Cases reported "Shock, Septic"

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1/839. Developing venous gangrene in deep vein thrombosis: intraarterial low-dose burst therapy with urokinase--case reports.

    Two patients with developing venous gangrene of the lower extremity and contraindications to systemic thrombolytic therapy are presented. Low-dose intraarterial burst therapy with urokinase provided rapid amelioration of symptoms and avoided amputation without any serious bleeding complications in both patients. ( info)

2/839. Toxic shock syndrome secondary to a dental abscess.

    A 9-year-old girl presented with arthralgia and myalgia which progressed to developing renal failure and overwhelming septic shock. The underlying cause was assumed to be a periodontal abscess from an upper right deciduous canine tooth. The pus from the abscess grew a toxic shock syndrome toxin 1-producing Staphylococcus aureus. This case illustrates the importance of an oral surgical review of patients presenting with features of toxic shock syndrome if the source of the infection is not immediately obvious. ( info)

3/839. Purulent pericarditis misdiagnosed as septic shock.

    BACKGROUND: Septic shock is common, with approximately 200,000 cases recognized annually. This syndrome is so well characterized that when a patient is febrile and in shock, septic shock may be diagnosed without regard to alternative possibilities. Purulent pericarditis is a relatively rare disorder in which fever and hypotension are common. Classic signs and symptoms, such as chest pain, pericardial friction rub, pulsus paradoxus, and elevation of jugular venous pressure, are seen in only 50%. methods: In this report, we describe four patients in whom purulent pericarditis and pericardial tamponade was initially misdiagnosed as septic shock. During a 3-month period, three men and one woman (mean age, 44.5 years) came to Kern Medical Center with purulent pericarditis and pericardial tamponade. These cases represented 13% of patients admitted with a diagnosis of septic shock. RESULTS: All patients were bacteremic, and the classic findings of pericardial tamponade were absent or relatively subtle. Hemodynamic findings of elevated systemic vascular resistance, low cardiac output, and normal pulmonary artery occlusion pressure were critical to the diagnosis. CONCLUSIONS: Consideration of purulent pericarditis is important in cases diagnosed as septic shock. Clinicians should be aware that patients with purulent pericarditis may not exhibit classic signs and symptoms, and a high index of suspicion is necessary for appropriate management. ( info)

4/839. Rapid and definitive diagnosis of infectious diseases using peripheral blood smears.

    A timely diagnosis is essential in the management of septicemia and septic shock. Three patients are described, all of whom presented with fever and one of whom was hypotensive at the time of admission. In each patient, rapid diagnosis of the cause of fever was possible because microorganisms were identified on a peripheral blood smear obtained at the time of admission. This identification permitted prompt initiation of appropriate antimicrobial therapy. In addition, a literature review of use of peripheral blood smears in the diagnosis of bacterial, fungal, and parasitic infections is provided. ( info)

5/839. Maximizing oxygen delivery when resuscitating patients from shock. Clinical guidelines as well as some practical pointers.

    In patients with shock and evidence of hypoperfusion, target therapy at increasing oxygen delivery and decreasing oxygen consumption. To augment delivery, increase arterial oxygenation (with mechanical ventilation and high levels of inspired oxygen), hemoglobin level to at least 10 g/dL (with transfusions of red blood cells), and cardiac output (with hydration and inotropic support). Avoid vasopressors because they increase afterload and thereby decrease cardiac output and oxygen delivery. To reduce oxygen consumption, consider antipyretics (to lower metabolic demand) and mechanical ventilation plus sedatives or paralytics (to decrease the work of breathing). Continue therapy until oxygen consumption is no longer coupled to delivery. ( info)

6/839. Fulminant lethal tuberculous pneumonia (sepsis tuberculosis gravissima) with ARDS in a non-immunocompromised western European middle-aged man.

    We report the case of a 42 years old, non-immunocompromised native Austrian living in Vienna. He presented at home with severe dyspnea and had to be intubated immediately. Shortly after hospital admission, he developed severe adult respiratory distress syndrome (ARDS) and septic shock with massive, bilobar patchy to confluent infiltrations and a need for norepinephrine. A CT-scan revealed severe loss of functional lung tissue with areas of consolidation and multiple communicating cystic spaces. air leaking into the mediastinum through fistulas produced pneumomediastinum, pneumoperitoneum, and a massive soft tissue emphysema. bronchoalveolar lavage performed within the first 24 hours of admission revealed of acid-fast bacilli. Even though appropriate tuberculostatic medication was started immediately, the patient succumbed the next day to ARDS due to massive tuberculous pneumonia and miliary disease (sepsis tuberculosis gravissima). ( info)

7/839. Infectious disease emergencies in primary care.

