I say — (almost) all septic patients need surgery, ventilatory and<\/p>\n
inotropic support, volume loading, and antibiotics. Accept it. Rivers<\/p>\n
data suggest that EARLY circulatory resuscitation is probably good for<\/p>\n
you. So, I teach the residents to ventilate septic patients early,<\/p>\n
accept that you will porbably need 40-60% oxygen and 5-12 PEEP during<\/p>\n
the peak of the septic illness, start inotropic support at once, aim for<\/p>\n
normotension, get good stable monitoring of MAP by art.line, HR from<\/p>\n
ECG, SPO2 from a finger and look at the ventilator peak pressures and<\/p>\n
the tidal volumes (we usually use pressure-regulated volume control on<\/p>\n
the Servo300) and then assess the ongoing effects of aliqouts of volume<\/p>\n
on MAP, HR, SpO2 signal\/noise ratio (pulse height), respiratory “swing”<\/p>\n
of MAP, urine volumes and peak airway pressures. Wean inotrope<\/p>\n
(noradrenaline) as tolerated. Accept that most septic patients need<\/p>\n
0.5-2 mg\/hr of noradrenaline. Just get over it. Accept that some<\/p>\n
patients will need drainage of pleural fluid collections (not many). Be<\/p>\n
aware of intra-abdominal hypertension and watch out for it. I have<\/p>\n
attached a snippet of my lecture on sepsis to our residents which talks<\/p>\n
about the extremely practical details. I know that some of this will<\/p>\n
fill “toyboys” (and girls) who need PA caths, TOEs, PiCCOs and Svo2<\/p>\n
before making decisions with horror. However, as I keep saying, your<\/p>\n
mileage may differ — mine certainly does.<\/p>\n
<\/p>\n
I take issue with your emphasis about sepsis and renal failure — Most<\/p>\n
patients in our unit do not need dialysis — we take the view that<\/p>\n
“renal failure is a capital offence” and try and reverse it aggressively<\/p>\n
at the beginning. However, if polyuria does not develop and oliguria<\/p>\n
supervenes we don’t try extraordinary measures (“saltwater drowning”,<\/p>\n
mannitol, frusemide, rain-dances etc) to get urine out of rocks. We just<\/p>\n
start CVVHDF.<\/p>\n
<\/p>\n
Sometimes in extremely co-morbid patients with sepsis the development of<\/p>\n
dialysis-dependent renal failure is an end-point (i.e. we would have<\/p>\n
decided that we would not dialyse these patients) but that is not very<\/p>\n
common. Here are some data I presented in Mumbai early this year by way<\/p>\n
of illustration — in 2002 we admitted 145 patients with severe sepsis,<\/p>\n
median age 60, 80% had co-morbidity, 26% had “serious co-morbidity”<\/p>\n
(Prior Health Status C or D — Knaus et al APACHE-I), 16\/145 (11%) had<\/p>\n
therapies withdrawn, 6\/16 had been “admitted with reservations”, 14\/16<\/p>\n
had prior “intention to withhold”, 11\/16 had had therapies withheld<\/p>\n
before being withdrawn and 16\/16 died in ICU 13 – 431, median 66 hours<\/p>\n
after admission. Another 9 patients died without withdrawal of therapy<\/p>\n
— total 25\/145 deaths or 18%. Only 12 of the 145 septic patients were<\/p>\n
dialysed (10 of whom survived).<\/p>\n
<\/p>\n
The recent (rather methodologically poor) studies of fluid restriction<\/p>\n
are to my mind largely showing that unncessary “salt-water drowning”<\/p>\n
perioperatively (including in the five days post-operatively) is bad for<\/p>\n
you (surprise). Since we don’t give resuscitation fluids (Na+140-154\/l)<\/p>\n
as maintenance fluids anyway (we give 1ml\/kg\/hr of D5W) then we were not<\/p>\n
altered in our practice by the Ann Surg Nov 2003 trial. We did<\/p>\n
participate (very heavy recruiting centre — 439 patients randomised) in<\/p>\n
the SAFE trial and that involved a lot of SAFE fluid (especially the<\/p>\n
“thin fluid” and especially in septic patients). As your can see from<\/p>\n
our mortality data on the previous jpg — survival was the same (~82%)<\/p>\n
during the SAFE trial as before and after it.<\/p>\n
<\/p>\n
I loved your comment about “advanced care” — it is very American. \ud83d\ude09<\/p>\n
Joan Cassell made the same comment when she came to work with us. I told<\/p>\n
her what I have said for many years — it is not technology that makes<\/p>\n
intensive care work — it is people who intensively care — and she<\/p>\n
liked it and included it in the paper. (Cassell J, Buchman TG, Streat S,<\/p>\n
Stewart RM. Surgeons, Intensivists and the covenant of care –<\/p>\n
administrative models and values affecting care at the end of life –<\/p>\n
Updated.\u00a0 Crit Care Med 2003;31(5):1551-1559). Let me be blunt — IMAO<\/p>\n
much of the invasive technotoys have been foisted unproven (they do<\/p>\n
measure something — I’m not disputing that, however — does it make a<\/p>\n
