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The vitreous chamber is the large space behind the lens containing gelatinous material arthritis tea discount celebrex 100mg without a prescription, the vitreous humour psoriatic arthritis medication side effects generic celebrex 200 mg visa. The main function of the eye is visual acuity which depends upon a transparent focussing system comprised by the cornea arthritis medication for dogs over the counter celebrex 200mg overnight delivery, lens arthritis pain dogs buy generic celebrex 100 mg online, transparent media consisting of aqueous and vitreous humours, and a normal retinal and neural conduction system. The basic defect lies in the developmental prematurity of the retinal blood vessels which are extremely sensitive to high dose of oxygen-therapy. The condition can have various inheritance patterns-autosomal dominant, autosomal recessive trait, or sex-linked recessive trait. The earliest clinical finding is night blindness due to loss of rods and may progress to total blindness. M/E the chalazion gives the appearance of a chronic inflammatory granuloma located in the tarsus and contains fat globules in the centre of the granulomas i. Panophthalmitis is the term used for inflammation involving retina, choroid and sclera and extending to the orbit. The exogenous agents may be bacteria, viruses or fungi introduced into the eye during an accidental or surgical perforating wound. The endogenous agents include opportunistic infections which may cause endophthalmitis via haematogenous route. Trachoma is widely prevalent in the developing countries of the world and is responsible for blindness on a large scale. The condition probably results from an autosensitivity reaction to injured uveal tissue. M/E There is granulomatous uveal inflammation consisting of epithelioid cells and lymphocytes affecting both the eyes. The condition develops in more than 60% of diabetics 15-20 years after the onset of disease, and in about 2% of diabetics causes blindness. Other ocular complications of diabetes include glaucoma, cataract and corneal disease. The risk is greater in type 1 diabetes mellitus than in type 2 diabetes mellitus, although in clinical practice there are more patients of diabetic retinopathy due to type 2 diabetes mellitus because of its higher prevalence. Background (non-proliferative) retinopathy this is the initial retinal capillary microangiopathy. Proliferative retinopathy (retinitis proliferans) After many years, retinopathy becomes proliferative. In acute severe hypertension as happens at the onset of malignant hypertension and in toxaemia of pregnancy, the vascular changes are in the form of spasms, while in chronic hypertension the changes are diffuse in the form of onionskin thickening of the arteriolar walls with narrowing of the lumina. M/E i) ii) iii) iv) v) vi) vii) Features of hypertensive retinopathy include the following: Variable degree of arteriolar narrowing. Clinically, the condition appears as raised yellowish lesions on the interpalpebral bulbar conjunctiva of both eyes in middle-aged and elderly patients. Pterygium is a lesion closely related to pinguecula but differs from the latter by being located at the limbus and often involves the cornea. It may occur spontaneously in older individuals past 50 years of age, or may be secondary to trauma in the region of head and neck. There are 3 pathogenetic mechanisms of retinal detachment: i) Pathologic processes in the vitreous or anterior segment, causing traction on the retina. The causes of such end-stage blind eye are trauma, glaucoma and intraocular inflammations. Glaucoma is one of the leading causes of blindness because of the ocular tissue damage produced by raised intraocular pressure. In all types of glaucoma, degenerative changes appear after some duration and eventually damage to the optic nerve and retina occurs. This is due to anatomic continuation of the subarachnoid space of the brain around the optic nerve so that raised intracranial pressure is passed onto the optic disc area. The condition occurs due to immunologically-mediated destruction of the lacrimal and salivary glands. M/E Many of the lesions can be placed in well-established categories such as tuberculous, syphilitic, mycotic, parasitic, foreign-body granuloma etc, while others show non-specific histologic appearance having abundant fibrous tissue, lymphoid follicles and inflammatory infiltrate with prominence of eosinophils. The tumour is seen mostly in the upper eyelid (basal cell carcinoma is seen more frequently in the lower eyelid). M/E the tumour may show well-differentiated lobules of tumour cells with sebaceous differentiation, or may be poorly-differentiated tumour requiring confirmation by fat stains. Spindle A melanoma is composed of uniform, spindle-shaped cells containing spindled nuclei.
