Sepsis

Now, in this talk we want to start thinking about the basic ideas of

sepsis

. The modern idea of ​​

sepsis

dates back to about 1992 and has been taken up by the Sepsis Survival Campaign and the guidelines have been modified so it is now a well-established concept, but it dates back to 1992 and the source of sepsis. The one we are thinking about begins with infection, so we notice that we have infection now. The infection will lead to acute inflammation, so there will be inflammation. The infecting microorganisms are not supposed to be there. They start a guest. inflammatory response and you probably know that that can lead to the local effects of heat pain redness swelling loss of function the local effects of inflammation heat pain redness swelling loss of function but how are these effects mediated?

What are the inflammatory mediators? Well, there are several inflammatory processes. mediator, you may have heard of prostaglandins for example, so there are inflammatory mediators produced by damaged tissue, so components are released from damaged tissue, these interact with tissue-based enzymes and are generated inflammatory mediators, so we get inflammatory mediators and it is these inflammatory mediators that actually generate the local characteristic of inflammation and the damaged cells will also release cytotypes, so there are inflammatory mediators and there are cytokines. Now cytokines are small proteins, they are small peptide units, polypeptide units and they communicate between cells, so the movement of cells is a movement of cytotypes, literally, so these are chemical agents produced. by a cell detected by another cell in essence they are a bit like the endocrine system they are the cytotypes they are messenger molecules now if there are many cytotypes and inflammatory mediators these will go to the body fluids and we will be distributed systemically now also if there is infection, normally infection bacterial or viral, these are antigens that the body recognizes as foreign and are detected by the white blood cells, the Luc coytes, in particular, all the lucaites, I was really going to say particularly. the macros, the monocytes, but the lucaites will generally recognize the antigen as foreign and when they do, the lucaites will also produce cytokines, so you can see that we are going to get cytokines from the damaged tissues along with inflammatory mediators and also the inflammatory mediators.

Inflammation are becoming inflamed as a result of the infection and the cytocytes released by the lucaites are also going to pass into the body fluids, so now we have body fluids that contain cytokines that circulate systemically and it is these types of cytocytes in the body fluids. that can lead to systemic inflammatory response syndrome systemic inflammatory response syndrome is systemic systemic because it affects the entire body inflammatory because it is caused by inflammatory mediators and proinflammatory cytotypes these cytotypes will be a proinflammatory systemic inflammatory response syndrome so we want to see for what we have this systemic inflammatory response syndrome, so we have noticed that there will be these cytotypes, there will be cinemas from here, cytotypes from here to types, from here I have a pen that works, so there will be There will be two batches of cyto and these will affect various tissues For example, they will affect the bone marrow, so the cytokines will affect the bone marrow, they will also affect the hepatocytes, the liver cells, they will also affect the hypothalamus in the brain and they will also affect the upper parts of the brain and we will also see that These effects of cytokines will increase the energy demand of the body, so some of the clinical characteristics of systemic inflammatory response syndrome will be caused by the effect of cytotypes on the hepatocytes of the hypothalamus of the bone marrow and the brain and others are going to be generated by this greater demand for energy that the body has, so what we want to do in the next slides is look at the medulla of the hypothalamus.

The cells and the brain see why this leads to increased energy demand and derive the clinical features of sepsis and this acute phase response, so sepsis is really an acute phase response, now the acute phase response. It does not have to be caused purely by an infection. is probably better at that, but it can also be caused by tissue injury, surgery or trauma in some neoplastic conditions, it can be an immunological reaction, but in this talk we will look at it as caused by an infection, particularly a bacterial infection, now sepsis is a combination of the infection with the systemic response to that infection and we have seen that sepsis, the infectious part of sepsis, will be recognized by the white blood cells, the Luc coytes, and they will respond by producing cytotypes and, in fact, the Cytotypes can also be produced by damaged tissue and one of the effects that the cytotypes will have is that the cytotypes will migrate to the bone marrow, particularly the red bone marrow, and the cytotypes will stimulate the red bone marrow and stimulate the red bone marrow to produce more white blood cells, so there will be lucco yosis.

