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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten cases of death due to heat stroke are described. They were all young men who collapsed during running exercise or route march and died in hospital later. Post-mortem examination was carried out in all cases. Death was due to disseminated intravascular coagulation with widespread microthrombus formation and coagulative necrosis involving many organs. Meteorological studies showed that at the time of the collapse the environmental temperature was higher than average although it may have been in the morning or evening.
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PMID:Acute heat stroke deaths. 722 95

A few cases of improvement in secondary renal amyloidosis following surgery (in particular, removal of the amylogenic foci) have been published, but cases of aggravation are much more numerous. The authors report on three patients whose renal function deteriorated dramatically after extra-renal surgery (pneumonectomy, aortic valve replacement, mitral valve replacement). None of the usual precipitating factors, such as DIC, cardiovascular collapse, sepsis or renal vein thrombosis, could be detected, but two patients had been under extracorporeal circulation. Such accidents appear to be unpredictable and irreversible. They can be seen in primary or secondary amyloidosis and whether or not surgery involves an amylogenic focus. Indeed, in two of their patients the diagnosis of amyloidosis was unknown before the operation. This suggests that in patients with suspected amyloidosis no major surgical operation should be undertaken without prior renal biopsy.
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PMID:[Dramatic aggravation of renal amyloidosis after surgery. Three cases (author's transl)]. 730 69

Heat stroke in distance runners is increasing in frequency. A case is reported of a 41-year-old man who collapsed during a 10-km "fun run" held when the temperature was 31.6 degrees C and the humidity 80%. Acute renal failure (serum creatinine level 1530 mumol/l [17.3 mg/dl]), rhabdomyolysis, disseminated intravascular coagulation and hepatic damage complicated the clinical picture. Repeated peritoneal dialysis and one cycle of hemodialysis because of a very high serum level of uric acid (1.23 mmol/l [20.7 mg/dl]) were required. Although the illness was prolonged, recovery was almost complete, and 4 months after the man's collapse the serum creatinine level had fallen to 133 mumol/l (1.5 mg/dl).
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PMID:Exertional heat stroke: the runner's nemesis. 738 6

Fatal Mycoplasma pneumoniae infection in a 30-yr-old woman is described. After 9 days of symptoms, the patient developed severe respiratory distress, rapidly progressive pneumonia, cardiovascular collapse, and acute renal failure. Death occurred 24 h after hospital admission. Postmortem examination demonstrated a diffuse membranous laryngotracheobronchitis, massive bilateral pneumonia, disseminated intravascular coagulation with widespread renal involvement, and hemorrhagic necrosis of the adrenal glands. Mycoplasma pneumoniae was isolated from the trachea, lungs, kidney, and brain, indicating hematogenous dissemination of the organism from its portal of entry in the respiratory tract.
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PMID:Fulminant Mycoplasma pneumoniae infection. Report of a fatal case, and a review of the literature. 741 24

We have used intraoperative autotransfusion in three cases of massive intraabdominal hemorrhage following blunt trauma. Based on this experience we recommend that: (1) To prevent sudden collapse the abdomen should be decompressed slowly through a small incision while blood is collected into the autotransfusion reservoir; (2) A skilled person is required to operate the autotransfusor; and (3) To prevent consumption coagulopathy, autotransfusion must be supplemented by the use of blood components, especially fresh frozen plasma.
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PMID:Intraoperative autotransfusion in blunt abdominal trauma. 746 73

An interesting case of acute poisoning by chromate compounds is reported. A 51-year-old man committed suicide by ingesting a fatal dose of sodium chromate solution. He unexpectedly lost consciousness 6 h after the ingestion and died approximately 20.5 h later. An examination of the blood showed noticeable hepatic damage and thrombocytopenia. The postmortem examination revealed extensive bleeding in the alimentary tract and a severe hepatic lesion due to hepatocellular necrosis. However, the renal disorder was unusually light in the microscopic and clinical findings. Moreover, the renal lesion was observed mainly in the distal tubules instead of the proximal tubules which is more typical in cases of acute poisonings by diverse heavy metals including chromium. The patient's death was assumed to have been caused by circulatory collapse due to internal bleeding and the direct toxicity of chromate compounds with hepatic malfunction and possibly disseminated intravascular coagulation (DIC).
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PMID:Unusual findings in a fatal case of poisoning with chromate compounds. 759 May 49

