Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An analysis of seven sporadic cases of Legionnaires' disease confirmed clinical features recorded during epidemics and identified aspects of the illness either unreported or not emphasized. Four patients had central nervous system abnormalities. Mental status changes included somnolence, obtundation, delirium, disorientation, and confusion. Three patients experienced visual hallucinations, and one patient without pneumonia had a grand mal seizure with residual memory deficit. Two patients had disseminated intravascular coagulation with thrombocytopenia, elevated split fibrin products, and prolonged partial thromboplastin and prothrombin times. Four patients had severe hypoxia; one patient had an exudative pleuritis. One patient whose treatment included erythromycin had radiologic improvement of his pneumonia despite deteriorating ventilatory function that led to death. The concept of Legionnaires' disease as a severe, diagnostically perplexing pneumonic illness is valid but too narrow. The emerging spectrum is that of a multisystem disease that, besides the lungs, often involves the central nervous system and can be accompanied by disseminated intravascular coagulation.
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PMID:Sporadic cases of Legionnaires' disease: the expanding clinical spectrum. 43 28

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

The Western diamondback rattlesnake, Crotalus atrox, is responsible for the majority of snakebites in Sonora, Mexico. We report 19 cases of children who were attacked by these snakes. Most of the rattlesnake attacks occurred in rural areas during the summer. The children's ages ranged from one to 15 years. The lower extremities, especially the legs, were most often bitten. The signs and symptoms presented by these patients included: pain, edema, limitation of motion, ecchymosis, bleeding and necrosis in the area of the bite, epistaxis, hematuria, and vomiting. Hospital treatment included: parenteral electrolyte solutions, antivenom serum, antibiotics, tetanus toxoid, blood transfusions, hydrocortisone, heparin, and peritoneal dialysis. In one case a fasciotomy was necessary. The observed complications on envenomations included: hemolysis, local necrosis, coagulation disorders, paresthesia, somnolence, and acute renal failure. One death occurred from disseminated intravascular coagulation.
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PMID:Rattlesnake bite complications in 19 children. 817 4

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91

Acetazolamide (Diamox) is a carbonic anhydrase inhibitor commonly used in patients with glaucoma in order to reduce intraocular pressure. Acetazolamide (AZ) is mostly excreted in the urine, therefore, the blood levels of AZ often tend to increase in patients with chronic renal failure. We experienced a case of chronic renal failure in a patient suffering from acute hemorrhagic gastritis associated with AZ intoxication. A 66-year-old female with chronic renal failure was referred to our hospital because of drowsiness and an acute deterioration of renal function. She had been treated with AZ, 500 mg per every day for eleven days for the treatment of glaucoma. Laboratory studies showed leukocyturia, thrombocytopenia, severe anemia, and tarry stools. The serum concentration of AZ was elevated to a maximum of 76.5 mg/ml. She was thus diagnosed as having AZ intoxication. On further examination, acute extensive hemorrhagic gastritis was also found by gastroscopy. Despite of the administration of intensive therapies, she died of disseminated intravascular coagulation (DIC) and septic shock due to bone marrow depression 6 days after admission. It is generally known that excessive blood levels of AZ inhibit not only the gastric juices but also prostaglandin levels and HCO3- excretion in the gastric mucosal barrier. We thus concluded that an excessive dose of AZ had probably destroyed the gastric mucosal barrier or thrombocytopenia due to bone marrow disorder and thus eventually led to the development of hemorrhagic gastritis. As far as we know, this is the first case report of acute hemorrhagic gastritis associated with AZ intoxication. Even though AZ tends to strongly bind to plasma protein and its clearance is generally poor by hemodialysis (HD), in our patient, HD was observed to be rather effective since the clearance of AZ was 45.8 ml/min on HD and 66 ml/min on direct hemoperfusion (DHP). DHP often reduces the number of platelets, also DHP needs a lot of heparin, therefore, we should have performed HD alone instead of DHP. In patients with an impaired renal function, AZ should therefore be administered very carefully in order to avoid an accumulation of the drug. In addition, HD alone should be used to remove any excessive amounts of AZ from the blood.
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PMID:Acute hemorrhagic gastritis associated with acetazolamide intoxication in a patient with chronic renal failure. 935 64

A 24-year-old, nulliparous woman in her 30th week of pregnancy was admitted due to threatened premature delivery. Ritodrin chloride relieved the premature contraction of the uterus but jaundice and drowsiness appeared 7 weeks later. Laboratory data revealed disseminated intravascular coagulation (DIC) with intrahepatic cholestasis, and ultrasound examination showed fatty liver. The patient was diagnosed with acute fatty liver of pregnancy (AFLP). Emergency delivery by Caesarean section was performed at 37 weeks of pregnancy and the liver function and DIC improved immediately. Liver biopsy 13 days after delivery showed nuclear swelling and cytoplasmic ballooning with mild fatty deposition. These findings were relatively compatible with acute AFLP. Higher magnification and electron microscopy revealed intracytoplasmic bacteria and fungus in the residual stage. The bacterial infection could be considered related to AFLP.
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PMID:Acute fatty liver of pregnancy showing microbial infection in the liver. 1119 91