Now some people now write one of the sepsis criteria. One of the ways we can recognize this systemic reaction that causes sepsis is that there will be more than 12,000 white blood cells per millimeter of blood, so if we have more than 12,000 white blood cells per cubic millimeter of blood, that is an indication of sepsis, like less than 4,000 cells per millimeter of blood because while cytokines stimulate the bone marrow to produce luccocytosis to produce more white blood cells. Sometimes the effects of the infection that caused sepsis can release toxins that actually inhibit the bone marrow and inhibit the bone marrow's ability to produce white blood cells effectively, so if someone's cells have more than 12,000 or less than 4,000, that is. actually, it is a criterion of sepsis, we should start thinking about the possibility of sepsis, in that case even the normal number of white blood cells could not be 5 to 10,000.

Now the cytokines greatly stimulate the bone marrow to produce a lot of white blood cells, so what we find is that we get immature forms of white blood cells. This is what hematologists call this a shift to the left, so there is an immature form, so normally the bone marrow would like to take a little longer to clear out your white blood cells, but the cytotypes say that No, there is an emergency situation here. there is an infection, we have an infection that causes sepsis, get these white blood cells out now to fight the infection because they are essential to fight the infection, so if someone has low levels of white blood cells, the lucenia, this is a life-threatening condition because does not have them. you have the white blood cells to fight the infection, this is the body mobilizing its effect mobilizing its response now that there is a serial infection, you may get an increase in the number of neutrophils because nutrifil are particularly good at fighting bacterial infection with their lobe nuclei usually three or four, they are small granules in the cytoplasm, so neutrophilia increases the number of neutrophils because they are particularly good at fighting bacterial infections, which means that if you find a neutrophilia it is probably caused by a bacterial infection , but there could also be lymphophilia.

Lymphocytosis is very often stimulated by a viral infection, so Luc coyos just means an increase in white blood cells in general, so neutrophil lymphocytes, of course, eosinophils are all types of lucites, but neutrophilia points towards bacterial lymphocytosis that points towards a viral infection or eosinophils are another type, very often these increase. in parasitic infections or in allergic conditions, asthma for example, so remember that if the cells are low, this could be what we call sepsis lucenia, a reduction in the number of white blood cells and that is very dangerous, very often it is caused by endotoxins.

Gram negative organisms now have other causes, it could be caused by cytotoxic chemotherapeutic agents or steroids or aplastic anemia or radiation, but in this case we are thinking of a lucenia caused by sepsis due to the inhibitory effect of the toxins of the bacteria in the marrow. bone itself, so we have a sepsis criterion that we can use to judge whether sepsis is present or not, the white blood cell count is greater than 12,000 or less than 4,000, but this occurs due to the effect of cytotypes on the bone. The marrow and cytotypes are there because the infection has induced the white blood cells to produce more cytokines, but the purpose of this is to produce luccocytosis so that we have more white blood cells to fight the infection.

More white blood cells can produce more antibodies. lymphocytes in particular will produce antibodies, more white blood cells such as neutrophils will carry out phagocytosis and we will attack this infection increasing the body's probability of survival, but it is interesting to note that this is mediated by cytokines, so the bone marrow knows that It's time to produce more. lucaites is because the cytotypes carry that message, the cytotypes, which are these little peptide chemical messengers, and as I said before, it's very analogous to the endocrine system that carries chemical messages throughout the body. It says, "Let's fight this infection with your share." of the brain just above the nasal passages now, for the purposes of this talk, we will look at its thermoregulatory properties.