Effectively every episode of double vision has an acute onset because double vision is either present or not reactive arthritis in feet purchase discount celebrex. What needs to be established is for how long double vision has been noticed and whether arthritis glucosamine discount 100mg celebrex otc, during the one or many episodes that have occurred rheumatoid arthritis pregnancy order celebrex 200mg otc, there has been change in the pattern arthritis in legs and feet symptoms 100 mg celebrex otc, as judged by the direction of separation of images and the directions of gaze in which double vision has been present, or severity, as judged by the distance separating the two images. It is also helpful to establish whether the double vision can be overcome with voluntary effort, because this implies a longstanding abnormality that has become more difficult to overcome (decompensated). Whenever an ocular motor cranial nerve palsy is diagnosed, it is essential to determine whether it is isolated or part of multiple cranial nerve dysfunction, including assessment of trigeminal nerve as well optic nerve function, not only to provide anatomical localization of the disease process but also as a guide to the likelihood of a serious underlying condition. In oculomotor nerve palsy, the presence of pupillary dysfunction, either 148 anisocoria or particularly an impaired response to light, provides an important clue to the possibility of a compressive lesion such as a posterior communicating artery aneurysm (see Chapter 14). Severe pain is another important clue to the presence of an aneurysm, but it also may occur in pituitary apoplexy (see earlier in the chapter). In all cases of double vision, careful attention needs to be paid to identification of any orbital signs, not least to avoid unnecessary investigation for a possible intracranial lesion. Internuclear ophthalmoplegia, in which there is impairment of adduction of one or both eyes, localizes to the medial longitudinal fasciculus within the brainstem (see Chapter 14). Horizontal gaze palsy, in which there is loss of conjugate horizontal gaze to one or both sides, localizes to the pons, whereas vertical gaze palsy localizes to the midbrain (see Chapter 14). Variability of double vision, during or between episodes, typically with increasing severity with fatigue that may also manifest as increasing ptosis, is suggestive of myasthenia gravis (see Chapter 14). Management Investigation of patients with binocular double vision depends on the clinical assessment. Many cases of isolated ocular motor cranial nerve palsy in patients over 50 are due to ischemic (microvascular) disease, which requires little investigation apart from exclusion of giant cell arteritis and review of vascular risk factors, and in which spontaneous recovery is the rule. In contrast, in isolated oculomotor nerve palsy, suspicion of posterior communicating artery aneurysm due to pupillary involvement, severity of pain, or age under 50 necessitates emergency imaging, with the outcome being much better if treatment can be undertaken prior to subarachnoid hemorrhage due to aneurysm rupture. Similarly, multiple cranial nerve dysfunction requires urgent investigation, usually guided primarily by a neurologist, who will also guide investigations when the disease process localizes to the brainstem. When clinical evaluation suggests decompensation of a longstanding abnormality, such as a congenital superior oblique (trochlear) palsy, further investigation may not be required, and initial treatment will be with prisms (see Chapter 14). In any patient with suspected myasthenia gravis, it is important to establish whether there is nonocular weakness suggesting generalized disease, especially 149 impairment of breathing or swallowing, for which emergency neurologic assessment is essential. Triage Acute isolated, dilated, unreactive pupil in an otherwise well individual is rarely due to a serious underlying condition, with the likely possibilities being the benign entity of tonic pupil (see Chapter 14) or pharmacologic mydriasis, such as from accidental ocular inoculation with an anticholinergic agent in travel sickness medication. In contrast, isolated, dilated, unreactive pupil in a patient with depressed conscious level due to head injury or other acute intracranial disease is an ominous sign, being suggestive of tentorial herniation. As discussed earlier, pupil involvement in oculomotor nerve palsy is an important clue to the possibility of a compressive lesion, including posterior communicating artery aneurysm. Pupillary light-near dissociation (impaired pupillary constriction to light with better constriction to near) is traditionally associated with central nervous system syphilis (Argyll Robertson pupils), but can be due to midbrain dysfunction, typically compression from a pineal tumor or dilated third ventricle in hydrocephalus, when usually there is also impairment of vertical eye movements. In all three instances, there will be no related ptosis or impairment of eye movements. Tonic pupil may be identified by the delayed dilation following a near response from which it derives its name; abnormal spiraling ("vermiform") movements of the iris when constricting to a light stimulus, best seen on slitlamp examination; or constriction to dilute (0. Pharmacologic mydriasis is characterized by lack of pupil constriction to bright light and standard-strength (2%) pilocarpine eye drops. Bilateral optic disk swelling is a characteristic feature of raised intracranial pressure and malignant (accelerated) systemic hypertension, both of which require emergency or urgent investigation and treatment (see Chapters 14 and 15). Triage Papilledema (optic disk swelling due to raised intracranial pressure) is usually identified as part of the examination of a patient with neurologic symptoms, particularly headache. It may be identified incidentally, such as during routine optometric examination, but even then, it still requires urgent head imaging to exclude an intracranial mass lesion. Blood pressure should be checked in every patient with bilateral optic disk swelling, even a child. Clinical Assessment When the abnormalities are florid, recognition of optic disk swelling is straightforward.
