Aggressive fluid therapy in Severe Septic Shock and ARDS.

Specialties CRNA

Published

This isn't meant to be an official scientific document, so I apologize in advance for the sloppy work.

It's been widely known that increased fluid volume can lead to edema. My theory is based upon the intentional inducement of mild to moderate edema in order to increase capillary leakage from intravascular to extravascular spaces. Increased capillary leakage would allow increased antibiotics to diffuse from intravascular to extravascular space. The fluids I would think most appropriate would be normal saline and lactated ringers. Large macromolecules, such as hespan and blood, should not be used as their properties would prevent diffusion in the appropriate direction. Maintainance of CVP=12 would seem to induce adequate edema, although that may be somewhat excessive, especially in pts with aneurysms.

In some cases of pneumonia-induced ARDS(from whatever specific microbial agent, such as TB, streptococcus, etc), pulmonary edema may be extraordinarily beneficial. It's my theory that bacteria may reside in areas of the lungs that antibiotics may have difficulty penetrating to. Induction of pulmonary edema would allow for increased diffusion of the antibiotic and allow for deeper penetration to needed tissues where bacteria may reside.

While intentionally induced pulmonary edema may exacerbate the ARDS, several modes of ventilation exist to support the patient during these times, including bilevel. The clinician's own judgement, experience, and pt's lab values, should be used to determine the best mode of ventilation while also following conventional medication for adequate ventilation (ie, paralysis and sedation for pts on bilevel).

There are a variety of complications to be considered. The two most notable are hemorrhage from aneurysms, which may result from weakened blood vessels and increased intravascular pressures, and cerebral edema. To prevent hemorrhage, a decrease in CVP may be used, although it may also decrease the amount of extravascular leakage needed for proper antibiotic concentration. Personal judgement and experience will play a factor. To prevent cerebral edema, which will occur in a small minority of patients, I would suggest use of an intracranial pressure monitoring device.

In addition for aggressive fluid therapy, hypothermic therapy would also play an important factor in pt outcome. There are a number of trial studies using hypothermia, and you may look any number of them up (I recommend the Cool MI studies) and see for yourself the benefits of hypothermia. The cool MI studies suggest a temp between 33-34 degrees Celsius.

Thoughts, comments?

My experience with pulmonary edema, especially severe, is very poor outcomes for the patient. This would be the last thing I would want to induce in anyone because a great number of times you can't oxygenate them no matter what vent setting you use. If this is a heart patient, the increased peep to ventilate a patient only causes major problems with the CO. I had a patient once in flash pulmonary edema on a peep of 36 (couldn't tolerate other vent settings) where the docs had to place bilat chest tubes prophylactally to prevent pneumos. Pulmonary edema is one of those instances (especially in renal patients) with which you can loose control very quickly.

i guess my only point here....

so you have an ards pt that already requires extensive measures to keep them alive...every question that is asked is only answered with an answer that requires another procedure on the patient...

first it is placing them in pulmonary edema....

then it is dialysis...

what next...heart transplant to fix the ARDS?!?!?!?

i do appreciate the posts - i learn so much from them - and love it.

but - i think in the quest for the betterment of medicine - pt's shouldn't suffer more, but less.

"I think that Dopamine 2-5 mcg/kg/min would benefit most of these pts, and I've seen many of the pts recover from their acute renal failure after being on renal dose dopamine."

There is no such thing as renal dose Dopamine. Show me the literature and educate me if you think differently.

Versatile Kat

Low dose dopamine 1-3mcg/kg/min increased renal blood flow and urine output ( Anesthesiology & critical Care Drug Handbook)

Renal effects of dopamine predominate when the dose of dopamine is less than 3mcg/kg/min. This dose can also inibit secretion of aldosterone which along with dopamine receptor stimulation results in increased urine output. B-adrenergic effects 3-10mcg, Alpha & Beta 10-20 mcg, predominantly Alpha at greater than 20mcg.

(Basics of Anesthesia. Stoelting & Miller)

Renal dose stimulates dopamine receptors ( D1, D2) in in the peripheral mesenteric and renal vascular beds.

Contrary to what we had been told for countless years, the popular opinion at the moments is that there is no longer such an infusion of dopamine which helps with renal perfusion. You will find sources to support renal dose dopamine, but they are now not considered current.