It is the temperature control center, so it is the POS responsible for thermoregulation, it regulates body temperature but it also plays a role. part in the initiation of the fear response produces hormone release factors from the anterior pituitary gland produces oxytocin and antidiuretic hormone has a sexually diamoric core and actually a difference between men and women tells us when it is time to start sexual activity you already know sexual desire sexual activity when the time comes to stop having sexual activity when the time comes to stop start eating when the time comes to stop eating with a cator center and the same for drinking generates thirst and tells us when we've had enough to drink, there are many homeostatic functions going on, but what we're seeing right now is that the cytotypes will affect the hypothalamus and the hypothalamus when stimulated by the sepsis-induced cytotypes will generate prostaglandins, so Cytokines stimulate the hypothalamus to produce prostaglandins and these prostaglandins affect the neurotransmitters in the hypothalamus now the hypothalamus has a set point, it tries to maintain the body temperature around 37 degrees centigrade but the neurotransmitters stimulated by the glans prostagland will increase that set point of adjustment. the set point maybe up to 38 39 even 40° centigrade now, what will happen here?

Let's imagine a graph here, so there is a graph. Now let's imagine that this line here is the set point of the hypothalamus, that's the set point, let's say 37° centigrade. and the body temperature that we will draw in yellow will follow that if the body is too hot there will be cooling mechanisms, if the body is too cold there will be warming mechanisms, but when the bacterial infection stimulates the production of cytotypes, the hypothalamus will produce prostaglandins that will stimulate the neurotransmitters to increase the set point, so this red line is the set point of the hypothalamus, so it will now increase, so the set point will now increase to maybe 39° centigrade, so the set point setting will now increase.

Now this is good because the immune system works best at warm temperatures, it works best at febrile temperatures, pyrexial temperatures, but going back to history we can see that that is the set point. Now the set point has increased, but the body temperature remains alone. 37 then we need to warm it up so that the hypothalamus induces warming mechanisms until again the set point and the actual body temperature are together now when the body temperature increased we call it pyrexia or fever or we say the person has fever. everything means the same and this is good because the immune system works better at pyrexial temperatures, so the immune system now works much better here at 39° Celsius than at 30.7° Celsius and also most bacteria feel very less comfortable and much less able to reproduce at 39 instead of 37° centigrade, so Ju is as if lucco yosis is part of the defensive response, so this part of the defensive response is necessary to improve immune function of the body, but can you see in this? point here where the set point rises to that point there where the body temperature reaches that period of time there throughout that period of time can you see the yellow line that is the body temperature is less than the set point that means? the hypothalamus is trying to warm us up and in that case, due toBecause the set point is high, the body temperature will feel cold and we will have chills, we will use charcoal, we will try to wrap ourselves in blankets and we may shiver and shake and try to warm up that is called RoR, so RoR is the body's shivering attempt to increase your temperature, but then when we get rid of the temperature and we feel it when we get rid of the infection if the infection goes away.

In the body, the set point can drop back down to normal again at 37 and hopefully the body temperature will follow that drop, follow the set point, so it will be back to approximately where the set point is. Now this is actually very dramatic if you take antifreeze, acetaminophen, non-steroidal anti-inflammatory drugs, all of these inhibit prostaglandins, they inhibit prostaglandins, so the prostaglandins no longer cause the change in neurotransmitters, which increases the set point, therefore, the set point will decrease dramatically. Therefore, if someone has a fever and has a high level. temperature and we take off the antifreeze covers, but can you see that means her body temperature is going down now this is good, it's going down here because the person is better, but if it goes down before the person gets better, if it went down there, well , the set point would go down first, so the set point would go down? and the body temperature would follow, can you see?

So we are lowering the body temperature, but we know that the immune system works best at these pyrexial temperatures, so by giving antipyretics we are actually reducing the efficiency of the immune system because this pyrexial response. The febal response is not an accident, it is the cytotypes which deliberately stimulate the hypothalamus to produce the Landin plastic to change the neurotransmitters and increase the SE point, so as a general principle, if someone has a bacterial infection, it is better not to give them antipyretics because the immune system works better at these pyrexial temperatures, so this is another defense mechanism facilitated by cytotypes in response to the presence of the bacterial infection that stimulates the hypothalamus to generate a pyrexial response to increase the efficiency of the immune system.

