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Diagnosis and Treatment of Spontaneous Bacterial Peritonitis

7/30/2015

A 59 year old male with a history of alcoholic cirrhosis presents complaining of shortness of breath and a rectal temperature of 101.1F. With knowing just this information the differential is vast. However, just like with any patient, a thorough search of the etiology of the fever is important. The patient does not have any abdominal tenderness, but a bedside sono shows the liver swimming in ascites. You wonder if this patient has SBP, and if so, what is the best way to treat it.

What is it? Spontaneous bacterial peritonitis is an infection that occurs in patients with cirrhosis and ascites. It is thought to be due to translocation of normal gut flora, and is a common infection in patients with decompensated cirrhosis. As such, the most common bacteria isolated from patients with SBP is E. coli. Other multi-drug resistant organisms can also be responsible and include Klebsiella strains, Enterococcus fecium, and Acinetobacter.

Why do I care? SBP is an infection, and like any infection can cause (severe) sepsis. However, it can also be complicated by acute renal failure and hepatorenal syndrome (HRS). If HRS is present, there is a 90% mortality rate, which is kinda high. Good news is there is something we can do to help prevent this.

What do I need to know? First step is to know that this is a possibility. The typical presentation is what we would expect: fever, chills, pain, diarrhea, and hepatic encephalopathy. However this is not always the case. An estimated 25% of patients with SBP will not have symptoms of the disease. Sometimes the disease is suggested in a patient with ascites and acute decompensation. But now on to the diagnostic criteria, which are based on findgins in the ascitic fluid.

PMN (neutrophil) count > 250 cells/mm3
Positive culture

Something else to know is that there may be bacteria that grow on culture, but it can be due to secondary peritonitis. Basically, the other causes of intra-abdominal infection (cholecystitis, diverticulitis, bowel perforation) can occur in these patients too. Diagnostic studies of ascitic fluid can help to separate primary from secondary disease. If suspected, this is what you should order:

Glucose
LDH
Protein concentration
Amylase
Bilirubin

If two or more of the following are present, then secondary peritonitis is confirmed: Ascites glucose < 50 mg/mL, ascites LDH > serum LDH, or ascites protein > 1.5 g/dL. If amylase and bilirubin are present, if suggest bowel perforation.

What do I need to do? Plain and simple, you need to perform a diagnostic paracentesis. Although this will be case by case, it is a procedure and diagnosis that should be considered in every patient with decompensated cirrhosis.

Once the diagnosis is made, treatment generally consists of a five day course of third-generation cephalosporin, quinolone or oxacillin. Typical treatment examples include:

Ceftriaxone 1 g daily
Cefotaxime 2 g TID

If a multi-drug resistant organism is suspected or on culture in the patient's history, add a second line agent such as Zosyn.

One last thing. As mentioned, HRS can complicate SBP. A treatment that has been shown to reduce the incidence of HRS, and death, is high dose albumin. As a bonus, you can give albumin 1.5 g/kg after the diagnosis is established. Treatment is 1.5 g/kg on day one and 1.0 g/kg on day three.

Case conclusion: You successfully perform a diagnostic paracentesis on your patient and find a PMN count of 320 cell/mm3. You start cefotaxime 2 g and with consultation with the inpatient team, give the patient 1.5 g/kg of albumin. The patient is admitted and has an uneventful hospital course.

References:

Salerno F, La Mura V. Treatment of spontaneous bacterial peritonitis. Dig Dis. 2015;33(4):582-5.

Matt and Mike Ultrasound podcast - paracentesis - not difficult, but like most things...better with ultrasound!

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Push Dose Pressors

7/21/2015

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What is it?
Push dose pressors are a great option to us in the ED. While the majority of us may be familiar with what these are and how to use them, we still could all use a refresher on their utility. Additionally, we now have 12 new faces in the department whom this may be a new concept for.

It is first important to note that EM Crit does the best job talking about this, and this is largely a review of his blog post (EM Crit Podcast 6 - Push Dose Pressors). That is because although push dose pressors have been used in the anesthesia world for decades, they are not as commonplace in the ED. Additionally, a literature search did not turn up much evidence. As such, much of their use and utility is from expert opinion and experience.

As the name implies, push dose pressors are administering a pressor in a bolus or "push dose" IV form. The two common drugs used in this scenario are epinephrine (alpha and beta) and phenylephrine (pure alpha).

Why does it matter?
These matter because they can be life saving interventions, in the right circumstances. A classic example is the hypotensive patient that needs to be intubated. Sure they may be fine with etomidate, but intubating an unstable patient may be nerve wracking and could potentially precipitate them coding. Or how about the unstable atrial fibrillation patient with RVR that does not convert after an initial shock? These are just two examples of why it matters to be able to temporarily raise the BP until you have the time or opportunity to stabilize the patient.

What do I need to know?
Our pharmacy helps us out and mixes dwindle epi and stocks it in the Pyxis. That's great, until you are in the real world and do not have this luxury. In that case, you need to know how to mix it.

