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We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

The purpose of this report is to examine health-related quality of life (HRQoL) as measured by the Medical Outcomes Study Short Form-36, across patient populations with chronic disorders and to compare quality of life (QoL) in these subjects with normative data on healthy persons. Six studies, within the Center for Research in Chronic Disorders at the University of Pittsburgh School of Nursing, in patients with urinary incontinence, prostate cancer, chronic obstructive pulmonary disease (COPD), acquired immune deficiency syndrome (AIDS), fibromyalgia and hyperlipidaemia provided the data for analysis. The results demonstrated that not only did the prostate cancer and hyperlipidaemia patients have the highest QoL across the chronic disorders, but their QoL was comparable to normative data on healthy persons. Homebound, elderly, incontinent patients had the lowest QoL for physical functioning, whereas patients hospitalized with AIDS had the lowest QoL in general health and social functioning. Patients with COPD had the lowest QoL in role-physical, role-emotional and mental health. Patients with fibromyalgia had the lowest QoL in bodily pain and vitality. Compared to normative data, patients with urinary incontinence, COPD, AIDS and fibromyalgia generally had lower QoL. Prostate cancer and hyperlipidaemia patients had QoL comparable to normative data. Compared to normative data, patients with urinary incontinence, COPD, AIDS and fibromyalgia had more variability for role-emotional. AIDS patients had more variability on physical functioning, bodily pain and social functioning compared to the normative data. These data suggest that patients with various chronic disorders may have QoL that is lower in most domains compared to a healthy population. However, there may be differences in the domains affected as well as the extent of variation across specific chronic disorders.
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PMID:Health-related quality of life in chronic disorders: a comparison across studies using the MOS SF-36. 948 Nov 51

This report describes the simultaneous manifestation of ischemic heart disease and nephrotic syndrome in a 37-year-old woman presenting with acute anterior myocardial infarction. Symptoms of nephrotic syndrome, such as facial and peripheral edema accompanied by proteinuria and hyperlipidemia, and onset of severe retrosternal pain developed within 24 h. Coronary angiography revealed a complete thrombotic occlusion of the proximal portion of the left anterior descending artery with no evidence of arteriosclerotic lesions. Histologic examination of renal biopsy, including electron microscopy, revealed evidence of minimal change glomerulonephritis. Ultrastructural studies demonstrated widespread effacement of epithelial foot processes. Elevated levels of circulating fibrinogen appeared to be an important factor for the hypercoagulable state in this patient, suggesting a causative relationship between coronary thrombosis and nephrotic syndrome.
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PMID:Simultaneous manifestation of acute myocardial infarction and nephrotic syndrome. 966 62

We experienced 23 cases of venous thrombosis after gynecological surgery for the past 12 years at Tokyo Women's Medical University Hospital, representing 0.345 % of all patients. Eighteen of the 23 cases had deep venous thrombosis (DVT) including five cases followed by pulmonary embolism (PE), and five cases had PE without any symptoms of DVT. The main risk factors for thrombosis in these 23 patients were (1) obesity, DM, hyperlipidemia; (2) huge abdominal tumor, severe adhesion; and (3) hemoconcentration, post-treatment of severe anemia. The onset of PE varied from 1 to 3 postoperative days, when the patients started to walk. Five cases had dyspnea, chest pain, and decreased PaO2 levels without leg pain, while five cases showed only calf pain and tenderness with decreased PaO2 levels. PE was confirmed by immediate diagnostic images such as RI venography with ventilation and perfusion lung scan, pulmonary arterial CT, or pulmonary arteriography. Two patients died and eight patients recovered. The best way of managing venous thrombosis might be as follows: (1) identify the risk factors of thrombosis before surgery; (2) perform prophylactic leg exercises in bed and/or active anticoagulant therapy depending on the degree of risk factors; (3) rapid diagnosis with the images; and (4) proper treatment.
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PMID:Management of venous thrombosis and pulmonary embolism after gynecological surgery. 983 10