We're thinking about the effects of cytokines induced by the presence of sepsis on the liver, liver cells, hepatocytes in particular, but just before we do that I want to point out that cytokines will affect muscle tissue and cause muscle catabolism. catabolism catabolism a catabolic process is one that breaks down things so that muscle proteins become amino acids, so the cytotypes induced by the septum will begin to break down the proteins in the muscle and release amino acids and the cytotypes also induced by the cytotypes will generate start . synthesizing acute phase proteins and these can increase by factors of 100 or hundreds in the blood now you don't normally feel hungry when you are sick you have anorexia can you see that amino acids are necessary to supply the building?

It blocks acute phase proteins, so during this emergency period, when the body is threatened by a life-threatening infection, the amino acids in the muscle are broken down and go to the liver and the liver converts them into acute phase proteins, so which, for example, you might have heard of CRP, this is C-reactive protein or you may have heard of another serum amloid protein or SAA, so both CRP and SAA are acute phase proteins. Now, what you're going to do is imagine that this is a bacterial cell. here what we don't want now sometimes the macres and the monocytes that would like to pho phage cyos this bacterial cell do not always recognize it so the PCR and the AAA the serum amalo protein will stick to the bacteria and label them therefore, these are called um the word for this is opsonin, they are opsonins, they will opsonize the bacteria and label them loud and clear for the destructive white blood cells to come and phagocytose them.

It's a bit like waving a red flag saying, "Me." I'm here come eat me increases the efficiency of the phagocytosis process, so again we can see that these acute phase proteins, CRP, CRP and serum ameloid protein are increasing the efficiency of the immune system. Now there is another acute phase protein. Fibrinogen is necessary, of course, for blood clotting, but it will actually tend to clump quite a few of the red blood cells that form together and, what these are, it will tend to clump groups of R red blood cells together in this way into clumps. in R A columns and these are going to be heavier than individual red blood cells, so this is what will increase the arthritic sedimentation rate, which is another clinical feature of sepsis and infection, so the presence of roua and increased arthritic sedimentation rate may also indicate sepsis. now in the short term the presence of these acute phase proteins is good they will do things like activate complement and you may remember that complement can form a membrane attack protein so stimulate complement so that complement can form a membrane attack protein, so if it's a bacterial cell, the complement is basically like tubes that go through it and will cause water to come in and the cell will burst the membrane attack proteins, so basically the complement it kills bacteria so it's good because the short term effects of the acute phase proteins will stimulate complement and the acute phase proteins will.

They also eliminate cellular debris and eliminate free radicals and neutralize protic enzymes and they are good, but if they remain there for a long time we can suffer the long-term effects of inflammation, but basically we see that these acute phase proteins, like Lucco yosis, like pyrexia, are improving the immune function of the body, so the effect of sepsis-induced cytotypes on the cell causes acute phase proteins to be facilitated by amino acids available through catabolism muscle tissue, but actually this is one of the reasons why if people are starving, if people are immunocompromised, they are much less able to generate an immune response and less able to produce immunoglobulins, as well as their lymphocytes, which are less capable of producing immunoglobulins. which of course are antibodies, so if someone is starving and has a protein shortage, their protein stores in the body are diminished, especially in long-term starvation, their immune system will be very compromised because they can't produce the acute phase proteins and cannot produce the antibodies to fight the infection, now the combination of cytotypes and inflammatory insults and possible hypoperfusion of the organ reduce the blood supply to the organ can reduce the efficiency of the lungs, liver, kidneys and also the brain. can affect the brain with its brain stem and cerebellum, so there can be cytotype effects in the brain and together these cause what we call AMS altered mental status, so AMS as a feature of sepsis now has some pretty obvious effects that we might notice that some people are sleepy, we call that suance and that's good because it means that the body rests and can recover from the infection and the inflammatory effects of the infection and of course Mala, remember to the lovely old doctor who gave me my introductory medical lecture. a long, long time ago and when you were describing the clinical features of almost every condition, you were talking about General Mala, the patient just doesn't feel well, you have Mala, you don't feel well and usually this is associated with anorexia, the patient doesn't I don't feel like eating so anorexia means a reduction in appetite now anorexia nervosa um actually it's a mistake Noma these patients are not anorexic they don't have a small appetite they can have a pretty deep appetite they just don't eat for various psychological reasons and um, there can be more serious effects and some patients can develop a delirium, delirium, they can become Delirium, this is like an acute state of confusion, so delirium is like an acute state of confusion and there can be disorientation over time. and the place of the person and especially in older people.

