Cases reported "Acute Disease"

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1/57. Acute hyperkalemia associated with intravenous epsilon-aminocaproic acid therapy.

    Epsilon-aminocaproic acid (Amicar) is used to treat severe hemorrhage refractory to usual medical management. This antifibrinolytic drug has been associated with a number of renal complications. However, there are no descriptions of this medication causing hyperkalemia. This report describes the development of hyperkalemia in a patient with underlying chronic renal insufficiency treated with intravenous epsilon-aminocaproic acid. The patient, who underwent coronary artery bypass grafting, had no other obvious cause for the acute increase in serum potassium concentration. Based on data in animals and humans, the cationic amino acids lysine and arginine have been shown to enter muscle cells in exchange for potassium and lead to hyperkalemia through a shift of potassium from the intracellular to the extracellular space. Epsilon-aminocaproic acid, a synthetic amino acid structurally similar to lysine and arginine, also has been noted to cause an acute increase in serum potassium in anephric dogs infused with this medication. It is probable that the mechanism underlying the increase in serum potassium with epsilon-aminocaproic acid is also based on the shift of potassium from the intracellular to the extracellular space. Hence, it appears that intravenous epsilon-aminocaproic acid can also cause hyperkalemia in humans.
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2/57. Neurotrophic corneal endothelial failure complicating acute horner syndrome.

    PURPOSE: The authors report the clinical findings of a unique case of rapid corneal endothelial decompensation in association with acute horner syndrome. STUDY DESIGN: Case report and literature review. methods: The authors followed a 38-year-old woman who developed horner syndrome after right jugular vein catheterization during cardiac valvular surgery. Shortly after the operation, horner syndrome accompanied by conjunctival hyperemia and stromal corneal edema developed in the right eye. Over the course of 4 months, the eye became painful, the corneal endothelial cell count dropped precipitously, and the stromal edema worsened, causing a difference of 100 microm in central corneal thickness compared to the unaffected eye. Deep stromal vascularization started at the limbus, resembling interstitial keratitis. RESULTS: A 3-week course of topical steroid treatment resulted in a dramatic improvement in the stromal corneal edema and regression of the deep stromal vascularization. Ocular and right hemicranial pain subsided shortly thereafter. CONCLUSION: The authors hypothesize that corneal endothelial failure in this unique case may have resulted from traumatic sympathectomy. According to experimental evidence in the reviewed ophthalmologic literature, sympathetic innervation may have a neurotrophic role in the cornea. Corneal pathology similar to the authors' case has been described in hemifacial atrophy (Parry-Robson syndrome), a disorder that is assumed to result from sympathetic denervation and that can be produced in animals by cervical sympathectomy. The authors therefore hypothesize that sympathetic denervation of the cornea may rarely cause endothelial decompensation and corneal edema. To the authors' knowledge, this is the first reported case of corneal endothelial failure in horner syndrome.
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3/57. Hyperacute cerebral enhancement: the earliest predictor of hemorrhage by MR imaging?

    A test to detect very early hemorrhage in acute cerebral infarct could offer a substantial increase in the safety and success of advanced stroke therapies, particularly when the use of thrombolytic therapies is contemplated. Currently, computed tomography is the standard test for the detection of cerebral hemorrhage but is not a valid predictor of potential areas of hemorrhagic transformation. A technique to evaluate the risk of hemorrhagic transformation in infarcted cerebral tissue has been conducted with contrast-enhanced magnetic resonance imaging in various animal stroke models. Knight demonstrated gadolinium-DTPA enhancement in the territory of occluded vessels immediately in rats after reperfusion. gadolinium enhancement was thought to predict areas of hemorrhagic transformation. Yenari and associates demonstrated in rabbit models that contrast-enhanced T1-weighted scans can reveal regions of blood-brain barrier disruption, characterized as hemorrhagic transformation in ischemic tissue. The authors report a clinical example in which hyperacute contrast-enhanced magnetic resonance imaging was the first indication of hemorrhagic transformation within 24 hours of onset of an acute cerebral infarct.
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4/57. Acute fish liver intoxication: report of three cases.