Peripheral arterial disease of the lower limbs is a manifestation of atherosclerosis, and may also affect other vascular territories such as the coronary and cerebral arteries. Progressive narrowing of the vessels up to total occlusion can present as intermittent claudication or pain at rest, with or without cutaneous lesions. Patients with intermittent claudication are at a low risk of amputation, and the symptom has to be regarded as a warning signal for myocardial infarction and stroke. Nevertheless, if the patient's walking distance is too limited to allow a near-normal life, symptomatic treatment to improve quality of life should be considered. Treatment may consist of walking exercise, surgical or interventional radiological revascularisation, or, in some cases, administration of vasoactive drugs. Antiplatelet agents should be administered in an attempt to limit disease progression and prevent cardiac and cerebrovascular complications, together with active measures to reduce established risk factors such as smoking, diabetes, hyperlipidaemia, and arterial hypertension. The presence of pain at rest indicates that a lower limb is jeopardised, especially when the criteria for critical ischaemia have also been met. These criteria include the presence of chronic (lasting for more than 2 weeks) symptoms of ischaemia at rest and a systolic blood pressure less than 50 mm Hg or 30 mm Hg at the ankle or big toe, respectively. In such a situation, revascularisation should be attempted whenever possible. If this is not possible or if the procedure has failed, prostacyclin administered intravenously for days or weeks is an alternative. After revascularisation, early reocclusion may be prevented by administering anticoagulants and late reocclusion by antiplatelet agents, in conjunction with eradication of risk factors. In all situations, therapeutic decision-making should be undertaken in a multidisciplinary setting and should include the following: specialists in angiology (an internist) and interventional radiology; a vascular surgeon; an orthopaedic surgeon, if necessary; and diabetes and infectious disease specialists.
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PMID:[Drug treatment strategies for peripheral obliterative arteriopathy]. 984 99

Aim of this paper is to describe and discuss, on the basis of the available current literature, the case of a female patient affected by a tophaceous gout associated with plurimetabolic syndrome. Hyperuricemia and gout may be seen today in all the populations of developed countries, with increasing frequency on the last fifty years. Increased production or reduced urinary excretion of uric acid (and hypoxanthine and xanthine) are the most important pathogenetic mechanisms of primary or secondary hyperuricemia. Gout is an acute rheumatic disorder (characterized by a limited range of manifestations) which occurs in humans in connection with deposition of crystals of monosodium urate (the final product of purine metabolism) in the articular and soft periarticular tissues. Hyperuricemia and/or gout are often associated with hyperinsulinemia, obesity, diabetes mellitus, hyperlipemia, hypertension and atherosclerosis to form the syndrome called "Plurimetabolic syndrome" or "Syndrome X". Here we report the clinical case of a 64-year-old female patient who had android obesity, type 2 diabetes mellitus, hypertension, dyslipidemia and hyperuricemia and had been suffering (over many years) from intermittent episodes of severe pain and inflammatory joint swelling (first metacarpo- and metatarso-phalangeal joints) with development of pronounced multiple tophi in bone articular and soft periarticular tissues. Hyperuricemia and acute episodes had never been treated with anti-hyperuricemic drugs because gouty arthritis had never been diagnosed. This severe tophaceous gout associated to multiple metabolic disorders prompted us to present knowledge on gout and to focus on the interrelationships between hyperuricemia and/or gout and plurimetabolic syndrome, important risk factors for coronary heart disease.
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PMID:[Tophaceous gout in plurimetabolic syndrome]. 1021 66

We encountered two cases of Pasteurella multocida subsp. septica isolation from exudates with seminal fluid-like odor from dog scratch and cat bite. Case 1: A 78-year-old male who had been diagnosed as having diabetes mellitus five years ago was scratched by the claw of a pet dog (Pekinese) on the back of the right hand. Since inflammation ascended to the arm, the patient visited Nihon University Itabashi hospital for a medical examination. Case 2: A 51-year-old female without a specific past history other than hyperlipidemia was bitten by a pet cat at the medical and lateral sides of the left carpus. The patient immediately opened the wound and washed it with tap water, followed by disinfection using a non-iodine disinfectant at home. Two hours later, the patient felt an unpleasant sensation and smelled a seminal fluid-like odor at the wound. The next morning, the entire left arm swelled and pain worsened, then the patient sought medical attention. The patients were treated with antibiotics and the wound completely healed on the 16 days from on set in Case 1 and on the 10 days from onset in Case 2. From these two cases, Pasteurella multocida subsp. septica was isolated from the exudate, suggesting that when wounds caused by animals smell like seminal fluid, the wound is infected with Pasteurellae. This finding may be an important clue for differentiation in clinical diagnosis.
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PMID:[Two cases of pasteurellosis accompanied by exudate with semen-like odor from the wound]. 1042 57

A 52-year-old man with diabetes mellitus, hyperlipidemia and smoking habit, experienced transient ischemic attacks (TIAs) with symptoms of left orbital pain, left blepharoptosis and hoarseness lasting for five minutes on March 10, 1997. Subsequently, the same symptoms repeated once or twice daily. On March 28, he had dysphagia, numbness and disturbance of pain and temperature sensation (segmental dissociated sensory disturbance) on the right side of the body above the level of the Th10, the right upper limb and face. The deficits persisted for more than 24 hours. Angiographic studies revealed an occlusion of the left vertebral artery immediately after branching of the posterior inferior cerebellar artery. MRI demonstrated a hyperintense lesion on MRI T2 weighted image in the left lateral medulla. About three months after the completed stroke, he had six episodes of TIAs of left Horner's sign and hoarseness. To our knowledge, this is the rare case that had frequent TIAs presenting the Wallenberg syndrome before and after the onset of lateral medullary infarction. We speculate that the TIAs resulted from microembolism from the proximal end of occluted left vertebral artery and failure of the microcirculation in and around the lateral portion of the medulla oblongata.
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PMID:[A case with frequent episodes of transient ischemic attack presenting the Wallenberg syndrome before and after the onset of brain infarction]. 1042 53