Polysomnography is very helpful in the evaluation of possible pediatric sleep-related respiratory disorders; a differentiation between obstructive versus central apnea can be obtained how to cure arthritis in feet naturally generic celebrex 200mg with mastercard. N Treatment Options Acute choking arthritis yoga classes order celebrex without prescription, with respiratory failure associated with airway foreign body obstruction psoriatic arthritis diet gluten generic 100mg celebrex free shipping, may be successfully treated at the scene using standard first aid techniques such as the Heimlich maneuver arthritis neck pain headaches cheap 100 mg celebrex, back blows, and abdominal thrusts. Even in less urgent settings, expeditious removal of airway foreign bodies is recommended and a workup may be performed. Medical Definitive management will, of course, depend upon the specific diagnosis. But in general terms, for the child with airway compromise continuous monitoring with pulse oximetry is necessary. Supplemental humidified oxygen, racemic epinephrine, or heliox may be implemented. Surgical Again, definitive management will, of course, depend upon the specific diagnosis. However, many cases of laryngomalacia may be managed with observation (see Chapter 6. Subglottic stenosis can be dilated, or a cricoid split or cartilage graft reconstruction performed (see Chapter 6. N Outcome and Follow-Up the child should be monitored closely overnight in case of bleeding or edema compromising airway. Child can be followed with the usual well-child checks, and immunizations should be kept up to date. Laryngomalacia is a temporary physiologic dysfunction due to abnormal flaccidity of laryngeal tissues or incoordination of supralaryngeal structures. Comorbidities, including prematurity, cardiovascular malformation, and neurologic and congenital or chromosomal abnormalities, are present in 41% of patients. N Clinical Signs and Symptoms Most commonly, patients present with intermittent inspiratory stridor that is relieved by neck extension and a prone position. In extreme cases, patients become cyanotic, have a poor oral intake, have chest retractions, and develop pectus excavatum. N Evaluation Physical Exam An examination of any child with a possible breathing problem should discern if there is an oxygenation problem, and if so, an oxygen requirement. In the physical examination, one should assess for the location of a possible obstruction and include auscultation, inspection for chest retraction, assessment for cyanosis and other anomalies such as micrognathia. To diagnose laryngomalacia and assess for other upper airway abnormalities, direct flexible endoscopic examination during respiration must be performed. Direct laryngoscopy and bronchoscopy in the operating room is the definitive evaluation. Pediatric Otolaryngology 513 Hollinger considered the occurrence of two or more synchronously as causal in airway obstruction. These factors include an inward collapse of aryepiglottic folds, an elongated epiglottis (flaccid) curled on itself, anterior and medial collapsing movements of the arytenoid cartilages, posterior and inferior displacement of the epiglottis, short aryepiglottic folds, and an overly acute angle of epiglottis. N Treatment Options Medical If an infant has good progress, which is indicated by adequate weight gain and normal development, then surgical therapy is not necessary. Surgical In one series of 985 patients with laryngomalacia, 12% required surgical intervention. Patients who should be considered for surgical management are those with severe stridor and failure to thrive, obstructive apnea, weight loss, severe chest deformity, cyanotic attacks, pulmonary hypertension, or cor pulmonale. Supraglottoplasty is performed using carbon dioxide laser or laryngeal microscissors, or other cold instruments such as pediatric ethmoid thru-cutting forceps. Most commonly, surgery involves removal of the prolapsing aryepiglottic fold with cuneiform cartilage or division of tight, short aryepiglottic fold. Unilateral supraglottoplasty has been advocated by some to reduce the risk of supraglottic stenosis. Potential complications include continued airway obstruction and posterior stenosis. In the event of continued airway obstruction, a tracheotomy may be necessary until the child "outgrows" laryngomalacia. The use of postoperative antibiotics has not been well evaluated in the literature and is controversial. N Outcome and Follow-Up Supraglottoplasty relieves symptoms of airway obstruction in 90% of patients. Congenital laryngeal stridor (laryngomalacia): etiologic factors and associated disorders.
