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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe conduction block as an unusual electrophysiologic manifestation in a patient with necrotizing angiopathy. The patient developed subacute symptoms over a 1-month period consisting of progressive pain, tingling, and weakness of the lower extremities. Physical examination revealed a pattern consistent with a polyneuropathy. Electrodiagnostic studies provided evidence of a conduction block in the left ulnar nerve. Pathologic studies confirmed the process to be a necrotizing angiopathy. This report establishes the role of conduction block in human nerve ischemia.
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PMID:Necrotizing angiopathy presenting with multifocal conduction blocks. 162 80

Two cases of subclavian steal syndrome are reported. Symptoms included light-headedness or syncope, reflecting vertebrobasilar insufficiency, and in one case, numbness and tingling in the left upper extremity, reflecting ischemia. Many persons with this syndrome are asymptomatic. Key findings include unilaterally decreased pulses and a significant difference in blood pressure between the upper extremities. Arch aortography, the "gold standard" of diagnosis, must be performed before surgical intervention.
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PMID:Subclavian steal syndrome. A report of two cases. 334 Jun 10

The elbow flexion test is a little known, inadequately standardized, and poorly understood clinical test for the cubital tunnel syndrome. To evaluate and define this test, 13 patients with clinical and electrophysiologic evidence of cubital tunnel syndrome were tested with elbow flexion in a standardized manner. This consisted of full elbow flexion with full extension of the wrists for three minutes. All patients noted the onset of or the increase in one or more of the symptoms of pain, numbness, or tingling with this test. Numbness and tingling followed the sensory distribution of the ulnar nerve, but pain was not limited to the ulnar nerve distribution. The symptom complex, rapid onset, and rapid resolution of symptoms support a locally induced segmental ulnar nerve ischemia as the cause of symptoms. This study demonstrates the elbow flexion test to be a useful, reliable, and provocative test for the cubital tunnel syndrome.
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PMID:The elbow flexion test. A clinical test for the cubital tunnel syndrome. 340 26

Compartment syndrome is a limb-threatening and occasionally life-threatening injury. It occurs whenever the tissue pressure (referred to as interstitial pressure) within a closed anatomic space is greater than the perfusion pressure. Untreated, compartment syndrome leads to tissue necrosis, permanent functional impairment and, if severe in large compartments, renal failure and death. Compartment syndrome can occur within any muscle group located in a compartment. It is most common following an event that severely damages a muscle, like a crushing or twisting injury. Mechanisms of injury that involve circumferential burns, ischemia and tourniquets can cause compartment syndrome. Motorcyclists who suffer lower-extermity injuries in accidents are a high-risk group. A tough membrane referred to as a fascia covers muscle groups, forming a compartment for the muscle. In normal circumstances, this arrangement allows the muscle to function more efficiently, but if the muscle is injured in any way, the fascia limits the amount of swelling that can occur. This in turn restricts the flow of blood through the affected region. The first compromised function within the compartment is the flow of lymph and venous blood. If there are sensory nerves running through the compartment, they will not function correctly, causing the numbness, tingling and, later, the pain associated with compartment syndrome. With more swelling, arterial flow is compromised, pain worsens and motor function is impaired. An artificial way of producing a compartment syndrome is to place a cast or splint around a damaged extermity, compressing it. This is a way emergency personnel can compromise an injury and cause long-term consequences for the patient. Recovery is achieved by surgically opening the compartment involved (a fasciotomy) and releasing the pressure. The muscle at first will swell outside the compartment, but then it recovers, swelling is reduced and normal function can be recovered. Prehospital treatment of extremity injuries that will prevent or limit compartment syndrome is immobilization, elevation and cooling. Recognition of the syndrome later in its course, as in this case, requires the EMT to remove the patient to an appropriate emergency department. Prehospital providers need to recognize that many mechanisms of injury can produce this syndrome, even those that seem relatively minor. All injured patients should be educated to seek care should the symptoms of numbness, deep pain and coolness to the distal extremity occur. This case involved a patient who, from a relatively minor mechanism of trauma, experienced an internal disruption of the muscle group controlling the thumb (thenar mass). The early swelling in the thenar compartment resulted in the patient experiencing a tingling sensation in his left thumb. In many cases, such an injury would be referred to as a "stinger" (a temporary neurological deficit due to a sudden and excessive stimulation of a neurologic plexus or junction). But this patient had more swelling in the compartment, resulting in a lack of circulation manifested by a cool extremity, poor capillary refill and decreased pulse oximetry. Luckily, this officer recognized the need for medical evaluation of what appeared to be a minor injury and was returned to duty with no permanent impairment.
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PMID:Compartment syndrome. 1450 55