    Infectious disease emergencies can be described as infectious processes that, if not recognized and treated immediately, can lead to significant morbidity or mortality. These emergencies can present as common or benign infections, fooling the primary care provider into using more conservative treatment strategies than are required. This review discusses the pathophysiology, history and physical findings, diagnostic criteria, and treatment strategies for the following infectious disease emergencies: acute bacterial meningitis, ehrlichiosis, rocky mountain spotted fever, meningococcemia, necrotizing soft tissue infections, toxic shock syndrome, food-borne illnesses, and infective endocarditis. Because most of the discussed infectious disease emergencies require hospital care, the primary care clinician must be able to judge when a referral to a specialist or a higher-level care facility is indicated. ( info)

8/839. Alpha1-antitrypsin deficiency and toxic shock: a Japanese autopsy case.

    A 74-year-old Japanese female presented with the sudden appearance of hemorrhagic purpuric ecchymoses on her lower extremities and with fever and chills, and died on the fifth day of hospitalization. A diagnosis of alpha1-antitrypsin (AT) deficiency was made postmortem. The liver weighed 1260 g. Histological sections from the liver revealed rather severe fatty changes of the hepatocytic parenchyma and partial loss of the normal hepatic architecture with fibrosis. The hepatocytes contained periodic acid-Schiff (PAS)-positive, diastase-resistant and alpha1-AT-positive intracytoplasmic globules. There was markedly increased inflammatory infiltration with severe edema and congestion, accompanied by fibrous, thickened pulmonary alveolar walls with fibrin deposition in the lungs (right, 410 g; left, 280 g), which suggest findings similar to those seen in multiple organ failure. Mild pulmonary emphysema was also present in the upper lobes of the lungs. Histological sections from the hemorrhagic necrotic ecchymoses of the skin showed marked neutrophil infiltration over the subcutaneous tissue with bleeding and blistering. A finding of thrombophlebitis was also found in the subcutaneous tissue. No bacteria were detected in the ecchymoses, the urine or the blood. plasma protein analysis revealed a lower level (9.5 micromol/L) of alpha1-AT and a higher level (330 U) of anti-streptolysin O (ASO). These findings suggest that the patient died of toxic shock-like syndrome and that alpha1-AT deficiency might have facilitated the development of the toxic shock. To our knowledge, this is the first case of toxic shock associated with alpha1-AT deficiency. ( info)

9/839. staphylococcal scalded skin syndrome in an adult associated with methicillin-resistant staphylococcus aureus.

    We report the first adult case of staphylococcal scalded skin syndrome (SSSS) due to methicillin-resistant staphylococcus aureus (MRSA). This case is particularly unusual as the MRSA produced toxic shock syndrome toxin 1 and enterotoxin, but not exfoliatoxin. SSSS was originally described in neonates and is thought to result from exfoliatins which produce subcorneal splitting of the epidermis and are only produced by certain strains of S. aureus. This case reflects the range of toxins that can be associated with SSSS and the clinical manifestations of MRSA infection in adult patients. ( info)

10/839. Effect of haemofiltration on pathological fibrinolysis due to severe sepsis: a case report.

    Bleeding due to coagulopathy is a frequent complication of severe sepsis, especially in burn patients. The primary treatment is aimed at the underlying cause but additional supportive measures, consisting mainly of coagulation factor replacement, are frequently necessary. We describe the salutary effect of continuous veno-venous haemofiltration (CVVH) with predilution on diffuse haemorrhage in a patient with severe septic shock and renal failure. The diffuse haemorrhage was initially treated with replacement of coagulation factors. prothrombin time and partial thromboplastin time became normal while diffuse bleeding continued and the thrombelastogram showed evidence of fibrinolysis. A short period of CVVH lead to the cessation of bleeding which was reflected by a normal thrombelastogram. ( info)
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