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)

Although snakebites are frequently seen in small animal practice in South Africa, boomslang (Dispholidus typus) bites are infrequent due to their shy habits. Boomslang venom is a potent procoagulent, causing a consumption coagulopathy and profuse haemorrhage. Boomslang monovalent antivenom is the most effective treatment. This case report describes and discusses 2 small dogs that were presented to a private practice after being bitten by the same boomslang. Boomslang monovalent antivenom administration to both resulted in cessation of bleeding within 45 minutes. One of the dogs developed severe adverse reactions to the antivenom, including vomiting, dyspnoea and nystagmus, which responded well to intravenous cortisone and symptomatic treatment.
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PMID:Boomslang envenomation in 2 dogs in Kwazulu-Natal, South Africa. 1766 67

This is the first report of the largest epidemic of dengue hemorrhagic fever (DHF) virus infection (2006) with IgM-confirmed cases from Karachi, Pakistan. Medical records of 172 IgM-positive patients were reviewed retrospectively for demographic, clinical and laboratory data. Patients were categorized into dengue fever (DF) and DHF according to the WHO severity grading scale. The mean+/-SD age of the patients was 25.9+/-12.8 years, 55.8% were males and the hemoconcentration was recorded in a small number of patients [10 (7.0%)]. Male gender [odds ratio (OR)=14.7, P=0.003), positive history of vomiting (OR=4.3, P=0.047), thrombocytopenia at presentation (OR=225.2, P<0.001) and monocytosis (OR=5.8, P=0.030) were independently associated with DHF, but not with DF. Five cases (2.9%) had a fatal outcome, with a male-to-female ratio of 1:4. Three were from a pediatric group (<15 years). Pulmonary hemorrhages, disseminated intravascular coagulation and cerebral edema preceded death in these patients. The results have highlighted significant findings, such as adult susceptibility to DHF, pronounced abdominal symptoms and lack of hemoconcentration at time of presentation in the study population. These findings may play an important role in the case definitions of future studies from this part of the world.
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PMID:Dengue outbreak in Karachi, Pakistan, 2006: experience at a tertiary care center. 1770 59

The clinical features of brown spider bites are the appearance of necrotic skin lesions, which can also be accompanied by systemic involvement, including weakness, vomiting, fever, convulsions, disseminated intravascular coagulation, intravascular hemolysis and renal disturbances. Severe systemic loxoscelism is much less common than the cutaneous form, but it may be the cause of clinical complications and even death following envenomation. Here, by using three recombinant dermonecrotic toxins, LiRecDT1, LiRecDT2 and LiRecDT3 (the major toxins found in the venom), we report the biological, immunological and structural differences for these members of this toxin family. Purified toxins evoked similar inflammatory reactions following injections into rabbit skin. Recombinant toxin treatments of MDCK cells with LiRecDT1 and LiRecDT2 changed cell viability, as evaluated by neutral red uptake and assessment of cell morphology through inverted microscopy, whereas LiRecDT3 caused only residual activity. Differences in cell cytotoxicity triggered by recombinant toxins were confirmed through a human red blood lysis assay, during which LiRecDT1 and LiRecDT2 caused a high degree of hemolysis compared to LiRecDT3, which induced only a small hemolytic effect. Additionally, biological differences for recombinant toxins were corroborated through mice lethality experiments, which showed animal mortality after LiRecDT1 and LiRecDT2 treatments, but an absence of lethality following LiRecDT3 exposure. Moreover, in experiments for edema, both the LiRecDT1 and the LiRecDT2 toxins evoked similar results, causing edema following toxin exposure, whereas LiRecDT3 caused only residual effects. Characterization of antigenic cross-reactivity using sera against crude venom toxins by immunoWestern blotting and immunodot blotting with recombinant LiRecDT1, LiRecDT2 and LiRecDT3 compared among themselves pointed to a higher cross-reactivity for LiRecDT1 compared to LiRecDT2 and LiRecDT3, corroborating structural and antigenic differences for these three toxins. Finally, evidence for structural differences among the recombinant toxins was strengthened by circular dichroism spectra, which suggested that the toxins were folded, and not aggregated or denatured proteins.
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PMID:Biological and structural comparison of recombinant phospholipase D toxins from Loxosceles intermedia (brown spider) venom. 1790 Jun 46

