Sepsis and Septic Shock

hello it's Eric strong from strong medicine in today's episode of intern crash course I'm discussing sepsis let's start by answering what is sepsis according to our current understanding sepsis is a life-threatening clinical syndrome caused by a dysregulated host response to infection resulting in a characteristic constellation of physiologic and biochemical abnormalities has a spectrum of severity in its mildest form one can see some vital sign abnormalities such as fever tachycardia and tachypnea along with leukocytosis if more severe the patient may develop hypotension responsive to infusions of IV fluids along with organ dysfunction specific signs of organ dysfunction can include low urine output and increased creatinine confusion or delirium hypoxemic respiratory failure liver failure and ileus sepsis induced cardiomyopathy and secondary heart failure and a variety of human toll object arrangements including thrombocytopenia elevated INR disseminated intravascular coagulation and even leukopenia if very severe the patient will experience hypotension that is resistant to IV fluids on account of peripheral vasodilation and they will have an elevation of serum lactate this specific combination is what is currently required for a diagnosis of septic shock and at some point the physiologic and biochemical Arrangements become so severe as to be irreversible at which point death is inevitable importantly this is a spectrum it's not meant to imply that patients necessarily pass through a smooth linear progression from the left side to the right there is a term that frequently comes up during discussions of sepsis the systemic inflammatory response syndrome or sirs the idea of sirs was introduced in 1991 as a tool for clinicians to identify those patients who were at the highest risk of death from sepsis service was said to be present if at least two of the following were present a temperature the either greater than 38 or less than 36 a pulse above 90 a respiratory rates above 20 or pco2 below 32 and either a white cell counts above 12 or less than four there was then a relationship defined between sepsis sirs and infection in which a patient was said to have sepsis when they met both sirs criteria and had clinical evidence of infection such as positive cultures or a consolidation on chest x-ray layered on top of this Venn diagram was another category of severe sepsis and severe sirs which is when either was associated with acute dysfunction of at least one organ system such as acute kidney injury or respiratory failure and then on top of this was the category of septic shock which is when severe sepsis or severe sirs was associated with hypotension refractory to fluids unfortunately there were problems with this paradigm most significantly the criteria for service proved to be too inclusive for example if a patient with chronic leukemia whose white blood cell counts was always elevated subtly developed rapid atrial fibrillation they would get classified as having the systemic inflammatory response syndrome and possibly put on a pathway to treat for sepsis even though they had neither an infection nor even inflammation another problem was the sense that the categories of severe sepsis and severe sirs ended up not being as clinically useful as clinicians expect that they would be as a consequence of these and other shortcomings when an international consensus conference on sepsis called sepsis 3 was held between 2014 and 2016 to come up with new definitions and new treatment guidelines they decided to simplify the paradigm quite a bit they got rid of the severe category and they got rid of sirs so as of 2016 in the eyes of academic medicine sirs was no more you'll still hear plenty of clinicians referring to serves on the wards which is the primary reason I'm still talking about it but professional societies and the medical literature has really tried to phase it out so now at this point here is our simplified substance paradigm a subset of patients with infection develop this regulated host response leading to sepsis and a subset of those patients have sepsis severe enough to lead to hypotension refractory to fluids and to an elevated lactate in which case we say they have septic shock this begs the question now if sirs and its associated criteria are no more how do we identify a patient whose infection is severe enough to be labeled sepsis well enter the sofa score sofa standing for a sequential organ failure assessment the sofa looks at six domains oxygenation coagulation liver function blood pressure level of consciousness and renal function each is scored based on severity of dysfunction between zero and four points leading to a maximum possible sofa score of 24 compared to deserves criteria the sofa score was a thought to more accurately identify the patient's at greatest risk of death but as you can immediately appreciate it's much more cumbersome because of this a streamlined version of sofa was also proposed called the quick sofa or cue sofa the cue sofa has just three