Rare cause of isolated severe coagulation failure in cirrhosis: traditional healing with fenugreek.

Patients with cirrhosis develop decompensation events during the natural history of the disease that encompass ascites, variceal bleeding, hepatic encephalopathy and jaundice. Coagulation failure, defined using the international normalised ratio, even though not a decompensation event, is important in patients with stratifying cirrhosis into those who require liver transplantation for long-term survival. Isolated coagulation failure in cirrhosis is rare and usually occurs with use of anticoagulants in the setting of vascular diseases. We reported the case of a patient with compensated cirrhosis in whom, isolated severe coagulation failure was found to be due to excessive use of fenugreek milk porridge as part of traditional healing. The coagulation failure was promptly reversed with avoidance of fenugreek and supplementation with vitamin K.

The impact of oral arsenic and all-trans-retinoic acid on coagulopathy in acute promyelocytic leukemia.

The aim of our study was to evaluate the impact of oral arsenic (the realgar-indigo naturalis formula, RIF) and all-trans retinoic acid (ATRA) on coagulopathy in acute promyelocytic leukemia (APL) compared with intravenous arsenic trioxide (ATO) and ATRA during induction. Mitoxantrone was added to all the patients at a dose of 1.4mg/m2 per day for 5-7 days. D-dimer levels, prothrombin time (PT), fibrinogen (Fbg) levels and the platelet count were comparably analyzed among 83 newly diagnosed APL patients treated with RIF (n=45) or with ATO (n=38). Since induction therapy with RIF and ATRA, the median levels of Fbg, PT and platelets were recovered to the normal range within 4days, 10days and 28days, respectively. The last day of platelet and plasma transfusion was day 12 (range: 0-24 days) and day 3 (range: 0-27 days), respectively. Among the 42 patients with a disseminated intravascular coagulation (DIC) score=4, the consumption of transfused platelets was less in the RIF group than that in the ATO group (P=0.037). In the 17 patients with a DIC score <4, prompt recovery of Fbg levels (P=0.028) was observed in the RIF group compared with that in the ATO group (P=0.401). RIF and ATO showed similar effects on the recovery of coagulopathy in APL patients. RIF had a potential beneficial effect in accelerating the recovery of thrombocytopenia and hypofibrinogenemia for subclinical DIC patients.

Improvement in blood fluidity by Kaempferia parviflora rhizome.

Improvement in blood fluidity leads to the prevention of various lifestyle-related diseases. A raw material for improving blood fluidity has been long desired in the research area of functional and supplemental foods. We successfully showed an improvement in blood fluidity by the Zingiberaceae plant, Kaempferia parviflora. The rhizome of the plant reduced the blood passage time through a micro slit using a disseminated intravascular coagulation model. The mechanism was attributed to the activation of fibrinolysis, as demonstrated by elongation of the euglobulin lysis time and an in-vitro fibrinolysis assay. The active principles were determined to be methoxyflavones. The results show that the rhizome of K. parviflora is a promising candidate preventive agent for treating lifestyle-related diseases.

A hyperbaric oxygen therapy approach to heat stroke with multiple organ dysfunction.

Here in we report the case of a patient who displayed a classic heat stroke with multiple organ dysfunction and hypercoagulable state resistant to conventional whole body cooling and antipyretic therapy, and necessitating the use of hyperbaric oxygen therapy (HBOT) to rescue him from death. A 49-year-old male laborer, suffering from heat stroke syndromes (e.g., hyperpyrexia, seizure and coma, and hypotension), was admitted to an emergency unit of a medical center hospital. The patient displayed multiple organ dysfunction with rhabdomyolysis, hepatic, renal, respiratory, and cerebral dysfunction, and disseminated intravascular coagulation (DIC). Both hyperpyrexia and multiple organ dysfunction were resistant to conventional treatment measures. HBOT was adopted to rescue the patient from heat stroke-induced death. Before HBOT, analyses of serum revealed hypercoagulable state or DIC as well as signs of rhabdomyolysis, and renal and hepatic failure. In addition, pulmonary edema, coma, hypotension, and hyperpyrexia occurred. HBOT was used successfully to combat these syndromes and to rescue the patient from heat stroke death. This case suggests that HBOT is useful for treatment of heat stroke with multiple organ dysfunction.

Disseminated intravascular coagulation (DIC).

Disseminated intravascular coagulation (DIC) is a condition that is seen in critical care areas in association with a number of precipitating conditions. DIC is often described as a paradoxical disease process of concurrent haemorrhage and thrombus formation, resulting in a range of clinical manifestations related to end organ ischaemia. This article will discuss the coagulation cascade as a basis for understanding the aetiology and pathophysiology of DIC. The discourse surrounding medical treatment will be highlighted to enable bedside nurses to understand the divergent orders they may receive from physicians for different patients. Management of the patient experiencing DIC will be approached from a multidisciplinary focus, as well as highlighting the specific nursing considerations and alternatives from an independent focus.

Hypothesis: disseminated intravascular inflammation as the inflammatory counterpart to disseminated intravascular coagulation.

