Cases reported "Diabetic Retinopathy"

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1/30. Acute gastric dilatation accompanied by diabetes mellitus.

    A 72-year-old man with diabetic triopathy was hospitalized with methicillin resistant staphylococcus aureus pneumonia. Six hours after the admission, his abdomen was fully expanded. An abdominal X-ray showed gastric dilatation. After insertion of a gastric tube to extract gastric air, his abdomen was flat and gastric dilatation improved. A positive Schellong test and decreased coefficient of RR interval in electrocardiogram variation indicated autonomic neuropathy, which may explain the reason for gastric hypomotility. Acute gastric dilatation in this patient may have occurred due to gastric hypomotility as a result of diabetic autonomic neuropathy in addition to gastric motility inhibition resulting from gastric autonomic nerve stimulation by bacterial toxin.
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2/30. Anatomic and histopathologic findings following a failed ahmed glaucoma valve device.

    Ahmed glaucoma valve implant (AGV) is one of the more commonly used implants in difficult glaucomas. The histology of a functioning bleb following AGV implantation and its anatomic relationship to the optic nerve when placed in the superionasal quadrant has been described. We report the histology of a failed bleb and the anatomic relationship between the optic nerve and the AGV end-plate when placed 9 mm from the limbus in a patient with neovascular glaucoma.
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3/30. Angiocentric T-cell lymphoma of the pancreas presenting as late-onset diabetes mellitus with diabetic retinopathy.

    Pancreatic lymphoma presenting with clinical diabetes mellitus (DM) is rare. We report angiocentric T-cell lymphoma of the pancreas in a 65-year-old Thai woman who presented with progressive deterioration of visual acuity of both eyes. She had diabetic retinopathy (DR) diagnosed only 20 months after the diagnosis of DM at the age of 63. She later developed erythematous rashes, fever, and deterioration of consciousness; she eventually died of shock. A skin biopsy and bone marrow examination revealed angiocentric T-cell lymphoma. At autopsy, the pancreas and both eyes were extensively infiltrated by lymphoma. Widespread involvement of nearly all organs but superficial lymphadenopathy was detected. In contrast to other typical cases of long-standing DM, only mild atherosclerosis was noted, and no DR was found. To the best of our knowledge, this is the first case of lymphoma involving the pancreas and both eyes producing clinical DM and DR.
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4/30. A suspected case of proximal diabetic neuropathy predominantly presenting with scapulohumeral muscle weakness and deep aching pain.

    A 48-year-old man with a 14-year history of type 2 diabetes with proliferative diabetic retinopathy and distal symmetrical diabetic polyneuropathy visited our hospital. Eight months later, he subacutely developed difficulty in both shoulder movement and trouble standing up from a squatting position. This was accompanied by severe bilateral shoulder and thigh pain. magnetic resonance imaging of the brain, cervical and lumbar spine, computed tomography of the shoulder and X-ray films of the cervical spine and shoulder revealed no abnormality. cerebrospinal fluid showed a mild elevation of protein (0.93 g/l) without cell infiltration. Antiganglioside antibodies and point mutation of mitochondrial dna at position 3243 were not found. Neuropathology of the sural nerve showed a moderate myelinated fiber loss, active axonal degeneration, but onion-bulb formation, endoneurial or epineurial vasculitis were not observed. electromyography revealed neurogenic changes in the proximal upper limb muscles. Nerve conduction studies revealed mild bilateral slowing in nerve conduction velocity in both of the upper and lower limbs. The diagnosis of this patients was suspected to be a proximal diabetic neuropathy (diabetic amyotrophy). The pain and muscle weakness had persisted more severely in the shoulder than in the thigh throughout the clinical course. His unbearable symptoms could be partially alleviated by an administration of a selective serotonin reuptake inhibitor, fluvoxamine maleate. Proximal diabetic neuropathy is a rare disabling type of neuropathy, which is characterized with subacute bilateral muscle weakness and wasting in the proximal part of the lower limbs. The involvement of the scapulohumeral region observed in this case is very unusual in proximal diabetic neuropathy.
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5/30. Dilated pupils and loss of accommodation following diode panretinal photocoagulation with sub-tenon local anaesthetic in four cases.

