We all recall the adrenalin rush in the field or emergency center resuscitation of the post traumatic hypotensive patient. We raise the blood pressure with the "treatment de jour" and get the patient to the operating room or ICU, only to face a complication or death later. We swell with pride as we brag that the patient was normotensive when he/she left our care. For decades, we have refused to even question whether or not our aggressive hyper resuscitation contributed to that death or complication. I have lived long enough to recall a long list of the techniques "de jour" to elevate the blood pressure:

Permissive Hypotension Bibliography

Trauma-List discussion of Permissive Hypotension in Trauma Resuscitation

• Elevation of the legs or Trendelenberg position
• Use of plasma
• Use of vasopressors (I have seen a long list used)
• Use of MAST
• Use of aggressive crystalloid fluid administration
• Use of hypertonic saline
• Use of rapid infusors
• Use of interosseous infusion

This subject cannot be debated without raising issues on terminology, etiology, classification, anomalies, outcomes, and tradition. We are creatures of habit, repeating and re-repeating the lectures of our teachers who, we are reticent to acknowledge, may have clay feet. A short list of terms or concepts which are germane include: end points of resuscitation, adequacy of resuscitation, renal failure, cytokine activation, down regulation of leukocytes, capillary leak, "obligatory" third space fluid accumulation, crystalloids, colloids, oxygen consumption, oxygen delivery, pulse versus blood pressure correlations, classification of shock, oxygen debt, reperfusion injury, and many others. Each of these concept areas precipitates a huge secondary discussion. In this editorial I will address but a few.

Whether from blunt or penetrating etiologies, less than 10% of all trauma victims have immediate post traumatic hypotension. The true percentage is somewhere between 6-8%. Those who have an injury and are not hypotensive are beyond the scope of this editorial or resuscitation debates. Of that 6-8%, fully 1/3 are hypotensive from causes other than blood loss, such as pneumothorax, gastric dilatation, drug ingestion, etc. In all series, the survival rate in this group is virtually 100%, regardless of treatment or non-treatment. This group should be excluded from any debate on resuscitation. In virtually every series of post traumatic hypotension since the Crimean War, 1/3 of the hypotensive patients die of their wounds, rather early in the course of their evaluation and treatment. This figure is uncanily reproducible and all of our trauma system, trauma center, and trauma surgeon development have not been able to reduce this "non-survivable" trauma classification. This group also should be excluded from any debate regarding trauma resuscitation. Unfortunately, most resuscitation papers include both of these two non-germane groups in their post traumatic hypotension analysis.

Only 2-3% of the entire trauma population has post traumatic hypotension which relates to the resuscitation debate. In this group, much like patients with leaking abdominal aortic aneurysms, there is a natural compensation with a blood pressure between 70/- and 85/-, with moderate maintinence of cerebral status and urinary output. In this group of patients, elevation of blood pressure to pre injury levels and prior to operative control of the bleeding site results in progressive and repeated re-bleeding, now with decreased platelets and clotting factors in each aliquot of blood loss. Aggressive resuscitation in this group of patients results in the now oft-repeated "cyclic hyper-resuscitation." In this group of patients, such hyper-resuscitation results in sicker patients in the ICU, often developing abdominal compartment syndromes, renal failure, coagulopathies, respiratory insufficiency, and prolonged ICU and hospital stays. One could easily suggest that such complications and any associated "preventable" deaths are clearly iatrogenic from over aggressive fluid management.

Several interesting non-trauma anomalies should be considered in applying logic to this subject. Virtually every textbook and training manual for EMS, nursing, emergency medicine, critical care, and trauma stipulate that patients presenting hypotensive following a rupture of an abdominal aortic aneurysm need to be kept hypotensive until proximal control of the aorta above the area of leakage. This preserves what intravascular volume remains and prevents new additional blood loss from the site of the rupture. In patients with dissecting aneurysm, all health care workers are taught to administer afterload reducing agents, induce hypotension and limit any treatment that would elevate blood pressure until a treatment strategy has been developed, which might include operative control of the dissection. Patients with pulmonary contusion are treated all over the world with fluid restriction to prevent the lung from acting like a sponge and developing pulmonary insufficiency. Seasoned internists often treat patients with bleeding duodenal ulcers following the principle, "keep the blood pressure low and don't give blood. If you raise the blood pressure, more bleeding will ensue."