    The livers of some larger fish such as shark, tuna and seabass have been reported to be responsible for a peculiar poisoning causing headaches and desquamation. This type of poisoning can also be induced by ingestion of the livers of the sea whale, the polar bear and the seal. Since these animals contain an extremely large quantity of vitamin a in their livers and the symptoms of poisoning in the patients resembled those of patients with acute hypervitaminosis a, the poisoning was believed to have been caused by excessive vitamin a intake. We observed an episode of acute fish liver intoxication in which 3 man experienced dizziness, headache, blurred vision, nausea, vomiting, fever, and desquamation after ingesting the liver of the grouper fish Cephalopholis boenak (C. boenak). One of the patients had full-blown symptoms and presented with a high fever, headache, dizziness, generalized aching pain, and superficial vesicles and bullae of the skin. The treatment was mainly supportive. In the follow-up period, he subsequently developed hair loss and diffuse peeling of the skin on his palms and soles. Acute fish liver intoxication is rare, especially in subtropical regions. Symptomatologically, the clinical pictures of these patients were comparable to acute hypervitaminosis a or retinoid intoxication. The average vitamin a content in the grouper (C. boenak) is high enough to cause acute vitamin a intoxication. Moreover, ethanol may play a potentiating role in this type of event.
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5/57. Cutaneous hypersensitivity reaction to injectable hyaluronic acid gel.

    BACKGROUND: Injectable hyaluronic acid gel is a non-animal biomaterial used for soft tissue augmentation. OBJECTIVE: The dermal implantation of this naturally occurring polysaccharide is reported to be well tolerated by patients, with a longer duration in tissue than bovine collagen without any major local or systemic side effects. We report a case of an acute hypersensitivity reaction in a woman after her third injection for improvement of melolabial fold wrinkles. methods: An adverse granulomatous-like response to the intradermal injection of a modified hyaluronic acid gel is described. RESULTS: The patient developed indurated and erythematous papulocystic nodules in the melolabial folds bilaterally at the sites of injection. CONCLUSION: Injectable hyaluronic acid gel can be associated with severe allergic reactions and patients should be warned of this possible treatment side effect.
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6/57. Neuronal representation of object orientation.

    The dissociation between object identity and object orientation observed in six patients with brain damage, has been taken as evidence for a view-invariant model of object recognition. However, there was also some indication that these patients were not generally agnosic for object orientation but were able to gain access to at least some information about objects' canonical upright. We studied a new case (KB) with spared knowledge of object identity and impaired perception of object orientation using a forced choice paradigm to contrast directly the patient's ability to perceive objects' canonical upright vs non-upright orientations. We presented 2D-pictures of objects with unambiguous canonical upright orientations in four different orientations (0 degrees, -90 degrees, 90 degrees, 180 degrees ). KB showed no impairment in identifying letters, objects, animals, or faces irrespective of their given orientation. Also, her knowledge of upright orientation of stimuli was perfectly preserved. In sharp contrast, KB was not able to judge the orientation when the stimuli were presented in a non-upright orientation. The findings give further support for a distributed view-based representation of objects in which neurons become tuned to the features present in certain views of an object. Since we see more upright than inverted animals and familiar objects, the statistics of these images leads to a larger number of neurons tuned for objects in an upright orientation. We suppose that probably for this reason KB's knowledge of upright orientation was found to be more robust against neuronal damage than knowledge of other orientations.
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7/57. Infiltrating T cells during liver graft-versus-host disease show a restricted T-cell repertoire.