People can become very difficult to deal with because they are delusional, they don't know where they are, they just act in a completely chaotic way because their brain doesn't work because older people don't have the redundancy that they have. They have no capacity to spare and are very prone to delirium due to infection. That said, younger people can have delirium too, of course. I remember when I was a child I had a fever and had quite strong hallucinations. Hallucination is a perception or perception without an external stimulus. and I remember having fever and visual hallucinations, the effect on my young brain is less likely to occur in adults but certainly occurs in children and in severe cases sepsis can induce an anal opathy very often caused by inflammatory insults and hypoperfusion , as well as by the cytoid. but there can be an enopathy, but the most common ones that we see are drowsiness, tiredness, not wanting to do anything, wanting to go to bed and the same, the very feeling of illness when you feel bad, that is the effect of the cytotypes in the brain, anorexia, delirium, hallucinations and Keal's opathy, so altered mental state is really the whole brain presentation of feeling sick and when you're not sick, you haven't been sick for a while, you forget about how horrible it is.

Is this Bad? This feeling of illness can be absolutely terrible. I remember when I had the flu, one time I was trying to go to bed and I couldn't do it. She was lying on the floor. I felt so bad that it was incredible and I remember thinking that I don't care if I live or die here, you know, I feel so sick that I don't care anymore because of the effect of the cytotypes that cause this extreme bad, this feeling of illness because of the effect on the brain and the way the brain generates the mind, so be empathetic, be kind, be generous to our sepsis patients because they are going through a really terrible, terrible time, they are not feeling well at all, so let's try Think about some of the other clinical features of sepsis. and although we cannot always explain them completely, we can begin to have some ideas that help us know that in sepsis there is anorexia but at the same time there is a greater demand for energy and this means that now there is a catabolic process in one of the hormones.

What stimulates the catabolic process being broken down is glucagon, so glucagon is produced by the alpha cells in the pancreatic eye and will break down glycogen into glucose and will also stimulate the process of gluconeogenesis producing glucose from n based molecules. in carbohydrates like fats and proteins and also that principle will be stress and one of the stress hormones is adrenaline, which of course is exactly the same as epinephrine and I think you can probably see that both of those things, glucon Genesis, produces glucose and adrenaline. Epinephrine also raises blood glucose levels, so we will get an increase in blood glucose, an increase in blood glucose levels, and we say if the blood glucose is greater than 6.6 milliliters per liter in a fasting patient or in an anorexic patient who is not diabetic.

That's a sepsis criterion in itself right now, in a sense glucose is good because it provides energy, but recent studies show that glucose actually needs to be controlled to optimize outcomes in sepsis, so in the clinical environment we don't want glucose. go up too much now there is also a greater demand for energy. I think you can see that oxygen will be used and carbon dioxide will be produced, so if the oxygen we use runs out, the amount of oxygen in the blood will decrease and it is energy as energy is produced, the carbon dioxide levels carbon will increase, so greater energy use will decrease the amount of oxygen remaining and increase the amount of carbon dioxide produced and that will be detected by the medulla oblongata, where the respiratory center is located and that will stimulate the respiratory rate, also the Decreased oxygen and increased carbon dioxide will increase heart rate which will also increase and if heart rate increases that will increase cardiac output and blood pressure is cardiac output multiplied by peripheral resistance, so we are going to have an increased in blood pressure and also if someone has chills and RoR, they will have peripheral vasoconstriction, peripheral vasoconstriction will reduce the amount of blood going to the surface of the body. retain warm blood in the center of the body, but it can also increase peripheral resistance, so these are other effects that we can see in sepsis, we can see an increase in glucose levels, we can see an increase in respiratory rate, an increase in heart rate and an increase in blood pressure and, in fact, very often.