The prevalence of diabetes and resultant complications continues to increase in many countries, including Brazil. A 1-day, multicenter descriptive study involving people with type 2 diabetes was conducted 1) to identify and describe indicators of foot neuropathy and ischemia and examine their relationship, and 2) to examine the relationship between existing risk factors and patient demographic and clinical variables. Seventy-nine (79) patients with an average age of 60.9 years (SD = 13.28) participated in the study. After obtaining a history, the feet of all participants were examined (assessment, palpation, and sensitivity tests using a 128-Hz tuning fork and a 10-g Semmes-Weinstein monofilament). The majority of study participants were women (57%) and the average length of time since diagnosis of diabetes for all participants was 7.76 years (SD = 6.69). The majority of participants were found to have neuropathic and ischemic changes, risk factors for the development of ulcers, or both. Thirty-one patients (42.47%) had cramps, 29 reported numbness (39.73%), 31 (39.24%) lacked sensory perception to the monofilament, 26 (35.62%) experienced tingling, 16 had paresthesia (22.86%), 15 (19.99%) lacked vibratory perception to the tuning fork, 14 felt burning (19.44%), and six had hyperesthesia (10.34%). Certain neuropathic and ischemic changes, as well as some risk factors, were observed more often in male and aged patients, respectively. Men were significantly more likely than women to lack vibratory perception or posterior tibial pulse and to have calluses and an ingrown toenail. Claw toe, lack of sensory perception to the monofilament, lack of posterior tibial pulse, lack of hair, reduced capillary filling, onychomycosis, ingrown toenail, and varices were significantly more common in older than in younger study participants. These results reinforce the importance of regular preventive foot examinations of patients with type 2 diabetes mellitus and confirm that nursing foot care can easily be expanded to include these much-needed assessments.
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PMID:Neuropathic and ischemic changes of the foot in Brazilian patients with diabetes. 1463 64

Acute compartment syndrome is a rare orthopedic emergency caused by orthopedic, vascular, iatrogenic, or soft tissue injury that elevates the pressure within a closed fascial space. Untreated acute compartment syndrome leads to ischemia of the muscles and nerves within the compartment with a resultant loss of motor and sensory function, death of skeletal muscle, and subsequent contracture and deformity. This article presents a case of compartment syndrome in a 33-year-old man following a peroneus longus muscle tear. The patient underwent emergent fasciotomy and decompression of the lateral compartment, and a hematoma located at the musculotendonous junction of the peroneus longus was evacuated. The patient was placed in a posterior splint with the ankle at 90 degrees and elevated. Postoperatively, the patient reported complete resolution of pain, numbness, and tingling. The patient underwent delayed skin closure on the second postoperative day and subsequently had an uneventful recovery. By 4 months postoperatively, he had resumed full activity. Knowledge of the signs and symptoms of compartment syndrome and a high index of suspicion is paramount as this injury can occur after a seemingly innocuous injury such as an ankle inversion injury.
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PMID:Acute isolated lateral leg compartment syndrome following a peroneus longus muscle tear. 1929 37

Persistent nerve injuries in context of peripheral nerve blocks are uncommon. Previous surveys and prospectively designed studies have specified neurological dysfunctions in different ways, which may cause the variability of data about incidence; so it has to be reckoned with about 5% after 1 week, 1% after 1 month and 0,01% after 6 months. Amongst the different locations interscalene blocks with their associated surgical procedures seem to have the highest incidence. Establishing the correlation between disabilities and the performed block technique often constitutes difficulties, especially when other reasons like patient positioning techniques, tractions, ischemia and surgery related nerve injuries have to be considered. Dysfunctions manifest as numbness, parasthesia, tingling sensation and/or amyasthenia. Fortunately long-term lesions, caused by nerve blocks are a rarity.
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PMID:[Nerve injuries associated with nerve blocks: clinic and incidence]. 2262 28