Meningitis and meningococcal sepsis are emergency conditions associated with high mortality. The outcome is worsened by the onset of disseminated intravascular coagulation. This may present, particularly in children, with the clinical picture of purpura fulminans, characterized by extensive necrotic-hemorrhagic skin lesions, ischemia of the extremities and multiorgan failure. It has been observed that depletion of coagulation inhibitors, particularly protein C, plays a key role in the development of this severe complication. We describe the case of a woman who presented in the Emergency Room with signs of meningitis, drowsiness, hypotension and petechie. Bacterioscopic examination of the cerebrospinal fluid evidenced characteristic gram-negative diplococci. Laboratory data disclosed initial disseminated intravascular coagulation with low levels of proteins C and S. Following intravenous infusion of antibiotics, fluids and fresh frozen plasma, the patient's condition rapidly improved. However, multiple skin lesions appeared on her fingers, toes and heels. It is likely that the infusion of coagulation inhibitors contained in fresh frozen plasma, prevented evolution to full-blown purpura fulminans. The first choice treatment for purpura fulminans in meningococcal sepsis is infusion of protein C concentrate, which is not, however, currently available on the market.
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PMID:[Meningococcal meningitis in the adult complicated by cutaneous necrosis: description of a clinical case]. 1120 31

An 80-year-old man who had undergone total gastrectomy and splenectomy for gastric cancer 13 years ago presented with headache, drowsiness, and high fever 1 month after a traffic accident. Brain CT scans revealed bilateral subdural fluid collections. Diffusion-weighted imaging (DWI) showed mixed high and low signal intensities in the left subdural fluid, and contrast-enhanced MR imaging revealed capsule enhancement of the left subdural fluid collection. The patient was diagnosed with left subdural empyema, and 2 burr-holes were drilled for drainage and irrigation. Operative findings revealed a neomembrane underneath the dura mater. Old hematoma and yellowish-white purulent fluid were present within the neomembrane. This confirmed the diagnosis of infected subdural hematoma (ISH). Abscess culture results were positive for Escherichia coli. The patient's symptoms resolved postoperatively with subsequent antibiotic therapy. However, 4 months after the operation, he suddenly died of severe sepsis and disseminated intravascular coagulation following cholecystitis, which was possibly associated with splenectomy. The clinical presentation, diagnosis, and treatment of an unusual case of ISH have been discussed. We emphasize that DWI and enhanced MR imaging may be useful for diagnosing ISH, and serial DWI evaluations may help in monitoring the therapeutic response in ISH.
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PMID:[Case of infected subdural hematoma diagnosed by diffusion-weighted imaging]. 1930 4

We report a 4-year-old boy with fulminating meningitis caused by Haemophilus influenzae (Hib). He suddenly developed fever, vomiting and then somnolence. As bacterial meningitis was suspected, treatment with antibiotics was started at 12 hours after the onset. However, there was a rapid progression of severe brain edema and brain hernia, leading to clinical brain death. His clinical course and neuroradiological findings mimicked those in patients with acute encephalopathy, with cytokine profiles in cerebrospinal fluid demonstrating a marked increase of inflammatory cytokines. From a review of the literature, fulminating Hib meningitis may be classified into two disease types: DIC plus multiple organ failure and acute brain swelling types. The present case belongs to the latter type, in which cytokine storm seems to play an important pathogenic role.
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PMID:[Fulminating meningitis caused by Haemophilus influenzae with rapid progression of severe brain edema similar to acute encephalopathy]. 1992 44

Chimeric antigen receptor T cells are a new and exciting immunotherapeutic approach to managing cancer, with impressive efficacy but potentially life-threatening inflammatory toxicities such as cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). Patients with severe CRS may develop capillary leak syndrome and disseminated intravascular coagulation, with a cytokine signature similar to that of macrophage activation syndrome/hemophagocytic lymphohistiocytosis. Moderate-to-severe CRS is managed with the IL-6 receptor antagonist tocilizumab with or without corticosteroids, with questions remaining regarding the optimal management of nonresponders. ICANS is an inflammatory neurotoxicity typically occurring after CRS and characterized by impaired blood-brain barrier integrity. Symptoms of encephalopathy range from mild confusion and aphasia to somnolence, obtundation, and in some cases seizures and cerebral edema. ICANS is currently managed with corticosteroids; however, the optimal dose and duration remain to be determined. Little information is available to guide the management of patients with steroid-refractory ICANS. Numerous cytokine-targeted therapies have been proposed to manage these inflammatory toxicities, but few clinical data are available. Management of inflammatory toxicities of chimeric antigen receptor T cells often requires multidisciplinary management and intensive care, during which allergists and immunologists may encounter patients with these unique toxicities.
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PMID:Cytokine release syndrome and neurotoxicity following CAR T-cell therapy for hematologic malignancies. 3277 58


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