criteria all of which can be assessed by physical exam alone the patient gets one point if the respiratory rate is 22 or greater one point if the systolic blood pressure is 100 or less and one point for any degree of altered mentation sepsis is said to be likely if the patient has either two or three points unfortunately despite initial enthusiasm for the cue sofa as an easy and more accurate replacement for sirs criteria its failed to catch on in many hospitals I'm returning to the spectrum of severity to make one final point about the shifting definition of sepsis based on the currently recommended framework labeling a patient as having sepsis requires them to have organ dysfunction so this spectrum has over time narrowed a bit moving away from the definitions how do you work up sepsis you need to identify the cause and identify complications to identify the cause the first step is a thorough physical exam then two sets of blood cultures a UA and urine culture and other relevant cultures for example a sputum culture any person with pneumonia and risk factors for unusual or multi drug-resistant pathogens such as bronchiectasis or a tracheostomy check a chest x-ray to look for pneumonia or a pleural effusion if there's a possibility of intra-abdominal pathology consider abdominal imaging which could be either a CT scan or bedside ultrasound depending on whether the patient is stable enough to go to the radiology department what should be checked to identify complications well a CBC will identify anemia and thrombocytopenia adi cpanel consisting of the inr PTT and fibrinogen along with a few other things will identify di see a basic metabolic panel will help to identify a ki and an elevated anion gap acidosis as serum lactate could help to identify systemic hypoperfusion I'm going to address this question mark at the end of the video lfts will identify ischemic hepatitis also known as a shock liver and identify hyperbilirubinemia which is a negative prognostic marker in sepsis an ABG will allow you to quantify hypoxemia and calculate the P to F ratio which is also a prognostic marker the ABG wanted to fight hypercapnia from ventilatory failure and will assess the pH among other things extremes of pH are believed to contribute to vasopressor unresponsiveness although I had already mentioned the chest x-ray as a tool to help identify the cause of sepsis it's also helpful to look for complications specifically non cardiogenic pulmonary edema from sepsis triggered ard s as well as iatrogenic cardiogenic pulmonary edema from excessive volume repletion a troponin will identify demand ischemia and a so-called type 2 MI and ECG will also help with that and can look for arrhythmias which may be really related to the intrinsic stress of infection or related to catecholamine access from pressors with beta agonist activity and last an echo will help to identify sepsis induced cardiomyopathy or undiagnosed pre-existing heart failure that might complicate treatment now when it comes to treatment what are the priorities first is of course ABCs meaning ensure the patient has a pulse and respirations but assuming that you don't need to immediately go down an ACLs pathway the next priority is restoring hemodynamics and there are two primary ways to do that the first is IV fluids given in rapid bolus is not via maintenance I have an entire brief video series dedicated to IV fluids but the profoundly oversimplified summary is that in almost all circumstances you should be using crystalloid fluid rather than colloid balanced solutions such as lactated ringers appear to be very slightly better than so-called normal saline and a very general guideline on the infused volume is 30 milliliters per kilogram within the first three hours but every patient is different and some will require much more than this the other primary way to restore human dynamics is with pressors continuously infused intravenous medications which act by either increasing peripheral vascular resistance increasing inotropy or both at this point there is strong expert consensus that norepinephrine should be the first choice pressure in septic shock if nor epi is insufficient vasopressin epinephrine dopamine dobutamine and phenol Efrain are all potentially reasonable as a second meant to add depending on the circumstances so in the young person with no evidence of cardiac compromise phenol Efrain a pure vaso constrictor is a sound choice but in an older person with a history of heart failure I don't my friend not a good choice at all and dopamine or dobutamine might be better the bottom line is to start nor epi for just about everyone but the choice of second presser is very patient dependence after hemodynamics is treating the underlying infection for this we want to use broad-spectrum antibiotics how broad and how many antibiotics depends on whether there is a specific infection suspected whether the patient has risk factors for antibiotic resistance and how sick they are overall there is some debate as to how quickly antibiotic should be delivered