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We report the survival of a multiply injured patient with exanguinating haemorrhage and an arterial pH of 6.5, following a road vehicle crash. The previously healthy 38 years old male driver veered off the motorway and collided with a tree. The ambulance arrived at the scene 9 min after being called by an eyewitness and, following rapid extrication from the wreckage; the patient arrived in hospital 27 min later (with a GCS of 6), and was immediately intubated. The patient had suffered near-complete amputation of the left leg at upper femoral shaft level, along with multiple distal fractures and open wounds. He also sustained a head injury and closed displaced fractures of left radius and ulna. The patient received 2 l of crystalloids in the pre-hospital phase. Once in hospital the haemorrhage was controlled with a pressure dressing and intra-venous fluids were kept to a minimum until he was taken promptly to theatre. His initial arterial blood sample revealed a pH of 6.57, pCo(2) of 9.18 kPa, a pO(2) of 70.11 kPa and a base excess of -27.5 mmol l(-1). The co-oximeter Hb was 5.8 g dl(-1). Haemorrhage was controlled in theatre where he was transfused a total of 30 U of blood, 1 pack of platelets, 12 U of fresh frozen plasma, 3.5 l of crystalloids and 1.5 l of colloid. Sodium bicarbonate was administered three times. He subsequently remained ventilated in intensive care unit (ICU). Over the following week he survived sepsis, disseminated intravascular coagulation and myoglobinuria (with transient renal failure) attributable to rhabdomyolysis secondary to muscle necrosis. He later underwent diversion colostomy and disarticulating amputation of the left femur after several debridements. After 6 weeks on ICU he made an excellent recovery will full return of his mental abilities. In this case, the serial arterial blood samples obtained were reliable. The lactic acidosis observed was the result of profound tissue hypo-perfusion and its rate of clearance seems to have greater prognostic value than its peak or initial value. Several factors may have contributed to the patient's survival: rapid retrieval from the scene; early intubation with excellent subsequent oxygenation (thus avoiding the dangerous combination of hypoxia and acidosis with synergistic influence on cardiac depression) and limited initial fluid resuscitation in the emergency department with prompt surgical intervention and vigorous restoration of organ perfusion after surgical haemostasis. Immediate operative haemostasis, coupled with restricted fluid administration beforehand and vigorous restoration of organ perfusion afterwards is now replacing the old resuscitation paradigm. Perhaps this shift in practice has helped this patient to survive.
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PMID:Survival with an arterial pH of 6.57 following major trauma with exsanguinating haemorrhage associated with traumatic amputation. 1200 26

The pathophysiological basis of hemorrhage in dengue infections remains poorly understood, despite the increasing global importance of these infections. A large prospective study of 167 Vietnamese children with dengue shock syndrome documented only minor prolongations of prothrombin and partial thromboplastin times but moderate to severe depression of plasma fibrinogen concentrations. A detailed study of 48 children revealed low plasma concentrations of the anticoagulant proteins C, S, and antithrombin III, which decreased with increasing severity of shock, probably because of capillary leakage. Concurrent increases in the levels of thrombomodulin, tissue factor, and plasminogen activator inhibitor type 1 (PAI-1) indicated increased production of these proteins. Thrombomodulin levels suggestive of endothelial activation correlated with increasing shock severity, whereas PAI-1 levels correlated with bleeding severity. Dengue virus can directly activate plasminogen in vitro. Rather than causing true disseminated intravascular coagulation, dengue infection may activate fibrinolysis primarily, degrading fibrinogen directly and prompting secondary activation of procoagulant homeostatic mechanisms.
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PMID:Coagulation abnormalities in dengue hemorrhagic Fever: serial investigations in 167 Vietnamese children with Dengue shock syndrome. 1211 93

A central position in the development of systemic inflammation is played by activation of the vascular endothelium and monocyte- macrophage system. Both are associated with the formation of inflammatory cytokines, the primary mission of which is mobilization of the organism to cope with the infection. The so-called acute stage response develops with typical clinical manifestations and laboratory values. When it is impossible to stop the inflammation the syndrome of systemic inflammatory response develops with excessive activity of inflammatory cytokines and immune mechanisms. This apparently favourable system can be highly toxic for the organism and can lead to the syndrome of multiorgan failure, to disseminated intravascular coagulation, to depression of the myocardium, refractory vasodilatation, hypertension and septic shock. The compensatory antagonistic mechanism which develops due to the formation of anti-inflammatory cytokines leads sometimes to the development of a balanced state of immunity which is most favourable from the prognostic aspect. In case of their excess however immunodepression develops which is equally dangerous for the patient as excessive cytokine activity. From what has been said ensues the need of regular monitoring of patients with sepsis and thus also detailed investigation of their immune system.
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PMID:[Role of cytokines in the development of local and systemic inflammation and septic shock]. 1242 7