difference — that’s not proven) on a gullible and easily seduced<\/p>\n
population of technoleaning ‘crats (no offence, really no offence) and<\/p>\n
have been slickly marketed as the “best thing since sliced bread which<\/p>\n
everyone else using and which you simply must have in order to stay up<\/p>\n
with the pack”. No $600 toilet seats here in NZ. However, we can and do<\/p>\n
use a lot of high-tech at times (but very selectively, accepting that<\/p>\n
the marginal benefits of it are small and will be confined to a small<\/p>\n
number of patients). We just don’t think that everyone needs a 30 foot<\/p>\n
gold plated cadillac limo to get them down to the corner store for a<\/p>\n
pepsi. Sometimes, it would be perfectly good to walk. I know that NASA<\/p>\n
is still smarting from that awful “metric versus imperial” (American<\/p>\n
empire that is) screwup on Mars a few years back but I agree with their<\/p>\n
faster, cheaper, better idea. Faster and cheaper can also mean “with<\/p>\n
better outcomes” in health care — it just takes application and<\/p>\n
innovation — and — and this is utterly crucial for the US of A who<\/p>\n
utterly refuse to face this — SELECTIVITY. This includes another one of<\/p>\n
those awful commie words Leo — RATIONING. Now I know that you (and many<\/p>\n
others) lament the waste of your time and everyones money that goes into<\/p>\n
non-selective ICU practice in many parts of the USA. However, this is<\/p>\n
what truly must be faced up to sooner (or in the standard US manner —<\/p>\n
later — much later — as later as you and your politicians can get away<\/p>\n
with). It is just silly to plumb every dying patient with every<\/p>\n
high-tech toy and probe and line and pump and just continue to accept<\/p>\n
this as the standard modus operandi. You know it Leo from your own hard<\/p>\n
working experience. You gotta go easy on this techie stuff and spend a<\/p>\n
great deal more time dealing with the “soft stuff” like setting limits<\/p>\n
on treatments and monitoring modes and toys and fancy pharmaceuticals.<\/p>\n
Easy for me to say. \ud83d\ude09<\/p>\n
<\/p>\n
Enough non-EBM opinion from me — Gord will be stressing the walls of<\/p>\n
his cerebral vasculature. However, some of this stuff really SHOULD be<\/p>\n
subjected to the kind of (difficult) studies that PACMAN and our own<\/p>\n
experience leads you to think about.<\/p>\n
<\/p>\n
Finally, lactate is a useful marker of badness — no question — (there<\/p>\n
is even quite good evidence for this) and rising or falling lactate<\/p>\n
during best clinical treatment gives a warning or a promise of things to<\/p>\n
come. However, there are few occasions when the course of clinical<\/p>\n
treatment with respect to the nature of CVS support is altered by<\/p>\n
knowing a lactate — or even serial lactates. We (that’s you too Leo I<\/p>\n
bet) try and resuscitate the patient as best we can and we watch the<\/p>\n
lactate. If it rises we worry (and we make sure that we had in fact done<\/p>\n
everything we should have) but we don’t usually change treatment.<\/p>\n
Similarly, if it falls we feel pleased with ourselevs and maybe we relax<\/p>\n
a bit — but we don’t withdraw all the CVS support we have put in place<\/p>\n
which seems to be a “good thing”.<\/p>\n
Immediately on admission ensure reliable standard monitoring (ECG, SpO2, MAP transduced from arterial line), place at least one large peripheral line for colloid and at least a quadruple lumen central line. Some patients need six central line lumens.<\/p>\n
Use standard curarisation\/sedation regimen \u0096 Pancuronium\/Morphine infusions, diazepam 5-10mg 6-12 hourly. Front-load the sedation \u0096 perhaps 20-40 mg diazepam (before complete curarisation if possible) to ensure no awareness under curarisation. Use Pressure Regulated Volume Control (PRVC) on Servo 300) to start with and continue this mode if respiratory failure is severe (FIO2>0.6 or PEEP>10). Start with 100% oxygen and 5 cm PEEP. Set VT to 10 \u0096 12 ml\/kg, adjust rate (10 \u0096 14) for normocarbia (35-45 mm Hg), and increase PEEP if necessary to control \u0093frothing\u0094 or for unsatisfactory SpO2 despite high FIO2 (0.6 or more). Adjust FIO2 and PEEP to obtain SpO2 95-98%. Keep peak airway pressure under 30 cm H2O Use standard I:E ratio (30%) for Servo 300 ventilator (see Servo Ventilation Charts) unless severe ARDS. Increased I:E ratio (e.g. 1:1) ventilation may help oxygenation but has risks, call Intensivist and discuss if you think this necessary. Be aware of PEEP effects on cardiac function, renal and hepatic blood flow and pulmonary (hyper)inflation..<\/p>\n
