of the respiratory muscles can be assessed by measuring maximal inspiratory and expiratory pressures. All diseases of the respiratory system causing hypoxemia are capable of causing pulmonary hypertension. However, pts with prolonged hypoxemia related to chronic obstructive pulmonary disease, interstitial lung disease, chest wall disease, and obesity-hypoventilation/obstructive sleep apnea are particularly likely to develop pulmonary hypertension. Normal tidal volume is approximately 500 mL and normal respiratory rate is approximately 15 breaths/min, leading to a total minute ventilation of approximately 7. Diffusion can be tested by measuring the diffusing capacity of the lung for a low (and safe) concentration of carbon monoxide (Dlco) during a 10-second breath-hold. A restrictive ventilatory defect with reduced Dlco suggests parenchymal lung disease. The pattern of normal spirometry, normal lung volumes, and reduced Dlco is consistent with pulmonary vascular disease. Gas exchange is critically dependent on proper matching of ventilation and perfusion. The actual content of O2 in blood is determined by both Po2 and hemoglobin concentration. The alveolar-arterial O2 difference [(A - a) gradient] can provide useful information when assessing abnormalities in gas exchange. Severe arterial hypoxemia rarely occurs purely due to alveolar hypoventilation while breathing air at sea level.
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A tight stenosis is associated with increased flow rate heart attack questions discount telmisartan 20 mg line, much like the increased flow of water through the end of a garden hose when a finger is placed over it hypertension grades purchase telmisartan 20mg visa. The flow rate and direction can be displayed as a graph (ie pulse pressure 28 cheap telmisartan 80 mg, duplex Doppler) or as colors superimposed on the cross-sectional images (ie blood pressure levels exercise 80 mg telmisartan with amex, color Doppler). A: Lateral image from an internal carotid catheter angiogram shows a large ophthalmic artery aneurysm. B: Lateral scout image of a catheter angiogram shows embolization coils in a large ophthalmic artery aneurysm and a stent in the adjacent internal carotid artery. C: Lateral image after the injection of contrast material into the internal carotid artery shows patency of the internal carotid artery and non-filling of the aneurysm. A properly draped ultrasound probe is used after the skull or vertebrae covering the lesion has been removed. Bifurcation of the common carotid artery-Both the morphology of the common carotid bifurcation and the severity of stenoses can be determined by ultrasound. Vasospasm and vascular stenosis-Transcranial Doppler ultrasonography can be performed in adults through the thin temporal squamosa to evaluate vasospasm in patients with subarachnoid hemorrhage and to detect intracranial vascular stenosis in patients with sickle cell anemia. Prenatal examination of the brain and spine- Ultrasound is routinely used for intrautero examination of the brain and spine. Subdural hematoma, hydrocephalus, and many anomalies of the brain and spine can be detected and, in some cases, treated before birth. Postnatal examination of the brain and spine- Open fontanelles are an excellent window for ultrasonic evaluation of the brain. Often, ultrasound can obtain good information about the condition of the spinal cord in the neonate. Technetium pertechnetate is injected intravenously for confirmation of brain death; failure of the tracer to accumulate in the brain indicates absence of cerebral blood flow. This procedure is also used to demonstrate communicating and normal pressure hydrocephalus, in which there is a lack of normal tracer accumulation over the cerebral convexities. Neonatal ultrasound shows hydrocephalus and hyperechoic intraventricular hemorrhage (arrows). Initial Examination and Immediate Interventions the examination begins with the detection and treatment of any immediate life-threatening condition (eg, hemorrhage, airway obstruction, hypotension, or cardiac arrhythmia). Finger-stick glucose is obtained, and if in doubt, 50% dextrose (plus thiamine and multivitamins) is given intravenously. Thiamine (and other multivitamins) is given with the glucose to prevent precipitation of Wernicke-Korsakoff syndrome. Abnormal motor responses to stimuli Abnormal respiratory patterns Abnormal pupillary responses Abnormal eye movements General Considerations Stupor and coma are reduced states of alertness that differ from syncope in being sustained and from sleep in being less easily reversed. They are clinically defined in terms of response to stimulation, and because terms such as lethargy, obtundation, stupor, and coma are not rigorously defined, an examiner should record both the minimal stimulus that produces a response (eg, voice, passive movement, pain) and the response itself (eg, groaning, purposeful movement, extensor posturing, no response). Delirium refers to severe inattentiveness, altered mental content, and sometimes hyperactivity. General Examination Examination includes skin, nails, and mucous membranes (cyanosis, pallor, cherry redness, jaundice, petechiae, decubiti, uremic frost, dry