Have a look at "Military medical revolution: Deployed hospital and en route care" in Journal of trauma 2012

Thanks Dr Herbert

Paramedics are taught to use presence or absence of a radial pulse as a rapid measure of adequate perfusion and therefore an indicator of blood loss

Stroke volume variation (SVV) in addition to heart rate, blood pressure and body temprature will determine the estimated blood loss volume. You may get an insite view by reading this article: http://211.144.68.84:9998/91keshi/Public/File/29/43-5/pdf/1-s2.0-S0041134511003629-main.pdf

What about heart rate? In a swine model of HS we find that critical reductions in blood volume triggers a prominent chronotropic response.

The answer to this is no different to the same question being asked inside a hospital, other than the interference by entrapment, ambient noise, clothing etc.

The fact remains that systolic blood pressure does not significantly drop until 30-40% of total blood volume is lost, with changes such as decreased pulse pressure occurring earlier, and heart rate and respiratory rate changes occurring even earlier.

Blood pressure maintenance is the results of a number of compensatory processes, including vasoconstriction, increased stroke volume, tachycardia etc, as oxygen saturations are the results of minute volume, gas transfer across the alveolar basement membrane, and oxygen content of alveolar gas. When we want to identify haemorrhage, respiratory failure or any other system failure, we need to spot it when the compensation is still continuing with varying degrees of effectiveness, not when compensation has failed, and blood pressure drops or oxygen saturations fall.

The key to assessment of clinical condition relies on systematic examination, focused history, a high index of suspicion for covert injury including haemorrhage, and finally repeated examinations of simple physiological variables and assessment of trend. The final key to assessment is to appreciate that all systems are interconnected, so that increasing haemorrhage causes evolving signs of poor perfusion in other systems, allowing pattern recognition.

Although pain, for instance, can cause a tachypnoea and a tachycardia, a similar picture after analgesia is much more predictive of underlying pathology. Decreased level or clouding of consciousness in concert with the preceding signs is haemorrhage until this is proven not to be true.

Having spent over a decade researching innovative noninvasive devices to use in early diagnostic strategies such as this, including CVS variability, ANS function etc, I have come to the conclusion that being a smart clinician and examining a patient in the way you were taught in school is superior to anything else.

Thanks colleagues. Although SVV is a good measure for fluid responsiveness of the patient but it is difficult to be performed in a prehospital setting and it does not give an estimation for volume of bleeding before initiating the therapeutic. Heart rate is readily available to assess in many patients, but there are many confounding factors when evaluating this parameter; confounding factors such as pain, distress, level of consciousness after a disaster, possible use of drugs or alcohol, etc could mimic the effects of blood loss during compensatory or non-compensatory levels of shock. As Dr Middleton wisely denoted, a comprehensive evaluation of the various parameters may gain the most reliable assessment; but as also wisely denoted by Kai Robinson, it needs certain levels of skillfulness of the care giver.

I think the current available methods during prehospital phase are kinds of subjective assessment, suffering from biases between various clinicians.

The main objective of Prehospital care of the patient with severe blood loss volume is to identify the presence or risk of hypoperfusion. Hypoperfusion is a lack of adequate oxygen delivery at a cellular level, due to decreased blood flow and oxygen delivery. Low BP is an indirect, imprecise measure of perfusion and tissue hypoxia may be present without low BP. Hypoperfusion triggers a systemic stress response, including tachycardia and peripheral vasoconstriction, but these responses are not exclusive signs of hypoperfusion. I think that the goal of volume therapy is to correct and prevent the risk of hypoperfusion. We are currently studying the role that tissue oxygen saturation (StO2) monitoring could play for the prehospital phase, in determining the volume status of patients and in guiding volume therapy efforts.

Dr Carchietti, I do agree with you. The definition of shock also emphasis on "inadequate tissue oxygenation" and thus it seems the question of "how much blood volume loss" should be corrected as "how much tissue oxygenation loss". However, what about those shock patients undergoing redistribution phenomenon? I mean, you may have a patient with ongoing uncontrolled internal hemorrhage; during the early phases of hemorrhage we may have a normal distribution of blood in various organs and evaluation of StO2 in each organ may represents the whole body status. As shock advances, redistribution phenomenon will be commenced, and various amounts of StO2 may happen in various body organs (e.g. higher in brain, lower in distal limbs). Is it possible to rely on available StO2 monitoring systems in prehospital phase, to guide the volume therapy efforts?

I can see that there is a great deal of academic excellence displayed in this discussion, but I think that this needs to be tempered with recognition of the clinical realities of the situation. There are good reasons that most ambulance services have adjusted their protocols to provide low volume resuscitation / hypotensive resuscitation / permissive hypotension, or whatever it is termed.

The fact is that we do not want much fluid resuscitation prehospital, or arguably even in the ED, when we have patients with significant covert haemorrhage, whether they are as described in clinical trauma texts as responders, transient responders or non-responders. We do need to maintain cerebral perfusion as a priority, followed by perfusion of other vital organs such as the heart, kidneys. liver and lungs, but then need to get them to a situation where they can be either be taken to surgery and the "tap turned off", haemorrhage stopped in some other way, such as via angio, or moved to a situation where they can be closely monitored, i.e. ICU.

