The UK’s National Institute for Health and Clinical Excellence has issued updated guidance on the management of acute upper gastrointestinal bleeding.
The initial resuscitation section recommends haemostatic blood product resuscitation for unstable patients in line with massive transfusion practice in trauma.
A risk assessment is recommended using the Blatchford score pre-endoscopy at first assessment, and the full Rockall score after endoscopy.
Consider early discharge for patients with a pre-endoscopy Blatchford score of 0.
In non-varicesal haemorrhage, acid-suppression drugs (proton pump inhibitors or H2-receptor antagonists) before endoscopy are not recommended.
Terlipressin should be given to patients with suspected variceal bleeding at presentation and continued until definitive haemostasis has been achieved, or after 5 days, unless there is another indication for its use.
Prophylactic antibiotic therapy should be offered at presentation to patients with suspected or confirmed variceal bleeding.
Click image to go to interactive pathway on NICE website
I had the honour of attending trauma rounds with leading South African trauma surgeons today at Groote Schuur Hospital in Cape Town. This was the first day of an intense week-long trauma education tour that I have organised for myself and three of my Sydney HEMS colleagues.
A technique for haemorrhage control in penetrating trauma is to place a Foley catheter (FC) in the wound and inflate the balloon to try to achieve compression of bleeding vascular structures. This has been life-saving in many cases and buys time to get the patient to a trauma or vascular surgeon or in some cases an interventional radiologist. Catheter is knotted (black arrow) to occlude lumen. The wound is sutured around the catheter (white arrow).
First described by Gilroy and colleagues from Baragwanath Hospital in Johannesburg1, another, larger case series was subsequently reported by Cape Town’s Navsaria2, the Professor who conducted today’s trauma round I attended. In his paper he describes:
An 18- or 20-G FC was introduced into the bleeding neck wound. An attempt was made to follow the wound tract. The balloon was inflated with 5 ml of water or until resistance was felt. The FC was either clamped or knotted on itself to prevent bleeding through the lumen. The neck wound was sutured in two layers around the catheter. Continued bleeding around the catheter was an indication to proceed to surgery.
There were no deaths attributable to the use of FC balloon tamponade.
Prof. Navsaria describes the following algorithm for the subsequent investigation and management of these patients:
I’ve been teaching this technique as an option in penetrating trauma for a few years but have never actually done it for real. Nice to finally see examples of its successful implementation by people who do this all the time. I’ve seen four patients with Foleys sticking out of their necks in the first 24 hours of being here.
1. Control of life-threatening haemorrhage from the neck: a new indication for balloon tamponade. Injury. 1992;23(8):557-9
[EXPAND Click to read abstract]
We report the use of a Foley catheter, placed through the wound, to provide balloon tamponade of major bleeding from the neck and supraclavicular fossae. In 10 consecutive explorations for exsanguinating injury in these regions balloon tamponade was used eight times, and was judged to be fully effective in four patients, partly effective in one, and ineffective in three patients.
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2. Foley catheter balloon tamponade for life-threatening hemorrhage in penetrating neck trauma World J Surg. 2006 Jul;30(7):1265-8
[EXPAND Click to read abstract]
BACKGROUND: Foley catheter (FC) balloon tamponade is a well-recognized technique employed to arrest hemorrhage from penetrating wounds. The aim of this study was to review our experience with this technique in penetrating neck wounds and to propose a management algorithm for patients with successful FC tamponade.
METHODS: A retrospective chart review (July 2004-June 2005 inclusive) was performed of patients identified from a prospectively collected penetrating neck injury computer database in whom FC balloon tamponade was used. The units’ policy for penetrating neck injuries is one of selective nonoperative management. All patients with successful FC tamponade underwent angiography. A venous injury was diagnosed if angiography was normal. Ancillary tests were performed as indicated. Removal of the FC was performed in the OR.