When someone gets sick, it isrespiratory rate which can often increase first, so this is a key clinical indicator, monitoring the patient's respiratory rate, but all of these things can indicate the onset of sepsis and we can use them to monitor the course of the disease. Sepsis also, for example, the degree of hyperglycemia is actually well correlated with the severity of sepsis, so there is a positive correlation here, we think about the graph, so if the blood glucose levels are there and the severity is here, severity of sepsis, blood glucose. Levels will tend to increase as sepsis becomes more severe with this positive correlation, so for us as clinical workers there are many things to pay attention to to monitor for the presence of sepsis, identify the presence of sepsis early and monitor the course and severity of sepsis. sepsis too, so now we're in a position to put some of these ideas together and look at our sepsis or severe sepsis screening tool.

Now two of the following, present and new to the patient, a temperature above 38° Celsius would indicate pyrexia. a temperature below 36° Celsius would represent cold sepsis, so that is a criterion if the patient's temperature is above 38 or below 36, if the heart rate is above 90 beats per minute or more than about a 20% above what the patient would normally expect, so there is a sticky cardiac response to sepsis as we mentioned due to the increased energy demand, likewise with respiratory rate to get more carbon dioxide out and more oxygen If the respiratory rate is greater than 20 breaths per minute, that would be a criterion for sepsis if there is alteration. mental status which is a criterion of sepsis if the white blood cell count indicates luccocytosis greater than 12,000 um per cubic millimeter of blood then that would indicate sepsis or if it is less than 4,000 cells per cubic millimeter of blood or if there is hyperglycemia greater than 6 .6 miles in a fasting patient in the absence of diabetes Now, if the answer to that question is yes, the patient has signs and symptoms of sepsis and then it is worth thinking about whether there is any significant history and the history suggests new infection and High risk conditions are pneumonia, urinary tract infection, abdominal condition such as abdominal pain, diarrhea, bloating or post-laparotomy meningitis, of course, you may have the possibility of mening Co or septicemia, cellulitis is a risk factor, as is septic arthritis, fasciitis or wound infection, endocarditis and uh. at any time there are indwelling catheters or intravenous lines or central lines as a risk now if the patient has two of the relevant characteristics, especially if there is a suggestive history, then we can consider that the patient does in fact have sepsis, are there any of the following present or new? the patient so the physical signs blood pressure less than 90 or a mean arterial pressure less than 65 mm in new Mercury or increased need for oxygen in other words if you have to increase oxygen to keep the patient's saturations above than 90, that would be significant and there are also relevant biochemical signs, so the increase in creatinine could indicate the development of acute kidney injury or a lot of muscle catabolism, both indicating potentially serious sepsis because if acute kidney injury is developing it means that there is organ failure, so sepsis is becoming severe or a urinary output of less than 0.5 m per kilogram for 2 hours, so in an adult we always want 0.5 m per kilogram per hour, which which means that in a 60 kg adult we want at least 30 MS of urine, in children we will look for more than that in children we will look for at least one Mill and in babies we will look for 2 Ms per kilogram per hour.

Another possible clinical feature is increased Billy Ruben. This can be caused by inflammation of the red blood cells and apoptosis, but also in septic patients, you can get a Col state, a CO stasis, the bile does not move properly through the body ducts, there is a chassis, which which means that bile can return to the liver and hepatocyte function can also be reduced if the platelets are depleted because the cytotypes will cause inflammation of the endothelial surfaces of the blood vessels, this will release tissue factor which will stimulate the development of thrombin, which will consume the platelets and there may also be small fiber clots in the vessels and uh aggregation, so coagulation abnormalities mean that the platelets become depleted, so the platelets would become low platelets, less than 100, which indicating thrombocytopenia, as with choral opathy, if the international normalized ratio is greater than 1.5, then that is a serious clinical indicator and an increase. in lactate means that the muscles and body tissues are hypopropagated.