Tissue factor (TF) and lipopolysaccharide (LPS) are frequently used to induce disseminated intravascular coagulation (DIC) in experimental animal models. Although the pathophysiology of DIC may differ depending on which agent is used for induction, previous studies on models of DIC have not distinguished which DIC-inducing agent was used. In the present paper, we evaluate the characteristics of TF-induced and LPS-induced DIC using two types of DIC models, with special reference to selected hemostatic parameters and pathological findings within the kidney. Male Wistar rats were administered TF (3.75 U/kg; sustained infusion for 4 h) or LPS (30 mg/kg; sustained infusion for 4 h) via the tail vein, and blood sampling was performed at 0, 1, 3, 4, 5, 7, 9, 11, and 28 h. Judging from changes in the levels of thrombin-antithrombin complex, fibrinogen levels, and platelet counts, it is reasonable to conclude that the severity of both types of experimental DIC is similar with regard to hemostatic activation and consumption coagulopathy. A marked elevation in the level of D-dimer was noted without any organ dysfunction or much fibrin deposition in the kidney upon administration of TF. However, a markedly prolonged period of elevation in plasminogen activator inhibitor activity, a prolonged depression in antithrombin III activity, severe organ failure, and a markedly prolonged period of fibrin deposition in the kidney was observed following LPS administration. A modest number of the rats from the TF-induced DIC model died during the experimental period, whereas a large number of rats died during LPS-induced DIC, especially after 9 h. Since the time course of the pathophysiology differed remarkably among the TF-induced and LPS-induced DIC models in rats, we recommend that TF-induced and LPS-induced DIC be approached as distinct models in order to determine the implications of their experimental and clinical use.
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PMID:Pathophysiology of disseminated intravascular coagulation (DIC) progresses at a different rate in tissue factor-induced and lipopolysaccharide-induced DIC models in rats. 1269 43

Disseminated intravascular coagulation (DIC) is a syndrome characterized by systemic intravascular activation of coagulation, leading to widespread deposition of fibrin in the circulation. Recent knowledge on important pathogenetic mechanisms that may lead to DIC has resulted in novel preventive and therapeutic approaches to patients with DIC. Thrombin generation proceeds via the (extrinsic) tissue factor/activated factor VII route and simultaneously occurring depression of inhibitory mechanisms, such as antithrombin and the protein C and protein S system. Also, impaired fibrin degradation, due to high circulating levels of plasminogen activator inhibitor type-I, contributes to enhanced intravascular fibrin deposition. Strategies aimed at the inhibition of coagulation activation may theoretically be justified and have been found beneficial in experimental and initial clinical studies. These strategies comprise inhibition of tissue factor-mediated activation of coagulation or restoration of physiological anticoagulant pathways, by means of the administration of antithrombin concentrate or (activated) protein C.
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PMID:Therapeutic intervention in disseminated intravascular coagulation: have we made any progress in the last millennium? 1291 85

Sepsis almost invariably leads to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation (DIC). There is compelling evidence from clinical and experimental studies that DIC is involved in the pathogenesis of microvascular dysfunction and contributes to organ failure. In addition, the massive and ongoing activation of coagulation, may deplete platelets and coagulation factors, which may in turn cause bleeding. Recent insights into important pathogenetic mechanisms that may lead to DIC have resulted in novel preventive and therapeutic approaches to patients with sepsis and a derangement of coagulation. Thrombin generation proceeds via the (extrinsic) tissue factor/factor VIIa route and simultaneously occurring depression of inhibitory mechanisms, such as antithrombin III and the protein C system. Also, impaired fibrin degradation, due to high circulating levels of PAI-1, contributes to enhanced intravascular fibrin deposition. Supportive strategies aimed at the inhibition of coagulation activation may be justified on theoretical grounds and have been found to be beneficial in experimental and initial clinical studies. These strategies comprise inhibition of tissue factor-mediated activation of coagulation or restoration of physiological anticoagulant pathways, by means of the administration of antithrombin concentrate or recombinant human activated protein C.
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PMID:Sepsis and disseminated intravascular coagulation. 1476 Feb 11