Neurosonography Intracranial Doppler sonography identifies flow of blood in arteries arthritis rheumatoid feet buy cheap celebrex 100 mg online, particularly the middle cerebral artery arthritis relief home remedies cheap 100mg celebrex visa. The absence of flow in the brain has been used to confirm brain death arthritis knee guard cheap celebrex 200 mg on-line, particularly in patients who have received sedative drugs that may alter some of the clinical findings (see Chapter 8) arthritis treatment lotions cheap celebrex uk. If the coma is due to a reversible stenosis or occlusion of a single vessel, it almost always will be in the vertebrobasilar, not the carotid, circulation. Once an imaging study has been performed, it is necessary to proceed with lumbar puncture as soon as possible for patients with no clear diagnosis. Similarly, occasional patients with bacterial meningitis or viral encephalitis may present with a depressed level of consciousness (sometimes after a missed seizure), and may not yet have sufficient meningismus to make the diagnosis of meningitis clear from examination. This may be particularly difficult to determine in patients who have underlying rigidity of the cervical spine (evidenced by resistance to lateral as well as flexion movements Examination of the Comatose Patient 81 of the neck). Nevertheless, it is imperative to identify infection as early as possible to allow the administration of antibiotics or antiviral agents. By the afternoon she had difficulty swallowing, her voice was hoarse, and her left limbs were clumsy. She was brought to the hospital by ambulance, and examination in the emergency department disclosed a lethargic patient who could be easily wakened. Pupils were equal and constricted from 3 to 2 mm with light, but the left eye was lower than the right, she complained of skewed diplopia, and there was difficulty maintaining gaze to the left. The tongue deviated to the right and there was distal weakness in her arms, and the left limbs were clumsy on fine motor tasks and showed dysmetria. Lumbar puncture disclosed 47 white blood cells/mm3 and elevated protein, and she recovered after being treated for Listeria monocytogenes. This case demonstrates the importance of examining the spinal fluid, even when a presumptive diagnosis of vascular disease is entertained. This is particularly true in patients with fever, elevated white blood cell count, or stiff neck, where infectious disease is a consideration. However, every patient with an undetermined cause of coma requires lumbar puncture as part of the routine evaluation. In these cases it is common to give antibiotics immediately and then do imaging and lumbar puncture up to a few hours later. Hence, deferring lumbar puncture in such cases until after the scanning procedure may do the patient harm. For this reason, when the evidence for meningitis is compelling, it may be necessary to do the lumbar puncture without benefit of prior imaging. As discussed in Chapters 4 and 5, the danger of this procedure is greatly overestimated. If the examination is nonfocal, and there is no evidence of papilledema on funduscopy, it is extremely rare to precipitate brain herniation by lumbar puncture. The benefit of establishing the exact microbial diagnosis far outweighs the risk of herniation. A critical but often overlooked component of the lumbar puncture is to measure and record the opening pressure. Elevated pressure may be a key sign that leads to diagnosis of venous sinus thrombosis, cerebral edema, or other serious conditions that can cause coma. If the tap is bloody, many clinicians send fluid from both tubes 1 and 4 for cell count. Nor does lack of a falling cell count indicate that the blood was there before the tap (the tip of the needle may be partially within or adjacent to a bleeding vein). Examination of the red blood cells under the microscope immediately after the tap may be helpful. Fresh red cells have the typical doughnut-shaped morphology, whereas crenelated cells indicate that they have been in the extravascular space for some time. A positive test indicates breakdown of red blood cells, which typically takes at least 6 hours to occur after a subarachnoid hemorrhage, and demonstrates that the blood was there before the tap. As the patient becomes more drowsy, higher voltage theta rhythms (4 to 7 Hz) become dominant; delta activity (1 to 3 Hz) predominates in patients who are deeply asleep or comatose. The alpha activity in such patients is usually more regular and less variable than in an awake patient, and it is not inhibited by opening the eyes. For example, triphasic waves are often seen in patients with hepatic encephalopathy, but can be seen in other metabolic disorders that cause coma.
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