If they are examined with hypop, the metabolism will change from aerobic to anaerobic and, as a consequence, lactic acid will be produced and passed into the blood as lactate. Now, if the answer to these questions is yes, then. the patient has severe sepsis start the severe sepsis pathway if the answer is no it may still be sepsis so we still want to give antibiotics with oxygen every hour Fluid therapy with national early warning score and we want to reassess the patient very regularly , so this is the clinical result of some of the theories that we just discussed, so again early recognition of sepsis is absolutely vital, suspecting that sepsis saves lives now that we think about the treatment of sepsis, for Of course, this must be individualized, but it's the place to start. is the severe sepsis care pathway known as sepsis 6 and time is of the essence here so we want to take note of when we start making these recordings and as we go we want to take note of the initial timing of the person who you do the assessment and the outcome or comment we might want to make so one of the key things here is to get senior staff involved quickly so speak to the senior registrar or the consultant and then some hospitals have critical care outreach teams nursing-based. who can be contacted, who can bring a lot of experience to the situation, firstly, we want to administer high oxygen flows of 15 liters per minute through a non-breathable bag and, in a patient without chronic obstructive pulmonary disease airways, we want to maintain oxygen saturations of 94.% or higher, so it contains main oxygen saturations, just be careful with patients with known chronic obstructive pear disease, particularly the presentation of bronchitis.

Now we need to know what organism is causing the infection, so before starting the antibiotics we want to take blood cultures to be able to identify the cause of the bacteremia before the antibiotics because obviously, if we give antibiotics that will kill the bacteria and distort the culture, also we want to do a complete blood count Ure or electrolytes liver function tests coagulation profile glucose and arterial blood gases if we have access to that facility and then consider other causes of infection urine swabs sputum send them for culture as quickly as possible but immediately ready we want to start with intravenous antibiotics, time is of the essence in sepsis the antibiotic, of course, will vary depending on what we believe is the cause of the sepsis, but it has to be intravenous and it has to be rapid so that as soon as the blood cultures come out antibiotics can enter, of course, we will not obtain the results of blood cultures.

I return for 24 48 hours so we can modify the antibiotic therapy, but since the mortality rate can increase in severe sepsis by about 1% every 10 minutes, we cannot wait until the antibiotics have to be given and then we will think about fluid resuscitation if patients are hypotensive, give 20 milligrams per kilogram sodium chloride or harmans bolus, which is actually quite a bit if you think about it, 20 Ms per kilogram of patient's body weight and consider repeating that up to a maximum of 60 Ms per kilogram if the patient is hypotensive. Now, if the patient is shocked, there is reduced perfusion of the body's tissues, if there is reduced perfusion of the body's tissues, they will become hypoxic and that will generate a change of metabolism from aerobic to anaerobic with the production of lactic acid, for example. what lactate is monitored.

Levels can indicate how the condition is going if lactate levels are rising shock is getting worse if lactate levels are falling hopefully shock is resolving so serum lactate and hemoglobin we want to ensure adequate hemoglobin for transport oxygen. In the body we do not want anemic hypoxia. Nowadays we do not normally use urinary catheters due to the risk of infection, but it is vital that we know that the patient has adequate urine output, so these patients need to be catheterized regularly. must be kept up to date and we are looking for a minimum of 0.5 m per kilogram per hour of urine output.

Hopefully, all of this will be completed within an hour in 1 hour. SE 66 has been completed and we can sign that and our designation, the patient does not Enhance specialist intervention may be required to assist with early goal-directed therapy, so we may wish to treat infected wounds or burns with debridement , for example, so that's basic sepsis 6, of course, it must be complicated and complemented by any other treatment for the condition. specifically, but this is what the sepsis survival campaign recommends to improve results in our septic septic potions, but it must be done early. This condition cannot wait.

Sepsis is a medical emergency and we must respond as such.