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

Patients suffering from vascular disease are often a challenge for the acute pain service. Ischaemia, impaired wound healing, stump and phantom limb pain often require a complex analgesic regimen. Invasive measures such as spinal or epidural catheters can be very helpful but carry the risk of infection, as shown by this case report. A 53-year-old woman with a ten-year history of diabetes developed arterial vascular disease. Her right lower leg had been amputated two years previously. She was now admitted with necroses of the left forefoot. A bypass operation was performed under general anaesthesia. Because of intractable ischaemic pain, she was provided with an epidural catheter by the acute pain service. The bypass occluded, however, and a few days later her left lower leg also had to be amputated, this operation being performed under epidural anaesthesia with bupivacaine. The catheter was subsequently used for postoperative pain control and as a means to prevent phantom limb pain. When signs of superficial catheter infection were noticed days later, the catheter was immediately removed. Intractable pain then developed in the left leg which could not be sufficiently controlled with opioids and NSAIDs, and so a second epidural catheter was inserted one segment rostrally. Several days later the infected vascular prosthesis had to be removed followed by amputation of the thigh, this operation also being performed in epidural anaesthesia. Eleven days after insertion of the first epidural catheter, the patient complained of low back pain and headache. Examination by a neurologist revealed no signs of intraspinal infection. The second epidural catheter dislocated at this point in time and it was decided to introduce a third one, this being the only means to treat the otherwise intractable stump pain. Ten days later meningism, Kernig's sign and leucocytosis developed. NMR tomography detected intraspinal fluid in the epidural space at the dorsal border of the spinal canal. A hemilaminectomy was performed. The spinal epidural space showed signs of inflammation of the adipose tissue, but no pus. A little necrotic material and residues of an old haematoma were removed and the epidural space was lavaged. Specimens taken from the epidural material revealed colonisation with staphylococcus epidermidis, which was sensitive to the broad spectrum antibiotics formerly given to the patient to treat the infection in the left stump. By the next day, all signs of epiduritis had disappeared and the patient recovered completely.
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PMID:[Epiduritis after long-term pain therapy with an epidural catheter--review of the literature with a current case report]. 932 67

The effect of failed vascular bypass surgery on final amputation level and stump complications is the subject of debate. The aim of this prospective cohort study was to assess the influence of previous infrainguinal bypass surgery on amputees in the authors' centre. Over a three-year period, 234 amputations (219 patients) were performed for critical ischemia. The cause of ischemia was either peripheral obstructive arterial disease (POAD) or diabetes mellitus (DM). Forty-eight percent (48%) (113 amputations) had ipsilateral vascular bypass surgery prior to amputation and 52% (121 amputations) had not. Final amputation level and the post-operative complications of infection, significant stump pain and delayed wound healing were used as the outcome measures for this study. At the end of the study period these outcome measures were used to compare the influence of previous bypass surgery on the two groups of amputees. There was a significantly higher rate of transfemoral amputations (TFA) (32.7%) vs. 16.5%; p < 0.05) and stump infection rate (42% vs. 23%; p < 0.05) in the bypass group. Significant stump pain (p = 0.23) and delayed wound healing (p = 0.24) was more prevalent in the bypass group although statistical significance could not be demonstrated.
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PMID:Major lower limb amputation following failed infrainguinal vascular bypass surgery: a prospective study on amputation levels and stump complications. 1141 Oct 2