We describe a 26-year-old female patient, who had attempted suicide with Endosulfan, and who presented to the Emergency Department with status epilepticus. She subsequently developed hypotension refractory to inotropes, intravascular hemolysis, disseminated intravascular coagulation (DIC), metabolic acidosis and, finally, cardiac arrest and death. Endosulfan is a chlorinated insecticide that causes central nervous system hyperstimulation. It is absorbed from the gastrointestinal tract, skin, and respiratory tract, and leads to nausea, vomiting, paraesthesia, giddiness, convulsion, coma, respiratory failure, and congestive cardiac failure. Hepatic, renal and myocardial toxicity, agranulocytosis, aplastic anemia, cerebral edema, DIC, thrombocytopenia, and skin reaction also have been reported. Management includes decontamination of skin and gastrointestinal tract, supportive care including treatment of status epilepticus, dysrhythmias, and mechanical ventilation. Mortality and morbidity rates are very high and there is no specific antidote. Atropine and catecholamines should be avoided.
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PMID:Endosulfan poisoning with intravascular hemolysis. 1797 61

Defined by the association of hemolysis, hepatic dysfunction and thrombocytopenia, the Hemolysis, Elevated Liver enzyme, Low Platelets (HELLP) syndrome can complicate preeclampsia and worsen maternal and fetal prognosis. It can be diagnosed in the immediate postpartum (30%) or in the absence of preeclampsia (10-20%). Clinical diagnosis can be difficult because there is no specific symptom. Abdominal pain or vomiting during the third trimester must lead to think about this diagnosis. Biological criteria are well defined: hemolysis by the presence of schistocytes, increased serum total bilirubin >12 mg/L or LDH >600 IU/L, hepatic dysfunction by increased transaminases and thrombocytopenia by a platelet count <100,000/microL. The evolution of those parameters is a major prognostic factor. With the HELLP syndrome, maternal morbidity is dramatically increased compared to isolated preeclampsia with complications such as eclampsia, placental abruptio, disseminated intravascular coagulation, pulmonary edema, acute renal insufficiency, subcapsular liver hematoma. The management of a HELLP syndrome requests level 3 hospital with intensive care units for neonate and mother. The treatment of this syndrome requires termination of the pregnancy as soon a possible, either by cesarean section or by vaginal delivery if cervical conditions are optimal (without any maternal or fetal complications). Before 32 weeks, a more expectative attitude could be acceptable with the prematurity permitting corticotherapy for fetal pulmonary maturation. This corticotherapy can improve temporary biological parameters but there are no proven benefits to consider improvement for long term maternal or fetal prognosis. During the postpartum, evolution is usually spontaneously favorable. Recurrences are not frequent.
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PMID:[Management of the HELLP syndrome]. 1900 44

A 58-year-old man was admitted to our hospital with fever, vomiting and disturbance of consciousness after common cold-like symptoms for 2 days. Physical examination showed high fever, moderate hypertension and tachycardia. There were no superficial lymph nodes swelling nor skin rashes. Cerebrospinal fluid (CSF) examination revealed increased protein level (467 mg/dl) and pleocytosis (508 cells/mm3), but no glucose was detected. CSF smear test detected the pneumococcus. Intravenous cefotaxime was administered along with intravenous immunoglobulins and steroid pulse therapy. However, DIC developed, so FOY therapy was started. With these treatments, level of consciousness gradually improved and he became able to eat. At 11th days after the onset, the patient suddenly developed left facial palsy and paresis of the left arm. Head T2-weighted magnetic resonance imaging demonstrated tumor-like hyperintensity signal lesions (28 x 16.6 mm) with ring enhancements in the right frontal lobe. Acute disseminated encephalomyelitis (ADEM) was diagnosed based on MRI and CSF findings, and then additional corticosteroid pulse therapy was administered twice. Herpes simplex virus and herpes zoster virus DNA in the CSF were undetectable by PCR. After 6 days of treatment with corticosteroid pulse therapy, left facial palsy and paresis of the left arm gradually improved and MRI showed the disappearance of tumor-like hyperintense signals. Although ADEM usually develops as a complication after viral infection such as measles, rubella, mumps and herpes zoster, this case suggests that ADEM complication should be considered even after pneumococcal meningoencephalitis.
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PMID:[A case of acute disseminated encephalomyelitis (ADEM) following treatment for pneumococcal meningoencephalitis]. 1934 73