RESULTS: During the study period, 220 patients with penetrating neck injuries were admitted to our unit. Foley catheter balloon tamponade was used in 18 patients and was successful in 17 patients. Angiography was positive in 3 patients, all of whom underwent surgery. The FC was successfully removed in 13 patients at a mean of 72 (range 48-96) hours. One patient bled after removal of the catheter, mandating emergency surgery.
CONCLUSION: Foley catheter balloon tamponade remains a useful adjunct in the management of selective patients with penetrating, bleeding neck wounds.
Do you have access to thromboelastometry in your Emergency Department? Further research by some of the first discoverers of acute traumatic coagulopathy involved using this tool to identify acute traumatic coagulopathy at 5 mins and predict the need for massive transfusion. Measures of coagulopathy more familiar to ED staff such as the INR took longer or (when point-of-care testing was employed) were less accurate.
OBJECTIVE: To identify an appropriate diagnostic tool for the early diagnosis of acute traumatic coagulopathy and validate this modality through prediction of transfusion requirements in trauma hemorrhage.
DESIGN: Prospective observational cohort study.
SETTING: Level 1 trauma center.
PATIENTS: Adult trauma patients who met the local criteria for full trauma team activation. Exclusion criteria included emergency department arrival >2 hrs after injury, >2000 mL of intravenous fluid before emergency department arrival, or transfer from another hospital.
INTERVENTIONS: None.
MEASUREMENTS: Blood was collected on arrival in the emergency department and analyzed with laboratory prothrombin time, point-of-care prothrombin time, and rotational thromboelastometry. Prothrombin time ratio was calculated and acute traumatic coagulopathy defined as laboratory prothrombin time ratio >1.2. Transfusion requirements were recorded for the first 12 hrs following admission.
MAIN RESULTS: Three hundred patients were included in the study. Laboratory prothrombin time results were available at a median of 78 (62-103) mins. Point-of-care prothrombin time ratio had reduced agreement with laboratory prothrombin time ratio in patients with acute traumatic coagulopathy, with 29% false-negative results. In acute traumatic coagulopathy, the rotational thromboelastometry clot amplitude at 5 mins was diminished by 42%, and this persisted throughout clot maturation. Rotational thromboelastometry clotting time was not significantly prolonged. Clot amplitude at a 5-min threshold of ≤35 mm had a detection rate of 77% for acute traumatic coagulopathy with a false-positive rate of 13%. Patients with clot amplitude at 5 mins ≤35 mm were more likely to receive red cell (46% vs. 17%, p < .001) and plasma (37% vs. 11%, p < .001) transfusions. The clot amplitude at 5 mins could identify patients who would require massive transfusion (detection rate of 71%, vs. 43% for prothrombin time ratio >1.2, p < .001).
CONCLUSIONS: In trauma hemorrhage, prothrombin time ratio is not rapidly available from the laboratory and point-of-care devices can be inaccurate. Acute traumatic coagulopathy is functionally characterized by a reduction in clot strength. With a threshold of clot amplitude at 5 mins of ≤35 mm, rotational thromboelastometry can identify acute traumatic coagulopathy at 5 mins and predict the need for massive transfusion.
Emergency physicians from Minnesota (and graduates of the amazing Hennepin Emergency Medicine Residency) describe a patient who developed cardiac tamponade after an ablation procedure for dysrhythmia. Attempts at pericardiocentesis by both emergency and cardiology staff were hindered by clotted blood, and so a left lateral thoracotomy was performed in the ED due to loss of pulse and lack of immediate availability of an operating room. A limited pericardial incision was made to allow drainage of sufficient blood to relieve tamponade while avoiding catastrophic blood loss from the underlying lesion, which turned out to be a 1.5-cm hole in the right ventricular outflow tract. The patient made a full recovery.