Find out if the patient responds to volume \u0096 give a rapid colloid infusion (500ml over 5 \u009610 minutes) and watch the patient closely! Look at peripheral temperature, urine output, heart rate on ECG, transduced MAP, peak airway pressures on the ventilator and continuous SpO2 (having set FIO2 and PEEP so that SpO2 is about 95%, not 100%) and answer two questions: i) Were there favourable changes in haemodynamics and clinical effects in keeping with a rise in cardiac output and oxygen delivery? (E.g. falling HR, rising MAP, oximeter begins to work, rise in SpO2, rise in evident peripheral warmth or colour, increase in urine volume). ii) Were there adverse effects on pulmonary function? (E.g. rising airway pressure, fall in oxygen saturation, frothing). If volume is beneficial and further benefit is desirable on clinical grounds then repeat the volume challenge. At some stage it will be clear that further volume merely worsens oxygenation and lung compliance. Many patients may need pleural fluid drainage at some stage and this may reveal further volume responsiveness. Lusitropic drugs (E.g. beta agonists, milrinone) and vasodilators (E.g. beta-agonists, milrinone, alpha-blockers) may need further volume loading for good effect.<\/p>\n
This is near-universal in severe sepsis1 and as such when used intelligently with DCCM standard monitoring most patients do not need pulmonary artery catheterisation. Aim to keep MAP 90 \u0096 110 and HR 90 \u0096 120 in SR for optimal cardiac function. Combinations of inotropes are often used \u0096 depending on haemodynamics \u0096 so be prepared to change as the patients\u0092 circulation changes. Start with noradrenaline first (>80% of patients with severe sepsis have noradrenaline), increase to 1 \u0096 2 mg\/hr if required for MAP. Remember NA is a mixed a,b-agonist. Some patients may benefit from the beta effect of additional dopamine \u0096 with an increase in rate (and sometimes contractility) but beware \u0096 AF or SVT are common. \u0093Renal\u0094 dopamine in sepsis is a myth5. Some patients require high doses of NA (5 \u009610 mg\/hr) and some of these may benefit from vasopressin or terlipressin. Dobutamine is used rarely (usually with noradrenaline) when BP will stand it and may help to increase output by chrono\/lusitropic effect in selected patients. Rare patients may benefit from adrenaline or milrinone. Give all patients digoxin after K+ repletion (for both inotropy and rhythm control) unless conduction disturbances contraindicate it. Be very cautious with amiodarone (heart block, vasodilatation, inotropic depression) in septic patients with abnormal hearts.<\/p>\n
Clinical assessment is most important. No CVP measures in DCCM patients except in transplant protocols or rarely at specialist instruction (e.g. caval surgery). Pulmonary artery catheterisation may occur rarely (DCCM specialist decision) when diagnosis is obscure.<\/p>\n
No specific therapy if pHa>7.2 and circulation is stable and improving \u0096 use serial pHa as sign of progress. If pHa is <7.2 and circulation is failing \u0096 give THAM (1 \u0096 2 mmol\/kg via CVL over 20 minutes) and consider continuous THAM infusion 0.25 \u0096 2 mmol\/kg\/hr when maximum CVS support will not keep pHa >7.2.<\/p>\n
<\/p>\n
1.\u00a0\u00a0\u00a0\u00a0\u00a0 Thomas MG, Streat SJ. Infections in Intensive Care Patients. Chapter 44 (pp 564-576) in Antibiotic and Chemotherapy. 8th Edition. Eds Finch R,Greenwood D, Norrby R, Whitley R. Churchill Livingstone. London 2003<\/p>\n
2.\u00a0\u00a0\u00a0\u00a0\u00a0 Bone, R.C., Balk, R.A., Cerra, F.B., Dellinger, R.P., Fein, A.M., Knaus, W.A., Schein, R.M., Sibbald, W.J.: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP\/SCCM Consensus Conference Committee. Chest 101:1644, 1992<\/p>\n
3.\u00a0\u00a0\u00a0\u00a0\u00a0 Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001 Nov 8;345(19):1368-77.<\/p>\n
4.\u00a0\u00a0\u00a0\u00a0\u00a0 Clark, M.A., Plank, L.D., Connolly, A.B., Streat, S.J., Hill, A.A., Gupta, R., Monk, D.N., Shenkin, A., Hill, G.L.: Effect of a chimeric antibody to tumor necrosis factor–a on cytokine and physiologic responses in patients with severe sepsis – a randomized clinical trial. Crit. Care Med. 26:1650, 1998<\/p>\n
5.\u00a0\u00a0\u00a0\u00a0\u00a0 Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet. 2000; 356(9248): 2139-43.<\/p>\n
6.\u00a0\u00a0\u00a0\u00a0\u00a0 Nasraway SA, Rackow EC, Astiz ME, Karras G, Weil MH. Inotropic response to digoxin and dopamine in patients with severe sepsis, cardiac failure, and systemic hypoperfusion. Chest. 1989 Mar;95(3):612-5.<\/p>\n
