There are 2 situations in the ED that warrant the use of prophylactic antibiotics; some cases of acute pancreatitis and chest tube insertions.
(thank you K.B. for this valuable info!)
Regarding Acute Pancreatitis, There's a 2009 article which was published in the Current Infectious Disease Reports, discussing the issue of the prophylactic abx in two main conditions: Severe Acute Pancreatitis ( SAP ) and Gall Stone Acute Pancreatitis ( AP ).
SAP:
- most common bacteria is Gram negative mostly E.Coli. Gram positive ( staph. Aureus & staph epidermidis ) were observed more in patients who recieved prophylactic antibiotics
- Infections of pancreatic necrosis & abscess formation is obsereved in about 30% in patients with Necrotizing Pancreatitis( NP ) & 10% in AP.
- Mortality & Morbidity is strongly determined in SAP by the early development of MSOF , extent of the necrosis, and sepsis caused by infected necrosis.
-Based on high quality , double blinded, randomized , placebo-controlled trials, Abx prophylaxis in SAP has no clinical benefit for reducuing pancreatic infection, decreasing morbidity, and improving hospital mortality.
- Two recent Meta-Analysis concluded that evidence based data do not support abx prophylaxis.
Therefore, the use of antibiotic in SAP is recommended on demand in patients who have SAP with multiorgan dysfunction at admission ( < 72 h ) , shock , and for those who develop acute respiratory distress & clinical signs of sepsis and show extended ( >50% ) pancreatic necrosis .
- Rational antibiotic treatment ( according to the sensitivity ) is recommended .
AP:
- Abx treatment in recommended for patients who additionally have acute cholecyctitis or cholangitis ( with common bile duct lithiasis ) and Fever > 38.5 C.
[References:
THE USE OF ANTIBIOTICS FOR ACUTE PANCREATITIS : IS There a Role?
Hans G.Beger, MD, Frank Gansauge, MD, Bertram Poch, MD and Michael Schwarz, MD
Current Infectious Disease Report 2009, 11:101-107]
As for prophylaxis in Chest Tube Insertion:
- The role of presumptive antibiotics for the prevention of empyema and pneumonia following chest tube insertion remains controversial.
- Risk Factors for infections such as : mechanism of injury, hemothorax, retained hydrothorax, alcoholism, or presence of chronic disease should be considered.
-When administered, Abx should have mainly a gram positive coverage.
- There's no Level 1 recommendation, Level 2 says that there's insufficient data to support routine use of antibiotics in patients who undergo chest tube due to spontaneous pneumothorax. Level 3 suggests antibiotics for those who have traumatic pneumo/hemothorax AND have additional risk factors for infections. However, In emergency situation Abx use shouldn't delay the insertion of the chest tube.
[References:
Guidlines prepared by the Department of surgical education , Orlando Regional Medical Center]
Thursday, May 6, 2010
Friday, April 23, 2010
Blood Pressure in Stroke
Today’s discussion: Why and How do you control the blood pressure in both ischemic and hemorrhagic stroke?
To know the rationale behind the need to lower the blood pressure in stroke and the limitations, we have to review the cerebral physiology and cerebral autoregulation.
Where CBF: cerebral blood flow
CPP: cerebal perfusion pressure
CVR: cerebral vascular resistance
The issue in ischemia is that it disrupts that cerebral autoregulation, so the CVR does not respond to changes in CPP.
Another thing to consider is that the impact of decreased cerebral blood flow (CBF) is related to both the magnitude and duration , therefore:
- CBF <10-15 mL for more than a short time = neuronal death. Labeled as “infarct”
- CBF 15-20 mL = neuronal functional impairment. Labeled as “penumbra”
The “Penumbra” is an area of high CBF, high O2 consumption, and preserved metabolic rate. This area is seen by PET, and sometimes with MRI. It’s ischemic, but not infarcted. It is very vulnerable to any decrease in blood pressure.