Cardiac dysrhythmias are a common problem in the United States. Radiofrequency ablation is being used more frequently as a treatment for these diagnoses. Although rare, serious complications such as cardiac tamponade have been reported as a result of ablation procedures. Traditionally, emergency department (ED) thoracotomy has been reserved for cases of traumatic arrest only. We report a case of a successful modified ED thoracotomy in a patient with postablation cardiac tamponade and subsequent obstructive shock who failed intravenous fluid resuscitation, pressor administration, and multiple attempts at pericardiocentesis. In this case, a modified approach was used to incise the pericardium. Although this was associated with large blood loss, we believed that using the traditional method of completely removing the pericardium would have resulted in uncontrolled hemorrhage. Instead, our method led to successful resuscitation of the patient until definitive care was available. A smaller pericardial incision than is traditionally used during ED thoracotomy deserves further consideration and research to determine whether and when it may be most useful as a temporizing treatment of cardiac tamponade when other methods have failed.
A small study on normal volunteers examined reversal of the new oral anticoagulants, Rivaroxaban and Dabigatran.
Rivaroxaban is a Factor Xa inhibitor and Dabigatran is a direct thrombin inhibitor. Image from "Australian Prescriber" website. Click for Original
We should note that this was a study on the reversal of effects on various coagulation tests, not on reversal of bleeding, which is what we would be interested in for our ED/critical care patients.
Nevertheless, it’s helpful to note that prothrombin complex concentrate appeared to reverse the effects of Rivaroxaban, but not of Dabigatran.
Background Rivaroxaban and dabigatran are new oral anticoagulants that specifically inhibit factor Xa and thrombin, respectively. Clinical studies on the prevention and treatment of venous and arterial thromboembolism show promising results. A major disadvantage of these anticoagulants is the absence of an antidote in case of serious bleeding or when an emergency intervention needs immediate correction of coagulation. This study evaluated the potential of prothrombin complex concentrate (PCC) to reverse the anticoagulant effect of these drugs.
Methods and Results In a randomized, double-blind, placebo-controlled study, 12 healthy male volunteers received rivaroxaban 20 mg twice daily (n=6) or dabigatran 150 mg twice daily (n=6) for 2½ days, followed by either a single bolus of 50 IU/kg PCC (Cofact) or a similar volume of saline. After a washout period, this procedure was repeated with the other anticoagulant treatment. Rivaroxaban induced a significant prolongation of the prothrombin time (15.8±1.3 versus 12.3±0.7 seconds at baseline; P<0.001) that was immediately and completely reversed by PCC (12.8±1.0; P<0.001). The endogenous thrombin potential was inhibited by rivaroxaban (51±22%; baseline, 92±22%; P=0.002) and normalized with PCC (114±26%; P<0.001), whereas saline had no effect. Dabigatran increased the activated partial thromboplastin time, ecarin clotting time (ECT), and thrombin time. Administration of PCC did not restore these coagulation tests.
Conclusion Prothrombin complex concentrate immediately and completely reverses the anticoagulant effect of rivaroxaban in healthy subjects but has no influence on the anticoagulant action of dabigatran at the PCC dose used in this study.
So what do we do about bleeding patients who are taking Dabigatran? If you haven’t seen it already, take a look at this video from HQMEDED.com made by my heroes at Hennepin County Medical Centre:
Acute traumatic coagulopathy (ATC) is present in up to 25% of major trauma patients by the time they arrive in hospital. A predictive tool called the coagulopathy of severe trauma (COAST) score was retrospectively derived and then prospectively validated in major trauma patients in the state of Victoria, Australia. The definition of ATC was INR > 1.5 (1.0–1.3) or aPTT of > 60 s (25–38 s) on hospital presentation.
The study claims that a subgroup of patients with acute traumatic coagulopathy can be accurately identified based on simple observations in the pre-hospital phase or immediately on presentation to the ED, and that this could improve the feasibility of prospective interventional studies. Perhaps this will lead on to evaluation of pre-hospital tranexamic acid or even blood products?
At the cutoff score of ≥3, 40 coagulopathic patients would have been missed with 60 patients correctly predicted. The authors argue that while the low sensitivity of the score missed these coagulopathic patients, they had significantly better outcomes (and contained a significantly higher proportion of patients with isolated severe head injury).