    AIM: To describe pupillary abnormalities associated with diode laser photocoagulation with subTenon's local anaesthetic. methods: We describe four cases of tonic pupils following diabetic panretinal photocoagulation with subTenon's local anaesthetic. RESULTS: Six pupils of four patients became dilated and sustained loss of accommodation with denervation hypersensitivity with 0.1% pilocarpine after undergoing panretinal photocoagulation with a subTenon's local anaesthetic. The numbers of burns were not excessive and in one patient it even occurred after only 1200 laser burns. CONCLUSION: Diode laser causes histological changes deeper in the retina and the choroid than in argon laser. Intense diode laser burns may cause damage to the short ciliary nerves traversing the choroid. In the unanaesthetised patient, pain arises when the laser burn hits these nerves and so may protect the eye from excess damage to the nerves. When the eye is anaesthetised with a subTenon's, local anaesthetic damage to the choroidal nerves may occur without the laser operator being aware that the burns are too intense.
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6/30. Combined pancreas and kidney transplantation in a lean type 2 diabetic patient. Effects on insulin secretion and sensitivity.

    BACKGROUND/AIMS: pancreas transplantation is an established method of treating Type 1 diabetes. It was our aim to test the consequences of pancreas transplantation in a Type 2 diabetic patient by determining insulin secretion and sensitivity before and after surgery. patients AND methods: A female patient with Type 2 diabetes and end-stage nephropathy was treated with combined pancreas and kidney transplantation. Before surgery and at 4 weeks, 6 months and 2 years afterwards, insulin sensitivity was measured using hyperinsulinemic euglycemic clamps and insulin secretion was quantified after oral glucose or intravenous glucagon challenges. RESULTS: The patient was insulin resistant before surgery (glucose infusion 4.6 mg. kg (-1). min (-1), normal range 6.4 /- 0.5 mg.kg( -1). min (-1). Insulin sensitivity declined further after transplantation (1.4 and 3.0 mg. kg -1. min -1 after 4 weeks and 6 months, respectively), but improved to 5.4 mg. kg (-1). min (-1) after 2 years. Insulin secretion was greatly impaired before surgery. Insulin and c-peptide responses after oral glucose and intravenous glucagon increased into the normal range from 6 months after surgery onwards and oral glucose tolerance remained non-diabetic (IGT). CONCLUSIONS: insulin resistance is first aggravated after pancreas transplantation, probably due to immunosuppressive treatment including glucocorticoids, but improves on the long term. The initially impaired insulin secretion from the transplant may also be explained by the action of glucocorticoids or by transient and reversible organ damage.
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7/30. Refractory ocular hypertension secondary to intravitreal injection of triamcinolone acetonide.

    PURPOSE: to report a case of severe ocular hypertension occurring as a complication after a single intravitreal injection of triamcinolone acetonide for the treatment of a diabetic cystoid macular edema. methods: interventional case report. RESULTS: a 63-year-old pseudophakic diabetic woman developed a severe and relatively sudden IOP increase to 50 mm Hg one month after receiving a single 4-mg intravitreal injection of triamcinolone acetonide for a chronic progressive macular cystoid edema. Previously the patient who did not develop corticosteroid-induced glaucoma secondary to her cataract surgery was treated with topical beta-blockers for a mild chronic bilateral ocular hypertension. A deep sclerectomy had to be performed in emergency to avoid optic nerve damage and allowed to successfully control the IOP with a 5 month follow-up. Concomitantly visual acuity could be increased from 0.05 before the intravitreal injection to 0.4. CONCLUSIONS: Although unfrequent in the literature, this observation confirms the risk of occurrence of a severe ocular hypertension after intravitreal injection of triamcinolone. A close monitoring of IOP is mandatory after intravitreal injection, especially in patients with altered trabecular function. This potentially devastating complication has to be weighed up with the benefices of intravitreal injection of triamcinolone for improving visual acuity in patients with clinically significant diabetic macular edema.
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8/30. Regression of optic nerve head neovascularization in proliferative diabetic retinopathy after intravitreal triamcinolone. Regression of diabetic optic disc neovascularization after intravitreal triamcinolone.