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

Infectious canine hepatitis in 4 Dogs in Switzerland. Four dogs presented with nonspecific symptoms of lethargy, vomiting, diarrhea, fever and weakness. Laboratory results were consistent with hepatopathy and disseminated intravascular coagulation. Three dogs died, one survived. In the three deceased dogs, a diagnosis of infectious canine hepatitis (ICH) was made based on histological findings and positive immunhistochemistry results for canine adenovirus-1 (CAV-1). In the surviving dog, an antemortem diagnosis of ICH was determined via positive polymerase chain reaction results from blood, occular, nasal and preputial discharge as well as from urine. Since the introduction of widespread vaccination, the incidence of CAV-1 infection in dogs is low. However, the disease has not been eradicated and should be considered when clinical signs consistent with ICH are present.
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PMID:[Infectious canine hepatitis in 4 dogs in Switzerland]. 2012 47

Disseminated intravascular coagulation (DIC) as a complication of surgery for ventriculoperitoneal (VP) shunts is extremely rare, and only one case has been documented in the literature. The authors present the case of a 9-year-old girl with shunted hydrocephalus who presented with a 3-day history of headaches and vomiting. A head CT showed enlarged ventricles compared with baseline. An emergent VP shunt revision was performed, during which an obstructed proximal catheter was found. Immediately after extubation, the patient became apneic and progressed to cardiopulmonary arrest. A breathing tube was reinserted followed by resuscitation attempts that led to extracorporeal membrane oxygenation. Soon after reintubation, bloody drainage was noted in the endotracheal tube, and subsequent laboratory studies were consistent with DIC. The patient died on postoperative Day 1, and autopsy findings confirmed DIC. Note that DIC is a recognized complication of trauma, particularly with brain injury, but it is rare with neurosurgical procedures. Disseminated intravascular coagulation should be considered if excessive bleeding occurs after any brain insult.
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PMID:Disseminated intravascular coagulation associated with ventriculoperitoneal shunt surgery. 2019 51

Patients receiving splenectomy are at risk of a fatal fulminant infection called overwhelming post-splenectomy infection (OPSI). Here we report a rare case of toxic shock syndrome (TSS) evoked by group B streptococcus (GBS) in an asplenic young woman, which we considered a case of OPSI. A 34-year old woman consulted our hospital complaining of vomiting, diarrhea and fever that developed early in the morning. As the physical examination and routine laboratory tests did not disclose any serious abnormalities, she returned home after symptomatic treatment under a provisional diagnosis of acute enterocolitis. However, the next morning, she was transferred to the hospital complicated by acute renal failure, severe liver damage, respiratory insufficiency, disseminated intravascular coagulation and hypotension. She was admitted to ICU and treated with intravenous antibiotics, frequent transfusions of platelet concentrates, hemodialysis, and non-invasive positive pressure ventilation. Blood cultures grew gram-positive cocci, which later proved to be Streptococcus agalactiae (GBS). We diagnosed the patient with TSS due to GBS. Organ damage and symptoms improved gradually with intensive treatment, she was discharged from the hospital 26 days after admission. Although cases of TSS due to GBS are very rare, we must be aware of the potential risk of OPSI in a splenectomized patient.
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PMID:[An overwhelming post-splenectomy infection with toxic shock syndrome by group B Streptococcus]. 2046 21


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