Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Raynaud's phenomenon is a frequent reason for seeking of medical attention, since it affects 3-5% of the population. It is characterized by sudden, transient and recurrent episodes of pallor and/or digital cyanosis, after exposure to cold or stressful situations. No known underlying illness is identified in over 80% of cases and consequently these cases are classified as primary Raynaud's phenomenon. Connective tissue diseases, particularly systemic sclerosis, are the main causes of the phenomenon. Once a complete clinical and physical evaluation rule out other causes, a nailfold capillaroscopy and antinuclear antibodies determination are the most useful adjunctive tests. Mild Raynaud's phenomenon can be managed almost exclusively with conservative non-pharmacological lifestyle modifications. However, if a patient develops a severe vascular condition a suitable vasodilator treatment is needed. When critical digital ischemia develops, intravenous treatment with prostaglandin analogues and surgery may be useful.
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PMID:[Raynaud's phenomenon]. 2002 66

Coexistence of thrombotic microangiopathy and adult-onset Still's disease is extremely rare. There is increasing evidence that this association could be more than just coincidental. We report on the case of a 34-year-old male diagnosed with adult-onset Still's disease and successfully treated with intravenous glucocorticoids. Nine months after onset the patient exhibited the presence of asymptomatic thrombocytopenia during treatment with chloroquine. The physical status was unremarkable except for pallor of the skin and mucosa. Laboratory evaluation revealed profound thrombocytopenia and hemolytic anemia. Coombs' tests were negative; renal function tests were all normal. The peripheral blood smear showed frequent schistocytes. Based on the presence of thrombocytopenia and microangiopathic hemolytic anemia, and with the exclusion of other known causes, the patient was diagnosed with thrombotic microangiopathy and successfully treated with plasma exchange and intravenous glucocorticoids. We also review the literature on the association between adult-onset Still's disease and thrombotic microangiopathy; our case is the 15(th) report on such an association. The mean age at onset of adult Still's disease in these cases was 31.60 years and the interval between the diagnosis of Still's disease and the onset of thrombotic microangiopathy ranged from 3 days to 17 years, with a female/male ratio of 2 : 1. In more than half the patients thrombotic microangiopathy occurred within the first 6 months after the diagnosis of the Still's disease. Eleven of the 15 (73%) patients were treated with plasmapheresis in addition to glucocorticoid therapy: eight of 11 (73%) had complete remission, the other three had permanent visual impairment and/or digital ischemia. Of the four patients who were not treated with plasmapheresis, two died, one developed end-stage renal disease and one had complete remission. Awareness of the possible development of thrombotic microangiopathy in patients with adult-onset Still's disease is critical, so that treatment can be initiated early and the complications and recurrence of thrombotic microangiopathy prevented. Patients with adult-onset Still's disease should be closely monitored for signs and symptoms of thrombotic microangiopathy during the first six months after diagnosis of the Still's disease.
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PMID:Thrombotic microangiopathy in adult-onset Still's disease: case report and review of the literature. 1989 Jul 48

Thrombosis of an abdominal aortic aneurysm is a rare devastating complication with an estimated mortality rate of 50%. Simultaneous acute pain, pallor and coldness of the lower limbs, mottling from the level of iliac crests or umbilicus, paraplegia and absence of femoral pulses are all manifestations of a sudden and acute interruption of blood flow through the aneurysmatic aorta. We report a case of an occlusion of an abdominal aortic aneurysm during hospitalization which was not manifested with symptoms of limb ischemia. In this case we feature the rare and unusually "silent" presentation of the event.
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PMID:"Silent" thrombosis of an abdominal aortic aneurysm not producing acute limb ischemia. 2073 87

Posterior elbow dislocations are the most common type of elbow dislocation and are usually caused by a fall on an outstretched hand. Although the incidence of elbow dislocation complications is rare, the emergency physician is responsible for evaluation and identification of concomitant neurovascular injuries. Failure to identify neurovascular compromise after elbow dislocation or reduction can potentially lead to severe morbidity with limb ischemia, neurologic changes, compartment syndrome, and potential loss of limb. Cyanosis, pallor, pulselessness, and marked pain should suggest vascular injury or compartment syndrome, both requiring immediate intervention. Patients in whom it is not clear if there is vascular injury should undergo further imaging with angiography, considered the gold standard for evaluation of arterial damage. It is important for the emergency physician to maintain a high level of suspicion and evaluate for neurovascular compromise on every patient with elbow dislocation despite the low overall incidence of severe injury.
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PMID:Orthopedic pitfalls in the ED: neurovascular injury associated with posterior elbow dislocations. 2088 16

Accidental intra-arterial injection of drugs is rare in pediatric patients. It is a source of considerable morbidity. Vessel proximity, aberrant vasculature, difficult procedures, and clerical errors can contribute to accidental intra-arterial injection. We report a case of a 7-year-old girl who had an accidental intra-arterial injection of 500 mg of floxacillin in her right elbow for open wound of the index. Initial signs and symptoms consisted of intense forearm pain and cyanosis. Two to 3 hours later, discoloration and nail bed pallor became evident, with no radial pulse. Rapid development of signs of acute ischemia prompted urgent brachial artery embolectomy and exploration and forearm fasciotomy. Postoperative heparin was administered. Postoperatively gangrene of the five fingers of the right hand developed. We present a comprehensive review of literature, highlighting available information on symptoms, pathogenesis, sequelae and management strategies for accidental intra-arterial injection. We believe that all physicians and ancillary personnel who administer intravenous therapy should be aware of this serious risk.
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PMID:[Fingers necrosis after an accidental intra-arterial injection of flucloxacilline: case report]. 2106 56