A variety of clinical conditions may cause systemic activation of coagulation, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation (DIC). DIC consists of a widespread systemic activation of coagulation, resulting in diffuse fibrin deposition in small and midsize vessels. There is compelling evidence from clinical and experimental studies that DIC is involved in the pathogenesis of microvascular dysfunction and contributes to organ failure. In addition, the massive and ongoing activation of coagulation, may result in depletion of platelets and coagulation factors, which may cause bleeding. Recent understanding of important pathogenetic mechanisms that may lead to DIC has resulted in novel preventive and therapeutic approaches to patients with sepsis and a derangement of coagulation. Thrombin generation proceeds via the (extrinsic) tissue factor/factor VIIa route and simultaneously occurring depression of inhibitory mechanisms, such as antithrombin III and the protein C system. Also, impaired fibrin degradation, due to high circulating levels of the fibrinolytic inhibitor plasminogen activator inhibitor, type 1 (PAI-1), contributes to enhanced intravascular fibrin deposition. Interestingly, an extensive cross-talk between activation of inflammation and coagulation exists, where inflammatory mediators (such as cytokines) not only activate the coagulation system, but vice versa activated coagulation proteases and protease inhibitors may modulate inflammation through specific cell receptors. Supportive strategies aimed at the inhibition of coagulation activation may theoretically be justified and have been found beneficial in experimental and initial clinical studies. These strategies comprise inhibition of tissue factor-mediated activation of coagulation or restoration of physiological anticoagulant pathways, for example by means of the administration of recombinant human activated protein C.
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PMID:New treatment strategies for disseminated intravascular coagulation based on current understanding of the pathophysiology. 1500 Mar 46

Coagulation abnormalities, ranging from a simple fall in platelet count to full-blown disseminated intravascular coagulation, are a common occurrence in critically ill patients and have been associated with increased mortality. In sepsis, activation of the extrinsic coagulation pathway by tissue factor induces increased coagulation, and simultaneous depression of the inhibitory mechanisms of coagulation, and suppression of the fibrinolytic system results in a procoagulant state that may lead to the formation of microvascular thrombi disturbing organ microcirculation and promoting the development of organ dysfunction. Many inflammatory mediators are involved in the activation of coagulation, but many coagulation proteins are themselves actively involved in the inflammatory process. In this article, we explore the complex relationship between inflammation and coagulation and how improved understanding of this interaction has led to the development of new therapeutic agents for patients with severe sepsis.
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PMID:Coagulation in sepsis. 1514 67

Sixteen fatal dog envenomations by the snake Vipera palaestinae over a 14-y period are described. Most envenomations occurred during the late night hours in the warm months, and 8/16 dogs were bitten on the limbs. The most frequent clinical signs upon admission were soft tissue swelling and edema, local pain, depression, bleeding, lameness, dyspnea, and 6 dogs were in shock. Thrombocytopenia was present in 14/16 cases and increased hematocrit (13/16) and hemoglobin (9/16) concentration were the most common hematological abnormalities upon admission. Biochemical abnormalities included increased activities of muscle enzymes and alkaline phosphatase, hypocalcemia, and hypocholesterolemia. Creatine kinase activity was markedly increased in 2 dogs. During hospitalization serious complications in many dogs were disseminated intravascular coagulation, acute renal failure, seizures, cardiac arrhythmias, acute necrotizing pancreatitis and severe laryngeal edema; these required intensive and expensive therapies. Specific antivenin (10 ml) administered to 8/16 dogs did not prevent death. Glucocorticosteroids were given in 8 cases; however, their use was associated with complications. Four dogs suffered sudden death, 2 of which died 1-2 d after discharge. Necropsy performed on 3/16 dogs found soft tissue swelling and local bleeding at the envenomation sites as well as bleeding in several distal body organs and tissues.
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PMID:Fatal Vipera xanthina palestinae envenomation in 16 dogs. 1548 52

Acute zinc poisoning has been observed in dogs following the ingestion of metallic zinc objects. A 1 1/2-y-old female miniature bull terrier exhibiting anorexia, vomiting, depression, fever (39.9 C), icterus and intravascular hemolysis was diagnosed with acute zinc poisoning. Anemia, Heinz body production, azotemia and bilirubinemia were also evident. Abnormal pancreatic, hepatic and renal functions were also apparent. A radio opaque object was observed in the stomach. Based upon an elevated plasma zinc level of 28.6 ppm, a tentative diagnosis of zinc poisoning was made. Following surgical removal of the metallic zinc object, a blood transfusion and fluid therapy were given to restore the normal blood volume. Heparin, Cephazolin and Raniditine were also given, although chelation therapy was not provided. Zinc levels in the plasma declined in a steady fashion (half-life = 7.6 d). Complications, such as disseminated intravascular coagulation, chronic pancreatitis, renal or hepatic failure, were not observed. By 20 d post surgery, only mild elevation of liver enzymes was evident. Measurements of the half-life of zinc may provide a useful indication of prognosis and the success of treatment.
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PMID:Diagnosis and treatment of zinc poisoning in a dog. 1548 53


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