On the other hand, leaving the blood pressure too high predisposes the patient to more bleeding and hematoma formation in hemorrhagic stroke, and to more edema and hemorrhagic transformation in ischemic stroke. However, clinical data supporting this theory is sparse.
A few pointers to keep in mind:
- Patients with chronically uncontrolled HTN have “reset” their “normal” CPP to a higher level, so their CBF decreases at a relatively higher MAP. Therefore, lowering their blood pressure too much can be detrimental.
- Patients with carotid stenosis will have even more compromised cerebral blood flow with acute reduction in blood pressure.
Now that we’re done with the logic behind it, here’s the most consistent data for management of BP in stroke (according to Rosen’s 6th Edition); most of it was reached by consensus:
As for ischemic strokes;
As for hemorrhagic strokes, these are the latest AHA guidelines:
A few pointers to remember:
- MAP= 1/3 SBP + 2/3 DBP
- Labetalol should be avoided in asthma, acute heart failure, or severe cardiac conduction abnormalities.
- In refractory HTN, other agents may be considered. However, drugs that cause precipitous decrease in bp should be avoided, such as sublingual nitroglycerin and calcium channel blockers (CCB)
So to sum it up:
- If the blood pressure is too high, the patient will rebleed (especially in hemorrhagic strokes).
- If the pressure is too low, the patient will infarct his penumbra (especially in ischemic stroke)
- Therefore, blood pressure must be controlled in acute stroke; in hemorrhagic stroke more than ischemic, and in patients managed with tPA more than non-thrombolytic candidates
To know the rationale behind the need to lower the blood pressure in stroke and the limitations, we have to review the cerebral physiology and cerebral autoregulation.
CPP: cerebal perfusion pressure
CVR: cerebral vascular resistance
The issue in ischemia is that it disrupts that cerebral autoregulation, so the CVR does not respond to changes in CPP.
Another thing to consider is that the impact of decreased cerebral blood flow (CBF) is related to both the magnitude and duration , therefore:
- CBF <10-15 mL for more than a short time = neuronal death. Labeled as “infarct”
- CBF 15-20 mL = neuronal functional impairment. Labeled as “penumbra”
The “Penumbra” is an area of high CBF, high O2 consumption, and preserved metabolic rate. This area is seen by PET, and sometimes with MRI. It’s ischemic, but not infarcted. It is very vulnerable to any decrease in blood pressure.
On the other hand, leaving the blood pressure too high predisposes the patient to more bleeding and hematoma formation in hemorrhagic stroke, and to more edema and hemorrhagic transformation in ischemic stroke. However, clinical data supporting this theory is sparse.
A few pointers to keep in mind:
- Patients with chronically uncontrolled HTN have “reset” their “normal” CPP to a higher level, so their CBF decreases at a relatively higher MAP. Therefore, lowering their blood pressure too much can be detrimental.
- Patients with carotid stenosis will have even more compromised cerebral blood flow with acute reduction in blood pressure.
Now that we’re done with the logic behind it, here’s the most consistent data for management of BP in stroke (according to Rosen’s 6th Edition); most of it was reached by consensus:
As for hemorrhagic strokes, these are the latest AHA guidelines:
A few pointers to remember:
- MAP= 1/3 SBP + 2/3 DBP
- Labetalol should be avoided in asthma, acute heart failure, or severe cardiac conduction abnormalities.
- In refractory HTN, other agents may be considered. However, drugs that cause precipitous decrease in bp should be avoided, such as sublingual nitroglycerin and calcium channel blockers (CCB)
So to sum it up:
- If the blood pressure is too high, the patient will rebleed (especially in hemorrhagic strokes).