Severe pallid breath-holding spells (BHSs) are based on parasympathetic hyperactivity, leading to cardiac asystole, pallor, brain ischemia, loss of consciousness, and reflex anoxic seizures. In recent years, an increasing number of patients with severe pallid BHSs have been successfully treated with pacemaker implantation. We present the case of a 13-month-old girl suffering from repeated severe pallid BHSs, causing asystole, loss of consciousness, and generalized anoxic seizures. She underwent treatment with oral glycopyrrolate, an anticholinergic drug, and an oral retard preparation of theophylline. The aim of the treatment was to decrease cardiac inhibition with glycopyrrolate and to bring about a positive chronotropic effect with theophylline. In our case, the combined therapy was effective in suppressing syncope and reflex anoxic seizures associated with BHSs This avoided the need for ventricular pacemaker implantation.
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PMID:Glycopyrrolate and theophylline for the treatment of severe pallid breath-holding spells. 2350 62

A 51-year-old man with several months of headache and progressive visual decline was found to have bilateral optic disc pallor with significant impairment of visual acuity. Despite a thorough ophthalmologic evaluation, the cause of visual loss could not be elucidated. MRI of the brain revealed a lesion in the left anterior Sylvian fissure as well as disseminated foci of subarachnoid fat consistent with a diagnosis of a ruptured dermoid cyst. The decision for open surgical resection was chosen to minimize the risk of cyst re-rupture and further visual or neurologic decline. The diagnosis of dermoid cyst was confirmed at the time of surgery. Vasospasm-induced ischemia of the optic nerves, optic chiasm or bilateral optic tracts secondary to the inflammatory reaction following cyst rupture is the most likely mechanism of visual loss in this patient. To the authors' knowledge, this report represents the first reported case of visual loss secondary to rupture of an intracranial dermoid cyst not related to mass effect of the tumor on the optic apparatus, visual pathways or visual cortex.
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PMID:Progressive visual loss following rupture of an intracranial dermoid cyst. 2389 50

Limb ischemia rarely occurs in utero. The diagnosis can be made by clinical observation at birth or a few hours later. Color duplex ultrasound is the first imaging test used to confirm the diagnosis. The etiology appears to be complex and multifactorial. We report 2 cases of intrauterine limb ischemia involving the upper limb in 2 newborns. Both children were heterozygous for the 5,10-methylenetetrahydrofolate reductase 677C>T gene variant. The first patient was born by caesarean section at 34 weeks of gestation. At delivery, the infant presented with pallor in his right upper limb and weak radial arterial pulsation. Doppler ultrasound and computed tomography angiography demonstrated a totally occlusive thrombus within the right brachial artery. The newborn underwent systemic thrombolysis with good recovery. The second patient was born via cesarean section at 37 weeks of gestation. At delivery, the infant presented with a motionless, cold, and gangrenous right upper limb. The demarcation line was just below the right elbow. Doppler ultrasound revealed a complete occlusion of the right subclavian artery. After failure of antithrombotic therapy, the limb was amputated with no further complication. We discuss the epidemiology, etiology, and clinical features of this rare pathology.
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PMID:[Intrauterine upper limb ischemia due to a heterozygous mutation (677C>T) of the methylene-tetrahydrofolatereductase gene]. 2433 83

Although the rapid and accurate diagnosis of both acute ischemic stroke and extremity ischemia is essential to the timely and appropriate treatment, it is not always easy to differentiate between true stroke and stroke mimics. Although in general, limb ischemia due to extremity embolism is not included in stroke mimics or misdiagnosis, limb arterial embolism should be considered in thedifferential diagnosis of acute monoparesis because the diagnosis maybe missed if the other typical manifestations of this presentation(pain, pallor, pulselessness, sensory loss, and coolness of the arm) are overlooked. Therefore, it is important to ensure that important signsare not missed whether the evaluation of the patient is done at thebedside. We report a case of a male patient presented to an emergency department with acute right upper extremity pain with headache, gait disturbance, and confused mentality. He was diagnosed by simultaneou sbrachial artery occlusion and acute stroke, which resulted in emergency surgical embolectomy and anticoagulation therapy.
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PMID:Simultaneous event of brachial artery occlusion and acute embolic stroke. 2522 78

CSF normally flows back and forth through the aqueduct during the cardiac cycle. During systole, the brain and intracranial vasculature expand and compress the lateral and third ventricles, forcing CSF craniocaudad. During diastole, they contract and flow through the aqueduct reverses. Hyperdynamic CSF flow through the aqueduct is seen when there is ventricular enlargement without cerebral atrophy. Therefore, patients presenting with clinical normal pressure hydrocephalus who have hyperdynamic CSF flow have been found to respond better to ventriculoperitoneal shunting than those with normal or decreased CSF flow. Patients with normal pressure hydrocephalus have also been found to have larger intracranial volumes than sex-matched controls, suggesting that they may have had benign external hydrocephalus as infants. While their arachnoidal granulations clearly have decreased CSF resorptive capacity, it now appears that this is fixed and that the arachnoidal granulations are not merely immature. Such patients appear to develop a parallel pathway for CSF to exit the ventricles through the extracellular space of the brain and the venous side of the glymphatic system. This pathway remains functional until late adulthood when the patient develops deep white matter ischemia, which is characterized histologically by myelin pallor (ie, loss of lipid). The attraction between the bare myelin protein and the CSF increases resistance to the extracellular outflow of CSF, causing it to back up, resulting in hydrocephalus. Thus idiopathic normal pressure hydrocephalus appears to be a "2 hit" disease: benign external hydrocephalus in infancy followed by deep white matter ischemia in late adulthood.
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PMID:CSF Flow in the Brain in the Context of Normal Pressure Hydrocephalus. 2535 13


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