7.\u00a0\u00a0\u00a0\u00a0\u00a0 Streat SJ, Plank LD, Hill GL. An overview of modern management of patients with critical injury and severe sepsis.\u00a0 World J Surg 2000 Jun;24(6):655-663<\/p>\n
8.\u00a0\u00a0\u00a0\u00a0\u00a0 Streat SJ. Abdominal surgical catastrophes. In Oh\u0092s Intensive Care Manual 5th Edition. Eds Soni N, Bersten A. Butterworth-Heinemann, 2003<\/p>\n
<\/p>\n
Leo,<\/p>\n
Here’s another approach.<\/p>\n
Unfortunately 50% of critically ill patients do not respond to fluid loading<\/p>\n
by increasing their cardiac output (CO) and oxygen delivery. Loading these<\/p>\n
patients aggressively is therefore harmful as their lungs, gut and all other<\/p>\n
organs\/tissues\u00a0 will just get more edematous. One has therefore to use those<\/p>\n
parameters that PREDICT the response to fluid loading before taking the<\/p>\n
decision to actually do it. The CVP and PCWP have been shown again and again<\/p>\n
and again to be poor predictors of fluid responsiveness. Volumetric<\/p>\n
parameters, like the EDA (TEE) and the ITBV are somewhat better. Functional<\/p>\n
hemodynamic parameters like the Systolic Pressure Variation, Pulse Pressure<\/p>\n
Variation and Stroke Volume Variation are the best predictors, but only in<\/p>\n
patients on fully controlled mechanical ventilation. The least one should do<\/p>\n
in these patients is monitor their CO, or its surrogate like the ScvO2. The measurement of CO is important since it will tell you, first and foremost, if the CO is low(!), as well as if, and by how much, does the CO respond to fluid loading. However, the CO value by itself, like the ScvO2 or SvO2 values, is not enough, since you still would not know why is it low. Many septic patients have significant myocardial depression, with or without hypovolemia and with or without hypotension. The Rivers data are impressive, but the success was achieved because the protocol was applied in the very early sepsis phase only, a phase in which most patients may indeed be hypovolemic. In later sepsis a more advanced hemodynamic monitoring is necessary in order to more accurately assess the cardiovascular status and prevent unnecessary and potentially harmful fluid loading.<\/p>\n
<\/p>\n
I think that it is somewhat more than that. We accept that there is\/will be a certain level of inotropic support (we use noradrenaline) required in patients with sepsis (that is mainly what we are talking about here — other general ICU patietns can be managed even easier). We establish what that “minimum dose” is, early in the course of the treatment, during intensive volume challenges (“Is the haematocrit down to 0.28 or so”?) and then give further volume, including sometimes as an infusion, according to the clinical circumstances — knowing some of the obligatory fluid losses. For example — if the patient has faecal peritonitis (our most common cause of severe sepsis, not community-acquired pneumonia which is second most common), then we understand that there will be “weeping” from the inflammed peritoneum — remember 1mm of exudate across the peritoneal surface equals about a litre of fluid. Similarly, there may well be increased luminal fluid — some of which will come up the NG tube and some of which will remain intraluminal. There may also be plasma volume loss into the interstitium — we accept that all of these things may amount to several hundred mls per hour for 12-24 hours, depending on the surgical situation. We are happy to give this and watch all the parameters I referred to before. At some stage (6-12 hours, 12-24 hours ..) we stop the volume and watch. We define the end of the resuscitation period as ‘haemodynamic stability’ as having been reached without a need for either escalating inotrope or further volume load. Usually this point is reached within 12 hours, sometimes 24. All this stuff requires a fair bit of ‘close clinical observation of the patient’. Our nurse:patient ratios in NZ and Australia for critically ill patients (such as severe sepsis) are 1:1 and this is fantastic. We watch the patients like hawks and teach the registrars (senior residents – we don’t have junior residents making decisions in ICU) to do likewise. I know this stuff might seem strange — but it works in our hands. Remember we put in hundreds of PA caths over 25 years and found over and over that they helped us less and less. Outcomes continue to improve at the same rate during their disappearance and afterward …<\/p>\n","protected":false},"excerpt":{"rendered":"
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