Introduction: The inability to accurately predict acute traumatic coagulopathy (ATC) has been a key factor in the low level of evidence guiding its management. The aim of this study was to develop a tool to accurately identify patients with ATC using pre-hospital variables without the use of pathology or radiological testing.
Methods: Retrospective data from the trauma registry on major trauma patients were used to identify vari- ables independently associated with coagulopathy. These variables were clinically evaluated to develop a scoring system to predict ATC, which was prospectively validated in the same setting.
Results: There were 1680 major trauma patients in the derivation dataset, with 151 patients being coagulopathic. Pre-hospital variables independently associated with ATC were entrapment (OR 1.85; 95% CI: 1.12–3.06), temperature (OR 0.60; 95% CI: 0.60–0.72), systolic blood pressure (OR 0.99; 95% CI: 0.98–0.99), abdominal or pelvic content injury (OR 2.0; 95% CI: 1.27–3.12) and pre-hospital chest decompression (OR 4.99; 2.77–8.99). The COAST score was developed, scoring points for entrapment, temperature <35 ◦ C, systolic blood pressure <100 mm Hg, abdominal or pelvic content injury and chest decompression. Prospectively validated using 1225 major trauma patients, a COAST score of ≥3 had a specificity of 96.4% with a sensitivity of 60.0%, with an area under the receiver operating characteristic curve of 0.83 (0.78–0.88).
Conclusions: The COAST score accurately identified a group of patients with ATC using pre-hospital obser- vations. This predictive tool can be used to select patients for inclusion into prospective studies examining management options for ATC. Mortality in these patients is high, potentially improving feasibility of outcome studies.
The overall effect of the antifibrinolytic drug tranexamic acid on outcome from major trauma was assessed in the CRASH-2 trial, reported here and here. Its effect on a nested cohort of 270 patients from the trial who had traumatic brain injury has now been published1.
Previous evaluation in nontraumatic subarachnoid haemorrhage patients showed tranexamic acid to be associated with cerebral ischaemia, whereas in CRASH-2 (in which a lower dose of tranexamic acid was used) there was a trend to fewer ischaemic lesions as well as smaller haematoma growth and decreased mortality. None of these outcomes were statistically significant so further research is warranted.
An accompanying editorial2 states:
…the CRASH-2 study also justifies a re-evaluation of the possible benefit of low dose short term TXA in patients with other types of intracranial haemorrhage. Many patients with aneurysmal subarachnoid haemorrhage still have to wait for one or two days before the aneurysm is occluded. In addition, at least 30% of patients with spontaneous intracerebral haemorrhage experience substantial haematoma growth in the first 24 hours after the onset of the haemorrhage. As well as the CRASH-2 trial we therefore need new trials investigating short course low dose TXA in patients with aneurysmal subarachnoid haemorrhage and intracerebral haemorrhage.
It looks like considerable enthusiasm for this drug will be around for a while. I look forward to more outcome data, particularly in regard to this challenging group of patients with traumatic and non-traumatic intracranial bleeding.
OBJECTIVE: To assess the effect of tranexamic acid (which reduces bleeding in surgical patients and reduces mortality due to bleeding in trauma patients) on intracranial haemorrhage in patients with traumatic brain injury.
METHODS: A nested, randomised, placebo controlled trial. All investigators were masked to treatment allocation. All analyses were by intention to treat. Patients 270 adult trauma patients with, or at risk of, significant extracranial bleeding within 8 hours of injury, who also had traumatic brain injury.
INTERVENTIONS: Patients randomly allocated to tranexamic acid (loading dose 1 g over 10 minutes, then infusion of 1 g over 8 hours) or matching placebo.
MAIN OUTCOME MEASURES: Intracranial haemorrhage growth (measured by computed tomography) between hospital admission and then 24-48 hours later, with adjustment for Glasgow coma score, age, time from injury to the scans, and initial haemorrhage volume.
