Permissive hypotension is only a penetrating trauma thing at the moment, although I have had some interesting discussions with Ken Mattox and some other luminaries of the surgical scene, and it would not surprise me if research wasn't carried out into permissive hypotension in blunt trauma as well. It's all about controlled versus not-controlled bleeding and bleeding into some cavities from blunt trauma may not be controlled at all.
This doesn't apply to traumatic brain injury however, as redcross has pointed out it is all about ICP, CPP and also cerebral blood flow (CBF). You can have high pressure with low flow depending on what the vessels are doing in the head (which is why we aim for a narrow window of EtCO2 after RSI in TBI)
Sepsis (which is Systemic Inflammatory Response Syndrome [SIRS] in the presence of a known or strongly suspected pathogen) is a clinical diagnosis. If a patient has 2 or more of the following:
Temperature >38C or less than 36C,
Heart rate > 90,
Resp rate > 20 (or PaCO2 <32mmHg)
White cell count abnormalities (high, low or lots of band cells - not that we will know this in the field unless it is an IFT)
then they have SIRS. These figures are from the surviving sepsis campaign guidelines for early goal directed therapy, whcih I think was published in NEJM off the top of my head.
SIRS can occur from a wide range of things like infection from bacterai, viruses or fungi, burns, trauma, pancreatitis, all sorts of things. The most common cause though is infection, and urosepsis is the most common type (followed by chest infection/pneumonia) It is also the second biggest killer in hospital, and can be quite subtle and thus not always easy to pick, particularly (as has been pointed out) in the elderly and the immunosuppressed.
Severe sepsis is the above criteria, plus signs of systemic hypoperfusion, such as hypotension, oliguria, altered mental status or organ dysfunction.
Septic shock is the same criteria, unresponsive to fluid resuscitation.
SIRS/Sepsis is a very complex interplay between the inflammatory cascade and the complement system and much of it is poorly understood. It is not the pathogen that causes the problems per se, but rather the host response to the pathogen.
One of the key pathological features in sepsis is that of microvascular dysfunction and leaky capillaries. These patients lose an enormous amount of fluid to third spacing and require very aggressive fluid resuscitation to normalise perfusion (which is one of the first steps in treating them). They also start making very large amounts of very poor quality urine, so as well as relative loss through fluid shifts, they have absolute fluid loss from the kidneys as well. The microvascular dysfunction will also lead to cold, shut down peripheries and the characteristic mottling of the skin that is seen in sepsis.
Myocardial dysfunction is often occuring in these patients as well, with something (probably NO) depressing myocardial function (stunning the myocardium) which exacerbates the shock state. If they patient survives, this myocardial stunning resolves itself without any long term cardiac issues, hence the term stunning or hibernation that is used.
Now, just to be a little more tricky, there can be two different shock states seen in these patients. One, cold shock, is reasonably obvious, has been discussed and is also generally late and bad as I think akulahawk and redcross pointed out. However the patient may also have what is known as warm shock, whcih is where things get a little trickier in identifying what is going on. Warm shock is a hyperdynamic shock state: that is the cardiac output remains normal or even elevated, however due to hugely increased metabolic demand, perfusion remains inadequate. There is a mismatch between supply and demand so that even though supply is normal or even raised, demand still outstrips it, and the organs remain poorly perfused.
These patients can present warm or normothermic (particularly in the patients who cannot mount a good fever such as the old, young or immunosuppressed) with flushed skin, bounding pulses and possibly normal blood pressures. However you need to take a good look at the diastolic BP. A wide pulse pressure (low diastolic) may be a clue that the patient is on their way to cardiovascular collapse, cold shock, and the coroner.
Where I work treatment would be (depending on the cirumstances, distance to hospital so on and so forth): Supplemental O2, possibly intubation (RSI)depending on the patients condition (we want to ensure adequate O2 delivery, and we also want to minimize workload and O2 demand), large bore IV access; aggressive fluid resuscitation; inotropic support if fluid resus alone does not improve perfusion. If we start inotropes (epinepherine/norepinepherine) we will also give low dose IV steroids as adrenal insufficiency is very common in these patients and the fact that we need to give exagenous catecholamines suggests that the endogenous ones aren't working so good no more. We may also give a 3rd generation cephalasporin like cefataxine of ceftriaxone, particularly if we suspect meningococcal sepsis, however we would weigh up the need to identify the pathogen in hospital with the need to acheive bacteriostasis before hand. With meningiococcal sepsis it doesn't matter if we are on the doorstep of the hospital, they get the antibugs.
Right, that's my typing done for the next 4 months. Hope I haven't bored you all to tears