The pathophysiological discussions are fascinating and valid, but in the end are not related to the prehospital realities which are - ABCDE primary survey (or CABCDE for catastrophic external haemorrhage), intervene in the systems you find the problem (open the airway when you find the obstruction rather than waiting until E is completed), and move quickly after extrication or loading to get to a hospital. Much prehospital morbidity and mortality has arisen from the mistaken perception that we need to concentrate on fluid resuscitation prehospital. We don't, we need to concentrate on getting them to (the right) hospital.

In 1989 Chudnofsky et al said 'We conclude that early administration of IV normal saline has no effect on hemodynamics or survival in this porcine hemorrhagic shock model simulating an urban prehospital care system' and in 1991 Bickell et al said 'From these data we conclude that, in this model of uncontrolled arterial hemorrhage resulting from abdominal aortotomy, rapidly administering lactated Ringer's solution intravenously significantly increases hemorrhage and death'. Almost all of the literature since this point has emphasised that not only does enthusiastic prehospital or even ED fluid resuscitation cause morbidity, or at least does not improve things, but moreover is not actually necessary in many instances.

Please have a look at a comprehensive set of abstract discussing this issue at http://www.trauma.org/archive/resus/permissivehypotension.html.

In my own prehospital practice, and in the ambulance service where I was medical director, the management of prehospital covert haemorrhage (i.e. high index of suspicion from mechanism + physiology / evidence of poor organ perfusion etc) was made very simple - titrate to the presence of a radial pulse (defined as approximately 70mmHg by Deakin et al) by giving 250ml boluses of crystalloid, stop fluid resuscitation if a pulse was present, and in all cases get them to definitive care asap. In the absence of signs of poor perfusion, and in this era of available alternatives to IV analgesia, such as intranasal opiates, there are strong arguments for not even delaying loading for cannulation but performing this in the back of the vehicle.

I suppose my point in all of this is that, however attractive StO2 monitoring, or other precise technological solutions to assessment of haemorrhage may be, in the prehospital phase at least they would add an unnecessary level of complexity because they would not really change the simple clinical management of someone in haemorragic shock.

Dr Siavash, also we have set immediately the question : "Is it possible to rely on available StO2 monitoring systems in prehospital phase, to guide the therapy volume efforts?"

Prospective studies demonstrated that changes in skeletal muscle StO2 showed a strong correlation with changes in DO2, blood base deficit (BD, and lactate). (J Trauma 2005, 58: 1119-1125)

Of course, I agree that the primary treatment of hemorrhagic shock is to control the source of bleeding as soon as possible and to replace fluid. The fluid replacement with attention to hypotensive resuscitation and expected evacuation time, is aimed toward normalization of tissue perfusion. I would stress that crystalloid fluid is the first choice for resuscitation in the absence of a radial pulse but, I think that crystalloid fluid is the first choice for resuscitation also in presence of a radial pulse with clinical evidence of poor tissue perfusion. In some cases, however, the clinical evidence may be a false evidence.

I agree that as shock advances, redistribution phenomenon will be commenced, but as we know, some organs, particularly the brain and kidneys, have remarkable autoregulation capacity. In conclusion I think that it is possible to rely on available StO2 monitoring systems in prehospital phase, to guide the volume therapy efforts, even more when must be ensured hypotensive resuscitation.

I disagree with Fabrizio. The sooner correct identification of volume loss can be made, the earlier appropriate intervention can begin. Better triage to the most capable center would also occur. In my humble opinion, poc ultrasound. Visit www.paramedicUltrasound.com

I do agree with you Peter

I agree with Fabrizio that the application of ATLS for HS classification can be misleading. However, you should not make the mistake opposite of oversimplifying the complexity of a proper treatment of patient bleeding. It 's true that you have to treat the patient and not the loss of blood, but this logo is misleading because it does not say how to can treat a hemorragic patient without treat bleeding.

To answer the question what can you do, not much right now but new treatments are on the way. Look up DARPA Foam. DARPA foam works in animals, human trials starting now.

Thanks Fabrizio, I agree with you that S/I is unreliable in many scenarios. Modified Shock Index may have some potential advantages over S/I.

Paul Middleton had also added valuable inputs on how to manage a prehospital patients in HS.

I agree that treatments have to be focused on the patient and not the blood loss, but the amount of blood loss volume is inevitably one of the major factors determining the HS patients’ general status. In fact losing blood is prior to formation of the detectable clinical signs. There is a time between these two events and we know that “time is trauma”.

The problem is that there are not pathognomonic signs for HS. Haemodynamic measures and other signs and symptoms of hemorrhagic shock may be affected by other confounding factors rather than the blood loss -such as head concussion, traumatic stress, previous usage of drugs or alcohol, medical conditions of a patient before accident, etc.. Furthermore, the confounding factors may have different effects on the various phases of shock.