    Data from animal models have shown that hepatic graft-versus-host disease (GVHD) may be mediated by donor T cells interacting with liver adhesion molecules, other minor histocompatibility antigens, or both. We hypothesized that T-cell infiltrates within a liver biopsy during clinical GVHD would show a restricted T-cell response because the T cells would be responding to a limited number of antigens. We studied the peripheral T-cell repertoire and the liver-infiltrating T-cell repertoire of a patient who developed skin GVHD and subsequent liver GVHD after a matched sibling bone marrow transplantation for acute myeloid leukemia. Spectratype analysis of peripheral blood at the time of liver GVHD revealed that the patient had reconstituted a complex peripheral T-cell repertoire as evidenced by the presence of complementarity-determining region 3 (CDR3) length heterogeneity in most of the T-cell families. The repertoire complexity was skewed in variable gene beta (VB) 5.3, VB4, VB7, VB8, and VB15. Spectratype analysis on the liver biopsy sample revealed a limited infiltrate with an oligoclonal expansion in VBs 4, 7, and 8. We evaluated the T-cell infiltrate in more detail by sequencing the relevant expansions noted by spectratype and developing probes for the predominant CDR3 sequences. These clonotype probes were hybridized to peripheral blood and liver samples from the patient, a T-cell line developed from the patient's peripheral blood at the time of the initial skin GVHD, the donor's blood and marrow, and control samples. The results showed that the T-cell infiltrate during liver GVHD is mediated by a limited number of T cells, and that those cells are mostly different from the ones expanded from the peripheral blood during an acute skin GVHD reaction. These data support the concept that liver GVHD is a response to tissue-specific minor histocompatibility antigens.
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8/57. New therapeutic perspectives for demyelinating retrobulbar optic neuritis.

    In patients with demyelinating retrobulbar optic neuritis (RON), a spontaneous or corticosteroid-induced improvement is generally observed within the first month, but this is clinically insignificant in 5%-7% of patients. We report the case histories of four patients who were considered to be "non-responders" to corticosteroids because their visus remained unchanged or had improved by only 1/10 after one month from intravenous corticoid therapy begun 2-7 days after disease onset, and who were therefore subsequently administered high intravenous doses of immunoglobulin. Three of these patients completely recovered in a period of 3-9 months; the fourth showed only a partial improvement, but this was consolidated after long-term continuation of the same therapy. These cases suggest the possible efficacy of early administration of intravenous immunoglobulin in RON patients who fail to respond to cortisone therapy. As recently demonstrated in animal models, it can be hypothesised that the result is due to immuno-mediated mechanisms of action that reduce autoimmune responses in the short- and medium-term, and in the long-term favour remyelination.
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9/57. leptospirosis mimicking acute cholecystitis among athletes participating in a triathlon.

    leptospirosis, a disease acquired by exposure to contaminated water, is characterized by fever accompanied by various symptoms, including abdominal pain. An acute febrile illness occurred in athletes who participated in an illinois triathlon in which the swimming event took place in a freshwater lake. Of 876 athletes, 120 sought medical care and 22 were hospitalized. Two of the athletes had their gallbladders removed because of abdominal pain and clinical suspicion of acute cholecystitis. We applied an immunohistochemical test for leptospirosis to these gallbladders and demonstrated bacterial antigens staining (granular and filamentous patterns) around blood vessels of the serosa and muscle layer. Rare intact bacteria were seen in 1 case. These results show that leptospirosis can mimic the clinical symptoms of acute cholecystitis. If a cholecystectomy is performed in febrile patients with suspicious environmental or animal exposure, pathologic studies for leptospirosis on formalin-fixed, paraffin-embedded tissues may be of great value.
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10/57. Fatal rhabdomyolysis after acute sodium monensin (Rumensin) toxicity: case report.

    myoglobinuria or rhabdomyolysis occurs when myoglobin escapes into the blood and then into the urine after acute muscle necrosis. It can be a serious medical condition leading to renal failure and death. There are many causes including exertion, crush syndromes, ischaemia, metabolic disorders, exogenous toxins and drugs, heat stroke and hereditary disorders such as malignant hyperthermia. We report the case of a 17 year-old boy who developed myoglobinuria, renal failure and death 11 days after ingesting sodium monensin, possibly with the intention of developing muscles. sodium monensin, the active principle of Rumensin(R), is a dietary additive used as a growth promoter for confined cattle. There are no previous reports of human intoxication. Accidental or experimental sodium monensin intoxication in animals produces similar findings to those seen in this case.
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