    The aim of this study is to report the clinical outcome of a diabetic patient with optic nerve head neovascularization treated with an intravitreal injection of triamcinolone acetonide. A 52-year-old patient presented with clinically significant diffuse macular edema and optic nerve head neovascularization due to proliferative diabetic retinopathy in her right eye. Despite grid laser photocoagulation in the macular region macular edema progressed and visual acuity declined. The patient received a single intravitreal injection of 4 mg triamcinolone acetonide with topical anesthesia. After injection of triamcinolone acetonide visual acuity increased and macular edema decreased. Furthermore optic nerve head neovascularization had markedly regressed. No complication was observed during follow-up period. Intravitreal injection of triamcinolone acetonide may be useful for treatment of optic nerve head neovascularization in patients with proliferative diabetic retinopathy.
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9/30. Bilateral hearing loss following a retrobulbar block.

    PURPOSE: Regional anesthesia is the most commonly used ophthalmological anesthetic technique in canada and the united states. Brainstem anesthesia is not an uncommon complication of retrobulbar blocks. Anesthesiologists are a prominent element in the ophthalmology suite, in part due to the complications possible with regional anesthesia. This is the first reported case of complete bilateral hearing loss following a retrobulbar block. CLINICAL FEATURES: A 46-yr-old male with type 1 diabetes mellitus presenting for ophthalmological surgery had a retrobulbar block performed by the ophthalmologist. Local anesthetic was injected through a 25 G, 1.5 inch needle, entering the orbit inferiorly on the temporal third of the lower lid. Shortly after the block was completed the patient experienced sudden hearing loss. On examination the hearing loss appeared to be complete and bilateral. The patient was alert and oriented; the remainder of the cranial nerve exam was normal. The patient's hearing loss gradually improved and three hours after the block his hearing had subjectively returned to normal. CONCLUSION: Brainstem anesthesia is not a rare complication of regional anesthesia for ophthalmological surgery. Symptoms include confusion, mental agitation, dizziness, blurred vision or blindness, ophthalmoplegia, deafness, tinnitus, dysphagia, dysarthria, respiratory depression to apnea, and/or limb paralysis. A connection between the subdural and subarachnoid spaces and the optic sheath exists. The effect on the central nervous system depends upon the amount of local anesthetic injected and the area to which it spreads.
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10/30. Hypertension, the endothelial cell, and the vascular complications of diabetes mellitus.

    Hypertension is a major factor that contributes to the development of the vascular complications of diabetes mellitus, which primarily include atherosclerosis, nephropathy, and retinopathy. The mechanism of the pathophysiological effects of hypertension lies at the cellular level in the blood vessel wall, which intimately involves the function and interaction of the endothelial and vascular smooth muscle cells. Both hypertension and diabetes mellitus alter endothelial cell structure and function. In large and medium size vessels and in the kidney, endothelial dysfunction leads to enhanced growth and vasoconstriction of vascular smooth muscle cells and mesangial cells, respectively. These changes in the cells of smooth muscle lineage play a key role in the development of both atherosclerosis and glomerulosclerosis. In diabetic retinopathy, damage and altered growth of retinal capillary endothelial cells is the major pathophysiological insult leading to proliferative lesions of the retina. Thus, the endothelium emerges as a key target organ of damage in diabetes mellitus; this damage is enhanced in the presence of hypertension. An overall approach to the understanding and treatment of diabetes mellitus and its complications will be to elucidate the mechanisms of vascular disease and endothelial cell dysfunction that occur in the setting of hypertension and diabetes.
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