Trauma and major haemorrhage

Author(s):  
Sheila Adam ◽  
Sue Osborne ◽  
John Welch

This chapter discusses the medical and nursing management of trauma patients from their initial assessment in the emergency department to their subsequent management in the critical care unit. Each section of the chapter covers a specific area of trauma and describes its underlying physiology, management, and associated complications. Injuries discussed include spinal, head, chest, cardiovascular, genitourinary, renal, abdominal, pelvic, musculoskeletal, burn injury, hypothermia, and drowning. Major complications, such as fat embolism syndrome, compartment syndrome, and rhabdomyolysis, are described in detail. The chapter also discusses the management of major haemorrhage and the complications of massive blood replacement therapy.

2015 ◽  
Vol 41 (01) ◽  
pp. 026-034 ◽  
Author(s):  
Satoshi Gando

Hemostasis and thrombosis in trauma patients consist of physiological hemostasis for wound healing and the pathological reaction of disseminated intravascular coagulation (DIC). Whole body trauma, isolated brain injury, and fat embolism syndrome, if extremely severe, can cause DIC and affect a patient's prognosis. Shock-induced hyperfibrinolysis causes DIC with the fibrinolytic phenotype, contributing to oozing-type severe bleeding. If uncontrolled, this phenotype progresses to thrombotic phenotype at the late stage of trauma, followed by microvascular thrombosis, leading to organ dysfunction. Another type of pathological hemostatic change is acute coagulopathy of trauma shock (ACOTS), which gives rise to activated protein C–mediated systemic hypocoagulation, resulting in bleeding. ACOTS occurs only in trauma associated with shock-induced hypoperfusion and there is nothing to suggest DIC in this phenomenon. This review will provide information about the recent advances in hemostasis and thrombosis in trauma and will clarify the pathogeneses of the pathological processes observed in trauma patients.


2011 ◽  
Vol 4 (3) ◽  
pp. 337 ◽  
Author(s):  
Nita D′souza ◽  
Kamran Farooque ◽  
Pramendra Agrawal ◽  
Babita Gupta ◽  
Chhavi Sawhney ◽  
...  

2020 ◽  
Vol 21 ◽  
pp. 475-480
Author(s):  
Miriam Alpert ◽  
Areg Grigorian ◽  
John Scolaro ◽  
James Learned ◽  
Matthew Dolich ◽  
...  

1996 ◽  
Vol 22 (S1) ◽  
pp. S108-S108
Author(s):  
M. Valente ◽  
G. Mancinelli ◽  
C. Münch ◽  
D. Corsi ◽  
G. Sambo ◽  
...  

2006 ◽  
Vol 17 (3-4) ◽  
pp. 75-79
Author(s):  
K. Mjahed ◽  
A. Bouhouri ◽  
Y. Alaoui ◽  
I. Tazi ◽  
A. R. El Adib ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Evgeni Brotfain ◽  
Leonid Koyfman ◽  
Ruslan Kutz ◽  
Amit Frenkel ◽  
Shaun E. Gruenbaum ◽  
...  

Fat embolism syndrome (FES) is a life-threatening condition in which multiorgan dysfunction manifests 48–72 hours after long bone or pelvis fractures. Right ventricular (RV) failure, especially in the setting of pulmonary hypertension, is a frequent feature of FES. We report our experience treating 2 young, previously healthy trauma patients who developed severe hypoxemia in the setting of FES. Neither patient had evidence of RV dysfunction on echocardiogram. The patients were treated with inhaled nitric oxide (NO), and their oxygenation significantly improved over the subsequent few days. Neither patient developed any cardiovascular compromise. Patients with FES that have severe hypoxemia and evidence of adult respiratory distress syndrome (ARDS) are likely at risk for developing RV failure. We recommend that these patients with FES and severe refractory hypoxemia should be treated with inhaled NO therapy prior to the onset of RV dysfunction.


Author(s):  
Luigi Vetrugno ◽  
Elena Bignami ◽  
Cristian Deana ◽  
Flavio Bassi ◽  
Maria Vargas ◽  
...  

Abstract Background The incidence of cerebral fat embolism (CFE) ranges from 0.9–11%, with a mean mortality rate of around 10%. Although no univocal explanation has been identified for the resulting fat embolism syndrome (FES), two hypotheses are widely thought: the ‘mechanical theory’, and the ‘chemical theory’. The present article provides a systematic review of published case reports of FES following a bone fracture. Methods We searched MEDLINE, Web of Science and Scopus to find any article related to FES. Inclusion criteria were: trauma patients; age ≥ 18 years; and the clinical diagnosis of CFE or FES. Studies were excluded if the bone fracture site was not specified. Results One hundred and seventy studies were included (268 cases). The male gender was most prominent (81.6% vs. 18.4%). The average age was 33 years (±18). The mean age for males (29 ± 14) was significantly lower than for females (51 ± 26) (p < 0.001). The femur was the most common fracture site (71% of cases). PFO was found in 12% of all cases. Univariate and multivariate regression analyses showed the male gender to be a risk factor for FES: RR 1.87 and 1.41, respectively (95%CI 1.27–2.48, p < 0.001; 95%CI 0.48–2.34, p < 0.001). Conclusions FES is most frequent in young men in the third decades of life following multiple leg fractures. FES may be more frequent after a burst fracture. The presence of PFO may be responsible for the acute presentation of cerebral embolisms, whereas FES is mostly delayed by 48–72 h.


2018 ◽  
Vol 6 ◽  
pp. 2050313X1878931 ◽  
Author(s):  
Siert TA Peters ◽  
Marieke J Witvliet ◽  
Anke Vennegoor ◽  
Birkitt ten Tusscher ◽  
Bauke Boden ◽  
...  

The fat embolism syndrome is a well-known complication in trauma patients. We describe a rare case of traumatic fat embolism that leads to paraplegia. A 19-year-old male motorcycle accident victim was presented to our hospital. After stabilization and trauma survey, he was diagnosed with bilateral femur fractures, a spleen laceration and a tear in the inferior vena cava, for which damage control surgery was performed. Post-operatively, the patient became paraplegic and developed a fluctuating consciousness, respiratory distress and petechiae. Fat embolism syndrome was considered as the most plausible cause of the paraplegia. The fat embolism syndrome is seen in approximately 1% of trauma patients, mostly those with bilateral fractures of the femur. Prevention of the syndrome depends on early stabilization of fractures. However, even with optimal care, this syndrome can still occur and may have dramatic consequences, as we demonstrate in this case.


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