An excellent review of the current British military practice to prevent and treat the acute coagulopathy of trauma shock (ACoTS) describes pathophysiology and treatment options and offers an algorithm for management. Key components of the system (when indicated according to their algorithm) outlined include:
Pre-hospital damage control shock resuscitation by a forward medical team, consisting of RSI with reduced dose thio or ketamine with suxamethonium or rocuronium, large bore sublclavian access, and early use of warmed blood products
1:1:1 packed red cells, fresh frozen plasma, and platelets,
Cryoprecipitate
Tranexamic acid
Recombinant activated factor VII
Permissive hypotension aiming for a systolic BP of 90 mmHg, using blood products and avoiding vasopressors according to a ‘flow rather than pressure’ philosophy
Avoiding hypothermia by giving warmed blood products and employing active patient warming methods
Buffering acidosis using Tris-hydroxymethyl aminomethane (THAM), which may be superior to bicarbonate by not affecting minute ventilation or coagulation, and maintaining its efficacy in hypothermic conditions
Minimising hypoperfusion with an anaesthetic strategy that provides effective analgesia and vasodilation, using high dose fentanyl and a low concentration volatile agent
Using fresh whole blood for resistant coagulopathy
International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding have been published. Here is a summary of the recommendations; a link to the full text document is at the bottom of this page.
Prognostic scales are recommended for early stratification of patients into low- and high-risk categories for rebleeding and mortality.
Blood transfusions should be administered to a patient with a hemoglobin level of 70 g/L or less.
In patients receiving anticoagulants, correction of coagulopathy is recommended but should not delay endoscopy.
Promotility agents should not be used routinely before endoscopy to increase the diagnostic yield.
Selected patients with acute ulcer bleeding who are at low risk for rebleeding on the basis of clinical and endoscopic criteria may be discharged promptly after endoscopy.
Preendoscopic PPI therapy may be considered to downstage the endoscopic lesion and decrease the need for endoscopic intervention but should not delay endoscopy (the observed lesion downstaging attributable to PPI therapy before endoscopy may be even more beneficial in situations in which early endoscopy may be delayed or when available endoscopic expertise may be suboptimal).
Early endoscopy (within 24 hours of presentation) is recommended for most patients with acute upper gastrointestinal bleeding.
A finding of a clot in an ulcer bed warrants targeted irrigation in an attempt at dislodgement, with appropriate treatment of the underlying lesion.
The role of endoscopic therapy for ulcers with adherent clots is controversial. Endoscopic therapy may be considered, although intensive PPI therapy alone may be sufficient.
Epinephrine injection alone provides suboptimal efficacy and should be used in combination with another method.
Clips, thermocoagulation, or sclerosant injection should be used in patients with high-risk lesions, alone or in combination with epinephrine injection
Routine second-look endoscopy is not recommended.
An intravenous bolus followed by continuous-infusion PPI therapy should be used to decrease rebleeding and mortality in patients with high-risk stigmata who have undergone successful endoscopic therapy.
Patients should be discharged with a prescription for a single daily-dose oral PPI for a duration as dictated by the underlying etiology.
Most patients who have undergone endoscopic hemostasis for high-risk stigmata should be hospitalized for at least 72 hours thereafter.
Where available, percutaneous embolization can be considered as an alternative to surgery for patients for whom endoscopic therapy has failed.
Patients with bleeding peptic ulcers should be tested for H. pylori and receive eradication therapy if it is present, with confirmation of eradication.
Negative H. pylori diagnostic tests obtained in the acute setting should be repeated
In patients with previous ulcer bleeding who require an NSAID, it should be recognized that treatment with a traditional NSAID plus PPI or a cyclooxygenase-2 (COX-2) inhibitor alone is still associated with a clinically important risk for recurrent ulcer bleeding.
In patients with previous ulcer bleeding who require an NSAID, the combination of a PPI and a COX-2 inhibitor is recommended to reduce the risk for recurrent bleeding from that of COX-2 inhibitors alone.
In patients who receive low-dose ASA and develop acute ulcer bleeding, ASA therapy should be restarted as soon as the risk for cardiovascular complication is thought to outweigh the risk for bleeding.
In patients with previous ulcer bleeding who require cardiovascular prophylaxis, it should be recognized that clopidogrel alone has a higher risk for rebleeding than ASA combined with a PPI.
International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding Ann Intern Med. 2010 Jan 19;152(2):101-13 (Full Text)
A volunteer study showed that tourniquets were just as effective at occluding distal blood flow measured by doppler signal when placed below the elbow or knee compared with above those joints. A makeshift windlass tourniquet, a rubber tube tourniquet, and a blood pressure cuff were all effective. Digital ‘pressure point control’ failed to maintain control of brachial or femoral artery flow. Tourniquets Revisited J Trauma. 2009 Mar;66(3):672-5
Haemostatic resuscitation of trauma patients, using high ratios of fresh frozen plasma (FFP) to packed red cells (PRBC), is growing in popularity as a result of military experience. Few data support the practice in civilian trauma. It is possible that some of the demonstrated mortality benefit is a result of survival bias: it takes time to obtain FFP, by which time severely injured patients may be dead. Therefore, those that receive large ratios of FFP:PRBC must have survived long enough to receive it. In other words FFP doesn’t lead to survival, but survival leads to FFP. Some evidence in favour of this explanation is provided on a study of 134 patients in the Journal of Trauma. Reanalysing data to correct for survival bias made an apparently significant survival benefit from high FFP:PRBC ratios go away. An interesting paper, although unlikely to dissuade us from paying attention to coagulopathy in trauma. I suspect the debate on optimal blood product resuscitation will be around for a while. The Relationship of Blood Product Ratio to Mortality: Survival Benefit or Survival Bias? J Trauma. 2009 Feb;66(2):358-62