London88 - I appreciate your verbatim from the drug guides, but that's not what I mean. I want to see journal articles stating that there is such a thing as "renal dose dopamine". As far as I know, there aren't any. Please school me!!! :confused:

If you cannot trust your textbooks, and I realize that by the time they are published there is new information rendering some of the info obsolete, what do you go by? If you cannot believe the text books and there is no available journal articles what is there to go by? Renal dose dopamine is what is still being taught in the CV class at my school. Wether or not this information is correct is debatable but that is what is being taught.

Specializes in Renal, Haemo and Peritoneal.

If you are dialysing an acute patient you need to keep them wet so you don't kill off their renal function. PAX.

In my ICU internship they taught us that there is no such thing as renal dose dopamine. They said the increased urine output just comes from improved flow overall.

London88 - I appreciate your verbatim from the drug guides, but that's not what I mean. I want to see journal articles stating that there is such a thing as "renal dose dopamine". As far as I know, there aren't any. Please school me!!! :confused:
Here's your articles. Two support benefits of renal dose dopamine, the third disputes this. PubMed is an easy tool to use for accessing current research articles. Most have links to the publisher to obtain the full article. Some of the most recent published articles will have only the abstract available. A trip to your friendly, local library is the only energy expenditure required to obtain the latest information.

Increasing renal blood flow: low-dose dopamine or medium-dose norepinephrine.

Chest. 2004 Jun;125(6):2260-7.

Di Giantomasso D, Morimatsu H, May CN, Bellomo R.

Department of Intensive Care, Austin and Repatriation Medical Centre, Heidelberg, Germany.

BACKGROUND AND OBJECTIVES: Many clinicians believe that low-dose dopamine (LDD) [2 micro g/kg/min] increases renal blood flow (RBF) and medium-dose norepinephrine (MD-NE) [0.4 micro g/kg/min] decreases RBF. They also believe that MD-NE might induce mesenteric and/or coronary ischemia. In fact, the effects of these drugs on renal and vital organ blood flow are poorly understood. The aim of this study was to compare the effects of 6 h of IV LDD and MD-NE infusion on mammalian renal, coronary, mesenteric, and sagittal blood flow. DESIGN: Randomized, controlled, experimental animal study. SETTING: Animal laboratory of tertiary physiology institute. SUBJECTS: Seven Merino cross sheep were studied. MEASUREMENTS AND RESULTS: We performed a staged insertion of transit-time flow probes around ascending aorta, sagittal sinus and circumflex coronary, superior mesenteric, and left renal arteries. We then randomized these animal with long-term embedded flow probes to either 6 h of placebo (saline solution) or drugs (MD-NE at 0.4 micro g/kg/min or LDD at 2 micro g/kg/min), and performed continuous measurement of systemic pressures, cardiac output (CO), and flow to vital organs. We also sampled blood and urine for the measurement of lactate, creatinine, and creatinine clearances at preset intervals. RESULTS: Compared to placebo, LDD did not affect systemic hemodynamics. However, it increased mean RBF by 20% (267.3 +/- 87.6 mL/min vs 222.0 +/- 74.4 mL/min, p = 0.028) without a detectable effect on other vital regional circulations. MD-NE, however, increased mean arterial pressure (101.0 +/- 8.3 mL/min vs 84.2 +/- 5.2 mL/min, p = 0.018) [mean +/- SD] and CO (4.93 +/- 1.45 L/min vs 3.81 +/- 0.57 L/min, p = 0.028). It also increased coronary blood flow (36.0 +/- 15.7 mL/min vs 23.0 +/- 10.7 mL/min, p = 0.018) and RBF (286.5 +/- 79.0 mL/min vs 222.0 +/- 74.4 mL/min, p = 0.018). MD-NE had no detectable effect on mesenteric or sagittal sinus flow. LDD infusion increased urine output, but did not change creatinine clearance. MD-NE infusion increased urine output significantly more than LDD but not creatinine clearance. CONCLUSIONS: Both LDD (2 micro g/kg/min) and MD-NE (0.4 micro g/kg/min) increased RBF and urine output. However, the effect of MD-NE was more pronounced. LDD did not affect other vital organ flows, but MD-NE increased coronary blood flow without any changes in mesenteric and sagittal sinus blood flow.