From 1990 to 1997, June, 296 patients (156 males and 140 females), aged 16 to 45 years, admitted in the Neurology Department of the University Hospital of Nancy (F) for ischemic stroke, were prospectively evaluated according to a standardized analysis of anamnestic and clinical data, angiography (90 p. 100 of cases), TEE (78 p. 100), hemostasis. Women were younger (mean age = 34.82 y) than men (36.87 y; p = 0.003), with a peak in the 4th decade. Clinical event was a TIA in 14.2 p. 100, a stroke in 51.7 p. 100; it concerned the anterior circulation in 64.5 p. 100, posterior circulation in 25 p. 100, multiple territories in 10.5 p. 100. History of TIA, cervical-cranial pain or Horner syndrome suggestive of dissection, pregnancy or post-partum were found respectively in 60 (20.3 p. 100), 34 (11.1 p. 100) and 13 (9.3 p. 100) cases. Risk factors concerned 87.2 p. 100 of patients, mainly smoking (55.1 p. 100), oral contraceptive (53 p. 100), hyperlipemia (35 p. 100), and were more frequent in case of atheroma and lacunar stroke (p < 0.0000). Etiology, according to TOAST classification, was: atheroma (8.4 p. 100), cardioembolism (8.7 p. 100), small-artery disease (7.1 p. 100), dissection (15.5 p. 100), other determined causes (11.1 p. 100), multiple causes (5.7 p. 100), undetermined cause (34.8 p. 100). Septal pathology was found 34 times. Patients whose stroke remained unexplained were younger (33.7 y vs 37.7, p = 0.002), had less risk factors (p < 0.0000), had more TIA (p = 0.005), more often in the carotid territory (p = 0.008), had a better prognosis (p = 0.01), and showed more often emboli at angiography (p = 0.001). During a mean follow-up of 33 months (median = 19), 21 recurrent strokes occurred and 6 patients died. 134 (46 p. 100) patients had no sequelae, 101 (34.7 p. 100) minor disability, 42 (14.4 p. 100) major sequelae. These results, compared to the main studies of the literature, suggest the interest of common definition criteria and classification of etiologies. In practice, hierarchisation of investigations may be proposed, and vascular risk factors should be tracked in young patients. In patients whose stroke remains unexplained, further studies, as atrial vulnerability, are needed.
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PMID:[Cerebral ischemic accidents in young subjects. A prospective study of 296 patients aged 16 to 45 years]. 1048 47

Thromboangiitis obliterans (TAO) has been reported to become less common in general population but more common in women, and in elderly patients. The authors looked at the clinical characteristics of TAO in Poland where there was no significant decrease of smoking and the extent of aging of the general population is less profound. They retrospectively reviewed the records of 377 patients with the diagnosis of TAO hospitalized in their institution from 1970 to 1995. If young smoking males demonstrated distal-extremity ischemia with no bruits audible over major arteries, upper limbs involvement, or superficial thrombophlebitis, the diagnosis of TAO was considered certain. When at least one of those criteria was missed, and in men older than 35 years, but in all females, typical arteriographic findings were required for the diagnosis of TAO. Connective-tissue disease, hyperlipidemia, diabetes, and hypercoagulable state were excluded. Three hundred forty-two men (91%), and 35 (9%) women had a mean age of 29.5 years at the onset of the disease (the oldest patient was 50 years old). The prevalence of TAO in southwest Poland is 8.1/100,000 and the incidence of the disease steadily declines; there was no increase of TAO in women. Three hundred thirty-seven (89%) experienced rest pain, 321 (85%) had ischemic necrosis, and 233 (62%) thrombophlebitis at some (continued on next page) time in the course of the disease. Raynaud's phenomenon occurred in only 39 patients (10%). Those patients who had quit smoking had a 50% decrease of the disease recurrences compared to their smoking period. Because the cause of declining incidence of TAO is obscure, the authors critically evaluated previously used explanations of this phenomenon. They did not confirm the observation of a change in the TAO clinical spectrum: occurrence in women did not increase, the aging of the TAO population was not observed. In Poland TAO is still a disease affecting the peripheral circulation of young smoking males with recurrent episodes of superficial thrombophlebitis and common involvement of the upper extremities; Raynaud's phenomenon is rather infrequent. Smoking cessation ameliorates the course of the disease but does not invariably stop further exacerbations.
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PMID:Sustained classic clinical spectrum of thromboangiitis obliterans (Buerger's disease). 1070 22


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