myxedema, hypo- or hyperpigmentation, signs of trauma), breath (acetone, alcohol), and fundi (papilledema, hypertensive or diabetic retinopathy, Roth spots, subhyaloid hemorrhage). Hypothermia might indicate cold exposure, hypothyroidism, hypoglycemia, or sepsis. The scalp should be palpated for signs of trauma and the ears and nose examined for blood or cerebrospinal fluid. Resistance to passive neck flexion suggests meningitis or subarachnoid hemorrhage; resistance in all directions suggests bone or joint disease, including fracture. Coma can be caused by any lesion-structural or metabolic- that disrupts the brainstem reticular activating system, the cerebral hemispheres to which it projects, or both. The causes of coma are usefully divided into supra- and infratentorial structural lesions and diffuse or metabolic disorders. By concentrating the neurologic examination on motor responses to stimuli, respirations, pupils, and eye movements, the clinician can usually identify which type of lesion is present. Motor responses-Inspection identifies limb position and spontaneous movements, either voluntary or involuntary (eg, seizure or myoclonus). A smaller pupil could indicate sympathetic dysfunction either intraparenchymally (eg, infarction of the lateral medulla) or extraparenchymally (eg, destruction of the superior cervical ganglion by lung cancer). Oculomotor nerve damage becomes obvious when the pupil becomes fully dilated and unreactive to light or when extraocular muscles innervated by the oculomotor nerve are affected. Sympathetic damage is evident when miosis is accompanied by other features of a Horner syndrome. Bilateral pinpoint (but reactive) pupils occur with pontine lesions (eg, hemorrhage) that transect descending sympathetic pathways. Unilateral or bilateral midposition and unreactive pupils occur with midbrain lesions that destroy both parasympathetic and sympathetic projections. Because the pupillary light reflex is consensual, retinal or optic nerve damage does not cause anisocoria. Rather, there is reduced response bilaterally when light is directed at the affected eye, but whether the light is directed at either the good or the bad eye, the pupils remain equal (the so-called afferent pupillary defect). With few exceptions, metabolic disorders do not cause unequal or unreactive pupils. Anticholinergic drugs, including amitriptyline, antiparkinsonian agents, and recreational use of Datura stramonium, can abolish pupillary reactivity. Hypothermia and severe sedative intoxication can cause not only unreactive pupils but a reversible state resembling brain death. Opioid drugs do not abolish pupillary light reactivity, but miosis can be so severe that reactivity is difficult to discern. Eyes conjugately deviated away from hemiparetic limbs indicate a destructive cerebral lesion affecting the frontal eye fields (and the motor cortex) on the side toward which the eyes are directed. Eyes turned toward paretic limbs favor a pontine lesion affecting the paramedian reticular formation (and the corticospinal tract) on the side away from which the eyes are directed. Conjugate eye deviation can also reflect a seizure generated by the frontal eye fields. Eyes dysconjugate at rest indicate paresis of individual muscles, internuclear ophthalmoplegia, or preexisting tropia or phoria. Eyes roving from side to side with a slow smooth velocity indicate nonwakefulness and an intact brainstem. If on inspection the eyes are seen to move conjugately and fully in both horizontal directions, further testing is usually unnecessary. Asymmetric movements or postures can signify either hemiparesis or focal seizures. Asymmetry of muscle tone suggests a structural lesion, but it may not be clear which side is abnormal. Appropriate responses to painful stimuli (eg, sternal rubbing, nailbed pressure) include limb withdrawal, fending off, grimacing, or vocalization. Inappropriate responses include so called decorticate posturing (flexion of arms and extension of legs) and decerebrate posturing (extension of arms and legs). In both decorticate and decerebrate posturing, there is usually internal rotation of the upper arms, and the limbs are flaccid and not moving in the absence of external stimulation. Spontaneous posturing should suggest seizures or an unrecognized stimulus such as airway obstruction or bladder distension. Decorticate and decerebrate postures are generated by lower brainstem structures and most often indicate upper brainstem damage, especially during transtentorial herniation secondary to a supratentorial mass lesion. They can also occur, however, in patients with metabolic derangement, including hepatic coma and sedative overdose. It usually signifies that the patient is not in imminent danger and does not, by itself, mandate artificial ventilation. Sustained hyperventilation is usually due to metabolic acidosis, hypoxia, pulmonary congestion, hepatic encephalopathy, or stimulation by analgesic drugs. So-called primary hyperventilation, with respiratory alkalosis, can follow upper brainstem damage, which may occur during the course of transtentorial herniation. Ataxic breathing signifies damage to the lower brainstem and mandates immediate ventilatory support.