A number of descriptive terms have emerged the last 5 years, including, "permissive hypotension," "purposeful hypotension," "fluid restriction," "selective minimal resuscitation," and others. These terms reflect a new trend to keep the blood pressure at a level that prevents any fresh clot from being dislodged, resulting in rebleeding. In large animal "uncontrolled hemorrhage" models, the clot is "popped" at approximately 80/-. This extremely reproducible level of hypotension is identical to the observations made in patients with penetrating or blunt trauma. Thus, both animal researchers and trauma personnel have adopted the term "pop a clot," to be that phenomena which occurs with aggressive resuscitation. "Pop a clot" occurs at a blood pressure of 80/-. Therefore, the concept of permissive or purposeful hypotension in patients with posttraumatic hypotension has great logic. This logic is supported by large animal "uncontrolled hemorrhage models" in more than 10 laboratories worldwide. Furthermore, in the few existing controlled randomized prehospital resuscitation trauma trials , this logic is reproduced and supported. It appears that the physiologists of the first half of the 20th century were correct in writing that in acute post traumatic hypotension, that hypotension caused by a long list of neurologic, hormonal, humeral, and (now we know) cytokines, is actually protective. When we interfere with that "protection," secondary consequences ensue, including death, prolonged hospitalization, renal failure, and abdominal compartment syndrome, among others.

These comments beg another issue - the effectiveness and utility of our "end point measurement of resuscitation." Traditionally, one of the mainstays of evaluating "shock" and determining the effectiveness of a resuscitation effort has been the blood pressure. Many factors affect blood pressure, both low and high. The systolic blood pressure perhaps is one of the LEAST RELIABLE measures of shock or as an end point in resuscitation. Other end points do need to be and will be developed. One could even predict that the well informed resuscitationist of the next 10 years will disallow the use of a peripheral blood pressure recording device in assessing the level of hypoperfusion and adequacy of any treatment (or non-treatment).

Aggressive cyclic hyper resuscitation using crystalloid fluids also has other hazardous and reproducible physiological consequences. At approximately 750ml of administered crystalloid solution, cytokines are activated and an iatrogenic dilutional coagulopathy occurs. Platelets, prothrombin time, PTT, and thromboelastograph evaluations demonstrate statistically abnormal difference compared to normal values in patients who have post traumatic hypotension and have received no or limited fluid resuscitation. The cyclic hyper resuscitated patient arrives in the operating room from the ambulance dock or the emergency center, already with a preventable coagulopathy even before the first incision or onset hypothermia. AND, those who caused the coagulopathy were never aware that they presented the surgeon with a situation that made optimal therapy much more difficult.

One can then question clinical protocols for patients in the ambulance or in an emergency department. In the field or in the emergency center, blood pressures should basically be abandoned as a tool to determine level of shock or adequacy of resuscitation. The ability for the patient to cerebrate or for the attendant to detect the presence of a peripheral pulse (roughly equivalent to a blood pressure of 80/-) can be used as the major trigger point in therapy. No IV lines should be started if the patient cerebrates normally or if a line is started, the rate of fluid administration should be to keep open only. Some clinicians would desire an intravenous portal just to be available in case the patient "crashes." In the absence of cerebration, the examiner looks for the presence of a radial or pedal pulse. If present, no lines are started and transport or treatment is determined on the basis of diagnosed injury. Should the peripheral pulse be absent, a solution of an acceptably standard fluid is given in aliquots of 25 ml. until a pulse returns. At that point, NO ADDITIONAL FLUID is administered. This approach has been recently used with success in some international military campaigns.

The recommendations for evaluation and therapy do not differ from those used in the evaluation and treatment of a leaking contained abdominal aortic aneurysm. In truth, these two patient groups are very similar. For whatever reason, the same surgeons (and other medical specialists) have applied one set of logic sequences to one disease process and a totally different set of logic to another. If the resuscitation studies from Houston using prospective randomized evaluation of the value of Military Antishock Trousers, hypertonic saline, and deliberate restriction of aggressive crystalloid fluid resuscitation have done anything, these studies have caused us to scientifically analyze our unfounded doctrines. Some who read this editorial will find these comments to be refreshing and support "what my gut has told me for a long time." Others will be offended and insulted, because it undermines some traditional teachings from the armamentaria of those who need rigid rules to accomplish their missions.

Regardless of the reflex response, remember:

"There is nothing more difficult to take in hand, more perilous to conduct, nor uncertain in its success,
than to take the lead in the introduction of a new order of things,
for the innovator has for enemies all of those who have done well under the old,
and lukewarm defenders in all of those who may do well under the new."
- Machiavelli

Kenneth L Mattox, MD
Professor & Vice Chair,
Michael E. DeBakey Department of Surgery,
Baylor College of Medicine

Chief of Staff/Chief of Surgery
Ben Taub General Hospital
Houston, Texas, USA

trauma.org 8:1, January 2003