We have identified a leukocyte activation syndrome that is occasionally associated with the transfusion of intraoperatively recovered erythrocytes. This syndrome appears to result from intravascular damage caused by leukocytes activated during the erythrocyte salvage process. We hypothesize that this syndrome is part of a larger disease grouping: disseminated intravascular inflammation (DII). DII is the analog of the coagulation disorder disseminated intravascular coagulation. In disseminated intravascular coagulation, the organ damage results from uncontrolled activation of the clotting pathway; in DII the damage is caused by leukocytes that have become activated by direct contact with bacteria or in rare instances--such as erythrocyte salvage--in the absence of bacteria and bacterial products. Recent studies of the hazards associated with intraoperative blood salvage indicate that activation of leukocytes can be achieved by exposure to activated platelets alone. If such activated leukocytes are reinfused along with the washed erythrocytes, widespread organ damage may result. The lung is the organ most severely affected by activated leukocytes. Adult respiratory distress syndrome is one outcome. It is likely that DII is a presently unrecognized pathophysiological process that complicates a variety of primary disease states and increases their lethality.

Acetic acid intoxication by rectal administration.

The enhanced toxicity of acid instilled directly into the rectum, without benefit of dilution and neutralization in the upper intestine, is evident in a case of acetic acid intoxication by accidental rectal administration of 50 mL of 9% acetic acid to a 5-year-old boy. The complications included necrosis of the colon, acute renal failure, acute liver dysfunction, disseminated intravascular coagulopathy (DIC) and sepsis.

The pathophysiologic role of fat in dysbaric osteonecrosis.

Dysbaric osteonecrosis (DON) can occur in humans and sheep after a single hyperbaric air exposure with inadequate decompression. The authors hypothesize that DON does not result from primary embolic or compressive effects of nitrogen bubbles on the osseous vasculature, but by secondary injury to the marrow adipose tissue by rapidly expanding nitrogen gas that triggers local, and possibly systemic, intravascular coagulation. A 28-year-old scallop diver remained at a depth of 92 feet in sea water for 4.5 hours on surface-supplied compressed air. Decompression sickness occurred after a no-stop ascent to the surface, and he died 70 minutes later. Autopsy showed multiple gas bubbles, not only within the great vessels, but in the fatty marrow of his femoral and humeral heads. Lipid and platelet aggregates were found on the surface of marrow bubbles. Fibrin-platelet thrombi were detected within dilated venous sinusoids adjacent to bubbles, and in veins, capillaries, and arterioles. Since pulmonary, renal, and intraosseous (subchondral) fat embolism and fibrin thromboses were observed, it is suggested that injured marrow adipocytes can release liquid fat, thromboplastin, and other vasoactive substances, which conceivably can also play a systemic procoagulant role in triggering disseminated intravascular coagulation and additional DON.

Amniotic fluid embolism associated with castor oil ingestion.

We report a case of an amniotic fluid embolism (AFE) causing a cardiorespiratory arrest associated temporally with ingestion of castor oil in a full-term normal pregnancy. Risk factors usually associated with AFE were not found in this patient.

[Activation of the blood kallikrein-kinin system in disseminated intravascular coagulation in rats. The significance of the pulmonary component and an attempt at correction with aspirin]. / Aktivatsiia kallikrein-kininovoi sistemy krovi pri disseminirovannom vnutrisosudistom svertyvanii u krys. Znachenie legochnogo komponenta i popytka korrektsii aspirinom.

It has been shown that the development in animals of disseminated intravascular coagulation (DIC) caused by long-term intravenous infusion of thrombin was accompanied by appreciable activation of the kallikrein-kinin system, being characteristic of acute pathological processes. In the initial stages of the process development, prekallikrein and kallikrein inhibitor were observed to be secreted from the lungs to arterial blood. Further development of DIC led to the depletion of the reserves of the kinin system. Pretreatment with a single low dose of acetylsalicylic acid considerably reduced the total animals' lethality and postponed blood kinin system activation determined by the development of DIC.

Left ventricular pump failure associated with diffuse coagulation in experimental intraoperative autotransfusion.

Autotransfusion of blood from the peritoneal cavity of pigs under a regimen of acid citrate dextrose solution 1:10 v/v for reservoir anticoagulation or systemic heparinization with 300 Iu/kg did not affect cardiac performance. Rapid deterioration of left ventricular pump performance was observed when low dose systemic heparin 100 Iu/kg was used. Evidence suggests that this is related to diffuse coagulation.

Participation of Hageman factor dependent pathways in human disease states.

Abnormalities of Hageman factor dependent pathways have been described in a wide variety of human disease states. Congenital deficiencies of factor XII (Hageman trait) prekallikrein (Fletcher trait) and high molecular weight kininogen (Williams, Fitzgerald and Flaujeac traits) although resulting in profound in vitro changes, do not cause in vivo difficulties. In contrast, deficiency of C1 esterase inhibitor (hereditary angioedema) results in significant morbidity and mortality. Acquired diseases may exhibit decreased synthesis of these three proteins in cirrhosis and dengue fever. In vivo activation of factor XII initiated pathways occur in septic shock, disseminated or localized intravascular coagulation, typhoid fever, polycythemia vera, hyperbetalipoproteinemia, coronary artery disease, nephrotic syndrome, transfusion reactions, hemodialysis and extracorporeal bypass. Activation of both the intrinsic system and tissue mediators contribute to the vasomotor phenomena in carcinoid syndrome and postgastrectomy dumping. Roles for factor XII, prekallikrein and kininogen have been suggested in gouty arthritis, allergic disorders and cystic fibrosis but the evidence is not yet convincing in these disorders.