Should we give prophylactic renal-dose dopamine after coronary artery bypass surgery?

J Card Surg. 2004 Mar-Apr;19(2):128-33.

Gatot I, Abramov D, Tsodikov V, Yeshaaiahu M, Orman S, Gavriel A, Chorni I, Tuvbin D, Tager S, Apelbom A.

Department of Cardiothoracic Surgery, Soroka Medical Center, Beer Sheva, Israel.

OBJECTIVE: A prospective double-blind randomized study undertaken to assess the effect of postoperative prophylactic "renal-dose" dopamine on post-coronary artery bypass grafting surgery's clinical outcome. METHODS: Eighty-five consecutive patients undergoing CABG operation were randomized to receive either 3-5 microg/kg/min dopamine (group D, n = 41) or saline as placebo (group P, n = 45) for 48 postoperative hours. Clinical outcome parameters were collected for four postoperative days. RESULTS: Preoperative and operative parameters were similar in both groups. Four patients from group P and none from group D reached an end-point of the study (oliguria, renal dysfunction) and received dopamine. Two patients from group P and none from group D needed an additional inotropic support. Mean arterial pressure values were similar during the first 24 hours after operation, but left atrial pressure values tended to be higher in group P (10 +/- 4 vs 7 +/- 3 mmH2O, p = 0.18). The mean pH was higher in group D at 8 hours after operation (7.38 +/- 0.2 vs 7.36 +/- 0.3, p = NS), due to higher bicarbonate levels (23 +/- 2 mmol/l vs 21 +/- 2, p = 0.49). The incidence of lung congestion in chest X-rays and CT scans was significantly higher in group P (50% vs 29%, p = 0.073 at 48 hours postoperatively). Room air blood O2 saturation and maximal expiratory volume tended to be higher in group D (at 72 hours after operation- 92 +/- 4 vs 90%+/- 5, p = 0.29 and 646 +/- 276 vs 485 ml +/- 206, p = 0.16, respectively). There was no statistical difference in urine output but the amount of furosemide given to patients in group P was significantly higher (during the first 8 hours 2.5 +/- 0.5 vs. 0.3 mg +/- 1.6, p = 0.07). Plasma creatinine levels were significantly lower in group D (at 24 hours 0.93 +/- 0.02 vs 1.05 mg/dL +/- 0.02, p = 0.02). Mobilization after surgery was faster in group D. CONCLUSIONS: Prophylactic dopamine administration after coronary artery bypass grafting surgery improves patient hemodynamic and renal status, reduces the need for additional medical support (inotropes and furosemide) and thus, provides stable postoperative course.

Is there still a place for dopamine in the modern intensive care unit?

Anesth Analg. 2004 Feb;98(2):461-8.

Debaveye YA, Van den Berghe GH.

Department of Intensive Care Medicine, Catholic University of Leuven, Leuven, Belgium.

For many years, dopamine was considered an essential drug in the intensive care unit (ICU) for its cardiovascular effects and, even more, for its supposedly protective effects on renal function and splanchnic mucosal perfusion. There is now ample scientific evidence that low dose dopamine is ineffective for prevention and treatment of acute renal failure and for protection of the gut. Until recently, low-dose dopamine was considered to be relatively free of side effects. However, it is now clear that low-dose dopamine, besides not achieving the preset goal of organ protection, may also be deleterious because it can induce renal failure in normo- and hypovolemic patients. Furthermore, dopamine may cause harm by impairing mucosal blood flow and by aggravating reduced gastric motility. Dopamine also suppresses the secretion and function of anterior pituitary hormones, thereby aggravating catabolism and cellular immune dysfunction and inducing central hypothyroidism. In addition, dopamine blunts the ventilatory drive, increasing the risk of respiratory failure in patients who are being weaned from mechanical ventilation. We conclude that there is no longer a place for low-dose dopamine in the ICU and that, in view of its side effects, its extended use as a vasopressor may also be questioned.

of course there is such a thing as renal dose dopamine with the inference being that with low dose dopamine you are able to provide for natriuresis and diuresis --- however what has been proven wrong was the belief that renal dose dopamine will prevent renal failure, or that somehow it improves outcome in renal failure.

Passin' Gas, thanks a million for the articles. :)

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