RESULTS: Of the 133 patients allocated to tranexamic acid and 137 allocated to placebo, 123 (92%) and 126 (92%) respectively provided information on the primary outcome. All patients provided information on clinical outcomes. The mean total haemorrhage growth was 5.9 ml (SD 26.8) and 8.1 mL (SD 29.2) in the tranexamic acid and placebo groups respectively (adjusted difference -3.8 mL (95% confidence interval -11.5 to 3.9)). New focal cerebral ischaemic lesions occurred in 6 (5%) patients in the tranexamic acid group versus 12 (9%) in the placebo group (adjusted odds ratio 0.51 (95% confidence interval 0.18 to 1.44)). There were 14 (11%) deaths in the tranexamic acid group and 24 (18%) in the placebo group (adjusted odds ratio 0.47 (0.21 to 1.04)).
CONCLUSIONS: This trial shows that neither moderate benefits nor moderate harmful effects of tranexamic acid in patients with traumatic brain injury can be excluded. However, the analysis provides grounds for further clinical trials evaluating the effect of tranexamic acid in this population
1. Effect of tranexamic acid in traumatic brain injury: a nested randomised, placebo controlled trial (CRASH-2 Intracranial Bleeding Study) BMJ. 2011 Jul 1;343:d379 (free text available)
2. Tranexamic acid for traumatic brain injury BMJ. 2011 Jul 1;343:d3958
Replacement of clotting factors in bleeding trauma patients seems to be of benefit, but are coagulation factor concentrates safer than fresh frozen plasma? This retrospective study suggests they might be; prospective studies are recommended.
INTRODUCTION: Clinical observations together with recent research highlighted the role of coagulopathy in acute trauma care and early aggressive treatment has been shown to reduce mortality. METHODS: Datasets from severely injured and bleeding patients with established coagulopathy upon emergency room (ER) arrival from two retrospective trauma databases, (i) TR-DGU (Germany) and (ii) Innsbruck Trauma Databank/ITB (Austria), that had received two different strategies of coagulopathy management during initial resuscitation, (i) fresh frozen plasma (FFP) without coagulation factor concentrates, and (ii) coagulation factor concentrates (fibrinogen and/or prothrombin complex concentrates) without FFP, were compared for morbidity, mortality and transfusion requirements using a matched-pair analysis approach. RESULTS: There were no major differences in basic characteristics and physiological variables upon ER admission between the two cohorts that were matched. ITB patients had received substantially less packed red blood cell (pRBC) concentrates within the first 6h after admission (median 1.0 (IQR(25-75) 0-3) vs 7.5 (IQR(25-75) 4-12) units; p CONCLUSION: Although there was no difference in overall mortality between both groups, significant differences with regard to morbidity and need for allogenic transfusion provide a signal supporting the management of acute post-traumatic coagulopathy with coagulation factor concentrates rather than with traditional FFP transfusions. Prospective and randomised clinical trials with sufficient patient numbers based upon this strategy are advocated.
The impact of fresh frozen plasma vs coagulation factor concentrates on morbidity and mortality in trauma-associated haemorrhage and massive transfusion. Injury. 2011 Jul;42(7):697-701
In some circles, ‘wuntwuntwun’ is in danger of becoming the new dogma of trauma fluid replacement (ie. 1 unit of plasma and 1 unit of platelets for every unit of red cells). Since it takes longer to thaw some plasma than it does to throw in some O negative packed red cells, some really sick patients may be dead before they get the plasma, biasing comparisons that show a reduced mortality in patients who were still alive to receive plasma. This ‘survivor bias’ has been suggested as a reason that high plasma:red cell ratios are associated with mortality reduction, although this has been challenged.
