Hemostasis and Thrombosis in Extreme Temperatures (Hypo- and Hyperthermia)

Levi, Marcel

doi:10.1055/s-0038-1648231

Cited by 36 publications

(23 citation statements)

References 47 publications

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“…Since it is well established that HIV increases the risk of antepartum and intrapartum infection, it is plausible that body temperature was a marker of intrapartum infection, such as chorioamnionitis, which has been shown to facilitate uterine atony and PPH . There is some evidence that body temperature in extreme situations may influence coagulation . However, higher body temperature may also affect uterine contractility, in turn amplifying uterine atony, known to be a major risk factor for PPH .…”

Section: Discussionmentioning

confidence: 99%

“…35 There is some evidence that body temperature in extreme situations may influence coagulation. 36,37 However, higher body temperature may also affect uterine contractility, in turn amplifying uterine atony, known to be a major risk factor for PPH. 38 We speculate that the combination of febrile infection in the setting of HIV, paired with higher severity of anemia (compared to HIV-negative patients) may exacerbate PPH, thereby resulting in a high mortality rate.…”

Section: Discussionmentioning

confidence: 99%

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Maternal death and postpartum hemorrhage in sub‐Saharan Africa – A pilot study in metropolitan Mozambique

Lancaster

Barnes

Correia

et al. 2020

Research and Practice in Thrombosis and Haemostasis

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Background Maternal mortality in sub‐Saharan Africa is approximately 500 to 1000 per 100 000 births (vs. approximately 5‐20 in developed countries). Postpartum hemorrhage (PPH) is deemed responsible for 30% to 50% of the deaths. Objective To study PPH, risk factors, and mortality in metropolitan Mozambique to inform future studies and intervention strategies. Materials/Methods Retrospective cross‐sectional data extraction from all charts available to us (n = 495) recording deliveries between January and June 2018 at Maputo Central Hospital. Data included age, maternal survival, HIV status, parity, delivery mode, complications, vital signs, laboratory values, and maternal/fetal data. PPH was determined by charted diagnosis, interventions for hemorrhaging, placental abruption, transfusion, or blood loss. Autopsy reports from all deceased patients (n = 35) were examined. Results Median age was 29 years with 17% HIV prevalence. Risk factors for PPH (frequency, 12%) included parity (adjusted odds ratios (AORs) for 3+ versus nulliparity, 7.20 (95% confidence interval [CI], 2.46‐21.10), gestation length (AOR, 0.86; CI, 0.81‐0.92 per week), and body temperature (AOR, 1.10; CI, 1.04‐1.16 per 0.1°C). Maternal mortality was strongly associated with PPH (AOR, 5.22; 95% CI, 2.26‐12.08) and HIV (AOR, 11.66; 95% CI, 4.72‐28.78). Laboratory values (n = 241) were available from mothers experiencing complications (approximately 50%). Anemia (prevalence 54%) was a strong predictor of PPH with an inverse relationship between hemoglobin levels on admission (AOR, 0.62; 95% CI, 0.50‐0.77 per g/dL higher hemoglobin) and the probability of later suffering from PPH. Mothers who died following PPH had lower median hemoglobin (6.2 g/dL) than mothers who survived (9.2 g/dL). Protocols to estimate peripartum blood loss were not used; antifibrinolytics and/or cryoprecipitate were unavailable. Conclusion Postpartum hemorrhage is a serious problem even in metropolitan areas of sub‐Saharan Africa, and anemia influenced bleeding and death substantially. To address this problem, it is critical to raise awareness and region‐specific prevention and intervention protocols.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Maternal death and postpartum hemorrhage in sub‐Saharan Africa – A pilot study in metropolitan Mozambique

Lancaster

Barnes

Correia

et al. 2020

Research and Practice in Thrombosis and Haemostasis

View full text Add to dashboard Cite

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“…In cases of mild to moderate hypothermia platelet function is affected but in severe hypothermia clotting factor enzyme activity is affected as well [3]. The optimal temperature to maintain balanced hemostasis is 37.5 C [5]. Whelihan et al found on in vitro experimentation that severe hypothermia leads to delay in thrombin generation secondary to delayed thrombin initiation; reduction on initial fibrinogen consumption and factor XIII activation [3].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, hypothermia affects global hemostasis and decreases the rate of clot formation and lysis without affecting the clot strength. Several studies in patients undergoing cooling after cardiac arrest or as part of laboratory studies have shown impairment of platelet function, and hypocoagulability [5]. In the setting of hypothermia, intracardiac thrombus as a direct consequence has not been described in the literature.…”