In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin < 5 g/dl (0/12), < 8 g/dl (2/12); serum creatinine > 265 mumol/l (3/12); blood glucose < 2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH < 7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia > 5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia < 30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12), < 125 mmol/l (2/12); rhabdomyolysis with creatine kinase > 1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intensive care aspects in severe tropical malaria: clinical aspects, therapy and prognostic factors]. 777 Jul 59

A 31-year-old multiparous pregnant woman forced into labour with oxytocin, suffered a sudden circulatory collapse and, after the birth of her child, a defibrination syndrome with uterine haemorrhage. In the absence of a local cause, either placental or cervico-uterine, a diagnosis of amniotic fluid embolism was made. The time course was favourable, mainly thanks to the absence of acute pulmonary cardiogenic oedema and to the use of an anti-shock G suit. The authors point out the lack of actual in vivo paraclinical means for confirming the diagnosis.
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PMID:[Amniotic embolism with favourable outcome]. 809 72

Three obstetrical patients who experienced cardiovascular collapse followed by disseminated intravascular coagulation were cared for by the author during residency training and 5 years of private practice. All patients survived. Their clinical courses were strongly reminiscent of those of patients described in the medical literature who ultimately died with the diagnosis of "amniotic fluid embolism." Paradoxically, the mere fact of survival is generally regarded as proof that a given individual did not have an amniotic fluid embolism. Proposed herein is a new clinical definition of amniotic fluid embolism syndrome that could apply to patients who survive as well as to those who die. With this definition in mind, the prevalence and prognosis of amniotic fluid embolism syndrome is reexamined. Finally, the traditional assumption that this syndrome is a result of amniotic fluid leakage into the maternal circulation is challenged. A new source is suggested and some new thoughts regarding treatment are provided.
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PMID:Nonfatal amniotic fluid embolism. Three possible cases and a new clinical definition. 811 30

Although up to several microns thick, the pericellular matrix is an elusive structure due to its invisibility with phase contrast or DIC microscopy. This matrix, which is readily visualized by the exclusion of large particles such as fixed red blood cells is important in embryonic development and in maintenance of cartilage. While it is known that the pericellular matrix which surrounds chondrocytes and a variety of other cells consists primarily of proteoglycans and hyaluronan with the latter binding to cell surface receptors, the macromolecular organization is still speculative. The macromolecular organization previously could not be determined because of the collapse of the cell coat with conventional fixation and dehydration techniques. Until now, there has been no way to study the dynamic arrangement of hyaluronan with its aggregated proteoglycans on living cells. In this study, the arrangement and mobility of hyaluronan-aggrecan complexes were directly observed in the pericellular matrix of living cells isolated from bovine articular cartilage. The complexes were labeled with 30- to 40-nm colloidal gold conjugated to 5-D-4, an antibody to keratan sulfate, and visualized with video-enhanced light microscopy. From our observations of the motion of pericellular matrix macromolecules, we report that the chondrocyte pericellular matrix is a dynamic structure consisting of individual tethered molecular complexes which project outward from the cell surface. These complexes undergo restricted rotation or wobbling. When the cells were cultured with ascorbic acid, which promotes production of matrix components, the size of the cell coat and the position of the gold probes relative to the plasma membrane were not changed. However, the rapidity and extent of the tethered motion were reduced. Treatment with Streptomyces hyaluronidase removed the molecules that displayed the tethered motion. Addition of hyaluronan and aggrecan to hyaluronidase-treated cells yielded the same labeling pattern and tethered motion observed with native cell coats. To determine if aggrecan was responsible for the extended configuration of the complexes, only hyaluronan was added to the hyaluronidase-treated cells. The position and mobility of the hyaluronan was detected using biotinylated hyaluronan binding region (b-HABR) and gold streptavidin. The gold-labeled b-HABR was found only near the cell surface. Based on these observations, the hyaluronan-aggrecan complexes composing the cell coat are proposed to be extended in a brush-like configuration in an analogous manner to that previously described for high density, grafted polymers in good solvents.
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PMID:The dynamic structure of the pericellular matrix on living cells. 827 5


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