Any of these factors may complicate the assessment and management of patients. This is specifically more complicated for patients in HS due to internal hemorrhage (such as liver hemorrhage or pelvic fx.). I think the current discussion should have been more focused on the ‘internal hemorrhage’, since this is where there is more problem in triage, volume therapy, etc.

The question is that whether to treat the symptoms, or the main problem, or both in the same time? I think, to make the decision we need some valuable information: how much blood loss? What is the stage of HS? How long the distance between the injury scene and the hospital? How much equipment we have? etc.

Furthermore, when we reached to the conclusion that the patient could not be survived until arrival to the hospital, we need reliable means for dealing with the main problem during the pre-hospital phase. Currently, almost all of the efforts to manage pre-hospital HS are focused on treating the symptoms and “maximum pressure on the speed pedal of the ambulance”.

Therefore besides current routine pre-hospital care, I think having a simple, rapid, accurate, and valid method for determining blood loss volume may have beneficial effects on assessing and managing patients in HS.

Thank you,

I do agree with your comments on SI. This is why I think SI is not reliable to determine the stage of HS. In my experience with lab animals using PowerLab Data Acquisition System with 0.001 mmHg accuracy, modified SI (which is based on the MABP) is more reliable than SI for determining HS stage, but with some inadequacies. The clinical benefits of estimating (or not estimating) blood loss volume are far beyond the scope of my question. Determining blood loss volume at the injury scene may have other advantages, even in forensic medicine or vet medicine.

Thank you Fabrizio,

as Holcomb stated: "Conventional prehospital care for hemorrhagic injury consists

of maintenance of the airway and ventilation; control of

accessible hemorrhage with bandages, direct pressure, and

occasionally tourniquets; and treatment of shock with intravenous

fluids. Despite this care, approximately 30–40% of

civilian and fully 90% of military casualties who die will do so

before they reach the hospital [2,3]. Unfortunately, the materials

and methods available to stop bleeding in the prehospital

care setting (gauze dressings, direct pressure, and tourniquets)

have not changed greatly in 2000 years [4]."

There are many questions remained unanswered about HS. and as we know, there is not a definite consensus about the ideal fluid for HS volume therapy. each fluid has some pros and cons. There are various protocols. According to my knowledge in basic medical researches on lab animals, I think permissive hypotension is a fair method for resuscitating HS patients, but needs special care to avoid ischemia/reperfusion injuries and other well-known consequences of hypotension in various body regions.

Great points and discussion, folks.

Being the curmudgeon that I am, here's a counterpoint: the volume of blood LOST is probably not as important as the volume (and degree of perfusion) of the blood REMAINING in the system. While pressure has been our metric since King Solomon was a corporal (chuckling), we now know that it is imperfect - catecholamine release, degree of pre-trauma dehydration and other factors can effect it independently of hemorrhage volume. Cardiac output (age, physical fitness and prior MI causing CHF all contributing / decrementing) also play.

What we need is a non-invasive, fairly accurate monitor that estimates remaining blood volume. Then we can fluid resuscitate to a specific (and minimally-adequate) target while speeding to surgery.

Thoughts?

I know this is a rather simplistic answer (but the original question was "the best means of estimating blood loss ie does the pt need more fluid, at the scene pre hosp ( simplisic & rapidly)" ), we use the method of raising the pt's legs to 30-45' if possible and see the haemodynamic responce - rise in BP then they require fluid no responce then they require inotropes. It is simple it works and as long as you look at the whole clinical picture before you Rx

I can understand your need to want to know the prehospital blood lost by the close relationship with the post lifesaving intervention ( hospital emergency room) as trauma and emergency surgery, amputation, blood transfusion, intubation, vasopressors…etc, that affecting the outcome.

Prehospital arena vital signs often fail to reflect the true severity of injury in trauma until compensatory mechanisms have been exhausted. But Heart Rate Variability (HRV) have indicated a superior diagnostic performance to predict poor outcome has been suggested to reflect impaired adaptation to physiologic stress and is an independent predictor of the need for Life Saving Interventions in prehospital chaotic medium.

Heart rate variability is generally considered to be a nonspecific

Indicator of health, mirroring the reaction plasticity of the autonomic

Nervous system. Loss of variability or regularization of the heart rate is

Believed to be a global index of poor health.

(NorrisPR et al.Heart rate Multiscale entropy at three hours predicts hospital mortality in 3,154 trauma patients. Shock2008;30(1):17–22)

(Peev MP et al. Real-time sample entropy predicts life-saving interventions after the Boston Marathon bombing. Journal of Critical Care 28(2013)1109.e1–1109.e4)

Mejaddam et al (Real-time heart rate entropy predicts the need for lifesaving

Interventions in trauma activation patients. J Trauma Acute Care Surg. 2013;75: 607-612)

have developed and miniaturized a device that allows

Instantaneous measurement of cardiac variability on a hand-held, portable monitor.

Saludos, Patricio

Fabrizio complete agreement regarding the heart rate .... but the Heart Rate Variability (HRV) is measured as a concept that the EKG R-R, which is affected by the autonome vegetative system and alters imperceptibly behaves long before heart rate and blood pressure.

Telemedicine? Scene Photo the blood loss?