First for epinephrine

Get a 10 mL NS flush
Remove 1 mL
Take a vial of "code dose" or 1:10,000 concentration of epinephrine. This has 1 mg in the 10 mL vial. This gives you 0.1 mg or 100 micrograms/mL
Draw up 1 mL (100 micrograms) into the NS flush
This gives you 10 mL of epinephrine with a final concentration of 10 mcg/mL

Phenylephrine

Get a 10 mg/mL vial of phenylephrine
Draw into a syringe
Inject into a bag of 100 mL of NS and shake
This gives you 100 mL of phenylephrine at a concentration of 100 mcg/mL

What do I need to do?
Dosing
Epinephrine

1-2 mL or 10-20 micrograms every 2-5 minutes
This would be equivalent to 2-10 mcg/min, which is a typical dosing order if you order an infusion in EPIC
Duration of action is 5-10 minutes

Phenylephrine

0.5-2 mL or 50-200 mcg every 2-5 minutes
This would be equivalent to 10-100 mcg/mL. A atypical dosing order would be 50-150 mcg/min
Duration of action 10-20 minutes

Hope you enjoyed the primer on push dose pressors. Keep them in the back of your mind, but remember to always use with caution and in the appropriate clinical scenario.

Disclaimer: This is for informational purposes only and is not intended to provide recommendations or provide clinical guidelines.

Submitted by Dr. Michael Craddick, PGY-2

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Acute Pericarditis: Review of the Diagnosis and Management

7/21/2015

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Acute pericarditis is a diagnosis many of us are familiar with. Since medical school, we have been taught the classic presentation of pleuritic chest pain that improves with leaning forward, worsens with lying flat, and has associated PR depressions and diffuse ST elevations on ECG. But is the diagnosis that easy? What is the required workup? Who needs to come in the hospital? What is the best way to treat This will be a brief review to cover these essential clinical questions.

What is it?
Acute pericarditis is, as the name would imply, an inflammation of the pericardium. The vast majority of these cases are idiopathic, but assumed to be due to a virus. The other 10-20% can have a specific cause such as connective tissue disease (SLE), cancer, or post-MI syndromes. Its true incidence is not known because mild cases may never be diagnosed, but it does make up around 5% of patients who will present to the ED with chest pain.

Why do I care?
Acute pericarditis is usually a self-limited condition with a low (~1%) mortality rate. Although 1/3 of cases may be associated with myocarditis, clinical heart failure and arrhythmias are rare at time of presentation. Further, the long-term prognosis for both idiopathic pericarditis and associated myocarditis is excellent. Even so, specific therapies are indicated for pericarditis and mismanagement of the condition can lead to its recurrence. It is still therefore important to recognize and treat this appropriately.

What do I need to know?
First step is making the diagnosis. To do this you need at least 2 of the following 4 criteria.
1. Chest pain consistent with pericarditis (ie - pleuritic chest pain that improves by leaning forward)
2. Pericardial friction rub (difficult to hear and inconsistent even when present)
3. Typical ECG signs (PR depressions and diffuse ST elevations)
4. Pericardial effusion (importance of learning and being efficient in bedside echo)

The diagnosis may not always be clear, and other causes of pleuritic chest pain may need to be excluded. If other causes are excluded and pericarditis is not confirmed, but remains the most likely, it should be treated as per recommendations.

Pericarditis may be idiopathic, but as mentioned above, can be seen in other specific conditions as well. The major considerations should be systemic lupus erythematous. Think about this as a possibility of any patient with SLE, or that fits with its classic demographics (young female).

What do I need to do?
A atypical chest pain workup should suffice for the majority of these patients. While sending a troponin is sometimes debatable, it is generally recommended. This will help to determine if co-existing myocarditis is present. This is important to consider for the young patient you might have only ordered a CXR and ECG on otherwise. CRP can be sent as well for evidence of inflammation, but remember it is not a specific test. A bedside or official echo should be done to evaluate for effusions. Pericardiocentesis does not need to be done unless there is tamponade. Further testing such as cardiac CT or MRI can be done, but often not necessary for uncomplicated pericarditis.

The recommended treatment options currently consist of NSAIDs and colchicine. A PPI should also be prescribed for gastric protection. Steroids are not recommended due to high rates of reoccurrence when prescribed. An exception would be for SLE.

Options for NSAIDs - duration of therapy 1-2 weeks

ibuprofen 600-800 mg every 6-8 hours
indomethacin 25-50 mg every 8 hours
aspirin 2-4 grams daily divided BID

Colchicine - duration of therapy 3 months

0.5 mg daily if < 70 kg
0.5 mg BID if > 70 kg

Unless there is a large effusion, evidence of tamponade, or a worrisome secondary cause of pericarditis, patients can be safely discharged home with outpatient follow up.

A little longer post than my others, but lots of good stuff here. For the podcast version of this, check out the Cardiology Corner section of the July edition of EM:RAP. Thanks for reading, now go save some lives.

References
LeWinter MM. Clinical practice: acute pericarditis. N Engl J Med. 2014 Dec 18;371(25):2410-6.

Submitted by Dr. Michael Craddick, PGY-2

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Diagnosis and Treatment of Spontaneous Bacterial Peritonitis

Push Dose Pressors

Acute Pericarditis: Review of the Diagnosis and Management

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