The survivor bias explanation receives some new support by the following (small) study from Journal of Trauma: BACKGROUND: In light of recent data, controversy surrounds the apparent 30-day survival benefit of patients achieving a fresh frozen plasma (FFP) to packed red blood cell (PRBC) ratio of at least 1:2 in the face of massive transfusions (MT) (≥10 units of PRBC within 24 hours of admission). We hypothesized that initial studies suffer from survival bias because they do not consider early deaths secondary to uncontrolled exsanguinating hemorrhage. To help resolve this controversy, we evaluated the temporal relationship between blood product administration and mortality in civilian trauma patients receiving MT. METHODS: Patients requiring MT over a 22-month period were identified from the resuscitation registry of a Level I trauma center. Shock severity at admission and timing of shock-trauma admission, blood product administration, and death were determined. Patients were divided into high- and low-ratio groups (≥1:2 and<1:2 FFP:PRBC, respectively) and compared. Kaplan-Meier analysis and log-rank test was used to examine 24-hour survival. RESULTS: One hundred three patients (63% blunt) were identified (66 high-ratio and 37 low-ratio). Those patients who achieved a high-ratio in 24 hours had improved survival. However, severity of shock was less in the high-group (base excess: -8.0 vs. -11.2, p=0.028; lactate: 6.3 vs. 8.4, p=0.03). Seventy-five patients received MT within 6 hours. Of these, 29 received a high-ratio in 6 hours. Again, severity of shock was less in the high-ratio group (base excess: -7.6 vs. -12.7, p=0.008; lactate: 6.7 vs. 9.4, p=0.02). For these patients, 6-hour mortality was less in the high-group (10% vs. 48%, p<0.002). After accounting for early deaths, groups were similar from 6 hours to 24 hours. CONCLUSIONS: Improved survival was observed in patients receiving a higher plasma ratio over the first 24 hours. However, temporal analysis of mortality using shorter time periods revealed those who achieve early high-ratio are in less shock and less likely to die early from uncontrolled hemorrhage compared with those who never achieve a high-ratio. Thus, the proposed survival advantage of a high-ratio may be because of selection of those not likely to die in the first place; that is, patients die with a low-ratio not because of a low-ratio.
The authors state “The current study underscores the need for well-designed prospective studies to address the important question of which ratio results in improved survival and stresses the importance of timing of blood product administration as this may impact survival.” Improved survival after hemostatic resuscitation: does the emperor have no clothes? J Trauma. 2011 Jan;70(1):97-102
Bleeding from an established tracheostomy (ie. ‘late bleeding’, as to opposed to peri-operative bleeding that is more common and often benign) may occur because of erosion of blood vessels in and around the stoma site. This is more likely if there has been infection of the stoma site. Such bleeding may settle with conservative management. More worryingly, however, is the prospect of such bleeding being the result of erosion of a major artery in the root of the neck where there has been pressure from the tracheostomy tube itself or the cuff tube. Most commonly, this erosion occurs into the right brachiocephalic artery (also known as the innominate artery), resulting in a tracheo-innominate artery fistula. This situation may be heralded in the preceding hours by a small, apparently insignificant, sentinel bleed. Bleeding from such a fistula will be massive. THIS IS A LIFE-THREATENING EMERGENCY and so decisions need to be rapidly made.
Call for help– senior medical and nursing staff, other health professionals with tracheostomy care skills (e.g. respiratory therapist, physiotherapist).
Clear airway – blood clots may need to be suctioned.
Replace blood products as required
Bleeding may be temporarily reduced or stopped by applying finger pressure to the root of the neck in the sternal notch, or by inflating the tracheostomy tube cuff (if present) with a 50ml syringe of air. This inflation should be done slowly and steadily to inflate the balloon to a maximum volume without bursting it. Depending on the type and size of the tracheostomy tube this may be anywhere between 10 and 35 ml.
Urgent referral for surgical exploration must now be made, if not already done so. In addition to an ENT or maxillofacial surgeon, it may be necessary to get help from a vascular surgeon. Sometimes, the damage can only be repaired utilising cardio-pulmonary bypass, and so a cardiothoracic surgeon may also be needed to help.
Consider palliation – it is well recognised that fatalities occur in this situation, and that this may be the mode of death for some patients with head and neck cancers