Section: Discussionmentioning

confidence: 99%

Accidental Hypothermia Associated with Intracardiac Thrombi

Acosta

Noman

Gohar

et al. 2019

Cureus

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Accidental hypothermia and thrombosis are rarely associated and encountered. A 66-year-old male and 62-year-old male were both admitted with accidental hypothermia. Patient 1 had a rectal temperature of 28.5 °Celcius (C). After 1 day of hospitalization, he developed worsening shortness of breath due to worsening pulmonary edema. Further investigation with echocardiogram showed large left ventricular thrombi as well and global hypokinesis and apical akinesis. Patient 2 had a rectal temperature of 28.5 °C, he was also discovered to have a multifactorial shock. Echocardiogram for shock evaluation showed small apical thrombus as well as global hypokinesis. Hypothermia has been associated with hypocoagulability rather than hypercoagulability secondary to platelet dysfunction and clotting factor enzyme derangements. Moreover, hypothermia has also been associated with myocardial dysfunction that could have predisposed the development of intracardiac thrombi. Further research needs to be done to help better understand these possible association.

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“…3,4 Heatstrokerelated coagulation activation and fibrin formation are clinically known as disseminated intravascular coagulation (DIC). [5][6][7][8] Previous studies have shown that DIC has been observed in 22 to 28% of the patients with heatstroke 9,10 and in 9.3% of the patients with heat-related illnesses. 10 A previous study has also shown that the presence of DIC was an independent strong prognostic factor for in-hospital mortality among patients with heatstroke.…”

mentioning

confidence: 99%

Treatment with Antithrombin or Thrombomodulin and Mortality from Heatstroke-Induced Disseminated Intravascular Coagulation: A Nationwide Observational Study

Ohbe

Isogai

et al. 2019

Semin Thromb Hemost

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Heatstroke-induced disseminated intravascular coagulation represents potential targets for specific intensive treatments. However, the effect of antithrombin or thrombomodulin treatment remains uncertain. Using a large nationwide inpatient database in Japan, this study aimed to evaluate whether treatment with antithrombin or thrombomodulin could reduce mortality among patients with heatstroke-induced disseminated intravascular coagulation. Using the Japanese Diagnosis Procedure Combination inpatient database from April 2014 to March 2017, we identified heatstroke patients who developed disseminated intravascular coagulation. We allocated patients who started treatment with antithrombin or thrombomodulin within 2 days after admission to the treatment group and allocated others to the control group. A primary outcome was in-hospital mortality. We used a doubly robust analysis to ensure the robustness of our findings. We also conducted two sensitivity analyses for thrombomodulin versus others and antithrombin versus others. We identified 1,606 eligible patients during the 81-month study period. Of these, 556 (35%) received antithrombin or thrombomodulin. The doubly robust analysis demonstrated that in-hospital mortality was significantly lower among patients in the treatment group than among those in the control group (risk difference −6.5%; 95% confidence interval: −12 to −1.4%). In-hospital mortality was significantly lower in patients with thrombomodulin than in others (risk difference −5.5%; 95% confidence interval: −9.5 to −1.6%). There was no significant difference in in-hospital mortality between patients with antithrombin and others (risk difference −4.2%; 95% confidence interval: −9.3 to 0.9%). Treatment with recombinant human thrombomodulin may be associated with lower in-hospital mortality among patients with heatstroke-induced disseminated intravascular coagulation.

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Hemostasis and Thrombosis in Extreme Temperatures (Hypo- and Hyperthermia)

Cited by 36 publications

References 47 publications

Maternal death and postpartum hemorrhage in sub‐Saharan Africa – A pilot study in metropolitan Mozambique

Maternal death and postpartum hemorrhage in sub‐Saharan Africa – A pilot study in metropolitan Mozambique

Accidental Hypothermia Associated with Intracardiac Thrombi

Treatment with Antithrombin or Thrombomodulin and Mortality from Heatstroke-Induced Disseminated Intravascular Coagulation: A Nationwide Observational Study

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