- If the pressure is too low, the patient will infarct his penumbra (especially in ischemic stroke)
- Therefore, blood pressure must be controlled in acute stroke; in hemorrhagic stroke more than ischemic, and in patients managed with tPA more than non-thrombolytic candidates
Arterial vs Venous Lactate
The other day, the supervising Consultant asked me to look up the difference between arterial and venous lactate. This was a direct result of my big mouth as I was the one who raised this point, since a lot of the articles that talked about lactate made a point to mention that it was “arterial” lactate, whereas some articles just said “lactate”.
The question is, are they really any different?
To answer this question, I googled it! (sorry pubmed lovers, I’m a “google” chick!)
And Here is what I got:
There are 3 studies that compare arterial and central venous lactate in patients in shock/cardiac arrest (J Resuscitation 2008;03:055 , Emerg Med J 2006;23:622-624, Crit Care 2005;9:44). They all came to the same conclusion; the levels are closely correlated. The first one even added that the levels more closely correlated if arterial lactate value was >5mmol/L.
I also came across a nice website (that is Google’s benefit ), called www.emedmag.com , in which there’s an article discussing the most important differences in values of ABGs and VBG, AGs, and finally, lactate.
This website came to the conclusion that since an elevated venous lactate (1.6 mmol/L or greater) is 100% sensitive and 89% specific in predicting elevated arterial lactate level, then a normal venous lactate should be enough, but an elevated venous lactate necessitates that an arterial lactate should be obtained. It cites a 1996 study by Younger of 48 ED patients as a basis for this conclusion. These results were bolstered by a 2000 study by Lavery on 375 hypovolemic patients.
While discussing the findings of my mini-search with my colleagues and seniors, we came to a discussion; is lactate higher in arterial blood or venous blood?
Logic says that it should be higher in venous blood than in arterial, as it is always a result of poor tissue perfusion, and is cleared by the liver, right?
NOT EXACTLY!
According to “The ICU Book” by Paul Marino; Lactate level is not indicative of poor tissue perfusion, but rather is a method of detecting global dysoxia. However, it sometimes indicates other things, such as hepatic insufficiency, thiamine deficiency, severe sepsis (as a direct result of endotoxins rather than O2 deprivation) and, finally, intracellular alkalosis.
It’s interesting how a discussion can clarify some of your most basic concepts!
The question is, are they really any different?
To answer this question, I googled it! (sorry pubmed lovers, I’m a “google” chick!)
And Here is what I got:
There are 3 studies that compare arterial and central venous lactate in patients in shock/cardiac arrest (J Resuscitation 2008;03:055 , Emerg Med J 2006;23:622-624, Crit Care 2005;9:44). They all came to the same conclusion; the levels are closely correlated. The first one even added that the levels more closely correlated if arterial lactate value was >5mmol/L.
I also came across a nice website (that is Google’s benefit ), called www.emedmag.com , in which there’s an article discussing the most important differences in values of ABGs and VBG, AGs, and finally, lactate.
This website came to the conclusion that since an elevated venous lactate (1.6 mmol/L or greater) is 100% sensitive and 89% specific in predicting elevated arterial lactate level, then a normal venous lactate should be enough, but an elevated venous lactate necessitates that an arterial lactate should be obtained. It cites a 1996 study by Younger of 48 ED patients as a basis for this conclusion. These results were bolstered by a 2000 study by Lavery on 375 hypovolemic patients.
While discussing the findings of my mini-search with my colleagues and seniors, we came to a discussion; is lactate higher in arterial blood or venous blood?
Logic says that it should be higher in venous blood than in arterial, as it is always a result of poor tissue perfusion, and is cleared by the liver, right?
NOT EXACTLY!
According to “The ICU Book” by Paul Marino; Lactate level is not indicative of poor tissue perfusion, but rather is a method of detecting global dysoxia. However, it sometimes indicates other things, such as hepatic insufficiency, thiamine deficiency, severe sepsis (as a direct result of endotoxins rather than O2 deprivation) and, finally, intracellular alkalosis.
It’s interesting how a discussion can clarify some of your most basic concepts!
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