This review deals with physiological and biological mechanisms of neuropathic pain, that is, pain induced by injury or disease of the nervous system. Animal models of neuropathic pain mostly use injury to a peripheral nerve, therefore, our focus is on results from nerve injury models. To make sure that the nerve injury models are related to pain, the behavior was assessed of animals following nerve injury, i.e. partial/total nerve transection/ligation or chronic nerve constriction. The following behaviors observed in such animals are considered to indicate pain: (a) autotomy, i.e. self-attack, assessed by counting the number of wounds implied, (b) hyperalgesia, i.e. strong withdrawal responses to a moderate heat stimulus, (c) allodynia, i.e. withdrawal in response to non-noxious tactile or cold stimuli. These behavioral parameters have been exploited to study the pharmacology and modulation of neuropathic pain. Nerve fibers develop abnormal ectopic excitability at or near the site of nerve injury. The mechanisms include unusual distributions of Na(+) channels, as well as abnormal responses to endogenous pain producing substances and cytokines such as tumor necrosis factor alpha (TNF-alpha). Persistent abnormal excitability of sensory nerve endings in a neuroma is considered a mechanism of stump pain after amputation. Any local nerve injury tends to spread to distant parts of the peripheral and central nervous system. This includes erratic mechano-sensitivity along the injured nerve including the cell bodies in the dorsal root ganglion (DRG) as well as ongoing activity in the dorsal horn. The spread of pathophysiology includes upregulation of nitric oxide synthase (NOS) in axotomized neurons, deafferentation hypersensitivity of spinal neurons following afferent cell death, long-term potentiation (LTP) of spinal synaptic transmission and attenuation of central pain inhibitory mechanisms. In particular, the efficacy of opioids at the spinal level is much decreased following nerve injury. Repeated or prolonged noxious stimulation and the persistent abnormal input following nerve injury activate a number of intracellular second messenger systems, implying phosphorylation by protein kinases, particularly protein kinase C (PKC). Intracellular signal cascades result in immediate early gene (IEG) induction which is considered as the overture of a widespread change in protein synthesis, a general basis for nervous system plasticity. Although these processes of increasing nervous system excitability may be considered as a strategy to compensate functional deficits following nerve injury, its by-product is widespread nervous system sensitization resulting in pain and hyperalgesia. An important sequela of nerve injury and other nervous system diseases such as virus attack is apoptosis of neurons in the peripheral and central nervous system. Apoptosis seems to induce neuronal sensitization and loss of inhibitory systems, and these irreversible processes might be in common to nervous system damage by brain trauma or ischemia as well as neuropathic pain. The cellular pathobiology including apoptosis suggests future strategies against neuropathic pain that emphasize preventive aspects.
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PMID:Pathobiology of neuropathic pain. 1169 24

May-Thurner syndrome (MTS) is a rarely diagnosed vascular abnormality that typically presents in young adults. The anomaly arises from compression of the left common iliac vein between the right iliac artery anteriorly and the lumbar vertebral body posteriorly, resulting in lower extremity venous outflow obstruction and recurrent deep vein thromboses (DVTs). We report the case of a 24-year-old female with a long history of recurrent DVTs and pulmonary emboli (PE) despite full anticoagulation. A computed tomography (CT) scan revealed findings consistent with MTS, and a left common iliac vein stent was placed. However, the patient continued to have DVTs while trialing several anticoagulation therapies, including rivaroxaban, enoxaparin, and warfarin. Eventually, the patient developed arterial thrombi resulting in critical limb ischemia, necessitating a right below knee amputation (BKA). One month status-post BKA, the patient was admitted for severe BKA stump pain secondary to infection and necrosis. She underwent BKA revision, but continued to experience pain post-operatively and was found to have new right common iliac artery, external iliac artery, and common femoral artery thrombosis in the setting of continued inpatient anticoagulation therapy with enoxaparin and aspirin. The patient returned to the operating room for emergent Fogarty thrombectomy, however, this was complicated by rupture of the balloon catheter secondary to migration of the left common iliac vein stent into the right common iliac artery lumen. A stent was placed in the right common iliac artery to shift the rogue vein stent, but the patient continued to have poor distal circulation of the BKA stump and eventually underwent an above knee amputation. Dual anti-platelet therapy (DAPT) with aspirin and clopidogrel in combination with enoxaparin were used to prevent in-stent thrombosis and future formation of arterial and venous thrombi. After the initiation of DAPT and enoxaparin, her clinical course was free of any further thromboembolic events. Clinicians should consider MTS in the differential diagnosis of younger adults presenting with recurrent DVTs or other unprovoked thromboembolic events. A two-pronged strategy of DAPT and anticoagulation was employed for successful prevention of thrombotic events.
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PMID:May-Thurner Syndrome: A Rare and Under-Appreciated Cause of Venous Thrombosis in a 18-Year-Old Healthy Female. 3230 Apr 23