The incidence of fungal endocarditis is increasing. While the pathogenic mechanisms are not fully understood, infection is associated with underlying heart disease and is most often attributable to Candida species. Candidal endocarditis complications include heart damage, inflammation, and emboli with resulting ischemia and tissue death. Candidal endocarditis is difficult to diagnose as blood cultures are often negative. Treatment includes surgical intervention and antifungal therapy. This case study describes a 41-year-old female complaining of acute onset of pain with numbness and tingling in both lower extremities. Prior history was significant for mycotic valve aneurysm and replacement secondary to culture-negative endocarditis. Evidence of limb-threatening ischemia led to a bilateral thrombectomy. During the thrombectomy white debris, later identified as Candida albicans, was encountered. A transesophogeal echocardiogram revealed a pedunculated mass which was determined to be the source of infection. The patient was placed on micafungin and voriconazole and discharged with a diagnosis of C. albicans fungal infection with descending aorta fungal mass. This case study illustrates an unusual presentation of candidal endocarditis with discussion of disease epidemiology, pathogenesis, diagnosis, and treatment.
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PMID:Candidal endocarditis presenting with bilateral lower limb ischemia. 2295 12

Hypothenar hammer syndrome (HHS) is characterized by digital ischemia after repetitive traumatic injury to the ulnar artery. Some hypothesize that susceptible patients have an intrinsic vasculopathy such as fibromuscular dysplasia (FMD). To investigate this hypothesis, we reviewed our institutional experience with this syndrome over 25 years. Clinical records were reviewed from all patients who underwent surgical treatment for HHS (1987 to 2011), and histologic features of excised ulnar arteries were characterized. A total of 67 patients (mean age 45 y; range, 21 to 75 y; 65 men) were treated for unilateral or bilateral disease. Common symptoms included digital pain (96% of cases), cold intolerance (79%), cyanosis (70%), numbness (54%), tingling (51%), and ulceration (40%). Angiography showed ulnar artery occlusion (89%), irregularity (56%), tortuosity (46%), and digital emboli (89%). Common pathologic features (from 75 specimens) included: luminal thrombosis (87%); intimal thickening (60%) and fibrosis (57%); internal elastic membrane disruption (95%); medial fibrosis (96%), hypertrophy (43%), neovascularization (49%), dilatation (29%), and disruption (25%); and adventitial neovascularization (53%). Specific features of dysplasia were present in 10 cases (15%), including smooth muscle disorganization and additional smooth muscle bundles outside the external elastic membrane, but typical FMD was not identified. Histologic features in HHS most often represent secondary changes consistent with repetitive trauma. Dysplastic features can be found in occasional cases, but FMD does not appear to contribute to HHS in most patients. Angiography should be interpreted with caution in superficial locations, as a string-of-beads appearance may simply reflect a posttraumatic corkscrew deformity of the ulnar artery.
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PMID:Surgical pathology of hypothenar hammer syndrome with new pathogenetic insights: A 25-year institutional experience with clinical and pathologic review of 67 cases. 2388 65

Transient ischemia produces postischemic tingling sensation. Ischemia also produces nerve conduction block that may modulate spinal neural circuits. In the present study, reduced mechanical thresholds for hindpaw-withdrawal reflex were found in mice after transient hindpaw ischemia, which was produced by a high pressure applied around the hindpaw for 30 min. The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors. Neural activities in the spinal cord and the primary somatosensory cortex (S1) were investigated using activity-dependent changes in endogenous fluorescence derived from mitochondrial flavoproteins. Ischemic treatment induced potentiation of the ipsilateral spinal and contralateral S1 responses to hindpaw stimulation. Both types of potentiation were blocked by spinal application of LY354740. The contralateral S1 responses, abolished by lesioning the ipsilateral dorsal column, reappeared after ischemic treatment, indicating that postischemic tingling sensation reflects a sensory modality shift from tactile sensation to nociception in the spinal cord. Changes in neural responses were investigated during ischemic treatment in the contralateral spinal cord and the ipsilateral S1. Potentiation already appeared during ischemic treatment for 30 min. The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.
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PMID:Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice. 2616 60


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