sepsis guideline state that a patient with sepsis should be receive antibiotics within one hour while some infectious disease doctors fear such a recommendation is leading to Doc's feeling obligated to give antibiotics before even having a proper opportunity to determine the probability the patient is even infected so they recommend giving antibiotics ASAP or as soon as is prudent which may in some cases be longer than an hour in addition to giving antibiotics you also need to address source control meaning draining abscesses or a/d seeing a potentially infected indwelling line if there are multiple options for addressing source control for example a percutaneous versus a surgical approach to draining an abscess there should be greater weight given towards whichever procedure can be safely performed the most quickly when treating the hypotensive septic patients what are the science that a patient has received an adequate amount of fluid resuscitation the mean arterial pressure is 65 or higher your an output is at least 0.5 milliliters per kilogram per hour the patient's mental status has normalized lactate is improving and for patients who are being mechanically ventilated there are a number of dynamic measures of human dynamics which are typically assessed to be an ultrasound there are a few important miscellaneous issues when it comes to treating sepsis first if it's felt that multiple antibiotics are required to cover both mrs a and gram negative organisms you should avoid the combination of vancomycin and pip Tazo better known as zosyn this is due to the increasingly recognized risk of kidney injury which appears to be relatively high for this specific combo alternatives that would provide similar coverage would be Vanka cefepime or vank plus a carbapenem while empiric steroids are not recommended routinely in septic shock they should be considered when shock is refractory meaning that the patient remains hypotensive despite receiving an appropriate amount of fluids and being on at least one presser the optimal choice of glucocorticoid and dose are not known some clinicians will also add the mineralocorticoid fludrocortisone but others feel that this is not necessary so-called early goal-directed therapy in which sepsis management is highly protocol eyes to target very specific hemodynamic goals which originally shown in 2001 to provide a huge mortality benefit compared to standard care however more recent studies have consistently failed to show benefits likely because standard care has gotten so much better since then and in the absence of ongoing hemorrhage or active myocardial ischemia red cell transfusions should only be given once the hemoglobin drops below 7 grams per deciliter although I won't take time to discuss them in depth there are two interesting additional issues in the management of sepsis specifically septic shock which are discussed in the ICU and emergency room from time to time the first is related to lactic acidosis you might recall that when I mentioned that serum lactate could potentially help identify systemic hypoperfusion I included a question mark afterwards the reason for this is that there is a minority opinion that the elevated lactate seen in septic shock may not be caused by tissue hypoxia and subsequent anaerobic respiration the alternative hypothesis is that in shock intrinsic beta-agonist activity leads to an increase in the rate of pyruvate production which then overwhelms the Krebs cycle ability to process it some of the accumulating pyruvate is then shunted into lactate a process that may be enhanced by thiamine deficiency thus lactate is really a marker of the body's intrinsic stress response rather than being a dangerous byproduct of anaerobic metabolism like I said this is a minority view and I won't offer a personal opinion on it other than to say that the debate about it is really interesting the other additional issue is vitamin C in 2016 a small retrospective study was published which found a possible very substantial mortality benefits to treating patients with septic shock the combination of high-dose intravenous vitamin C thiamine and hydrocortisone the authors put forward about 10 different overlapping mechanisms by which this combination of medications could have led to such benefits but to date there have been no follow-up randomized controlled trials to confirm this very early preliminary finding at this time high dose of vitamin C remains investigative only and should not be routinely used outside of a clinical trial there are links to more info on lactic acidosis and vitamin C and sepsis in the video description below thanks for watching [Music]

Channel: Strong Medicine

Views: 147,895

Keywords: sepsis, septic, shock, septic shock, pressor, norepinepherine, fluids, normal saline, medical education, med ed, foamed, foam, icu, sepsis 3, sirs, systemic inflammatory response syndrome, lactic acidosis, lactic acid, vitamin C, strong medicine, intern crash course

Id: 3EVpyBORw5Y

Length: 17min 21sec (1041 seconds)

Published: Tue Nov 19 2019