Management of Ascites

Today at morning report, we discussed the management of ascites.

I wanted to share with you some guidelines and literature:



Chronic Outpatient Management of Ascites

1. Sodium restriction (88 mmol/day [2000 mg/day])


2. Diuretics (oral spironolactone with or without oral furosemide).


3. Fluid restriction only if serum sodium is less than 120 to 125 mmol/L.

Chronic Outpatient Management of REFRACTORY Ascites

1. Serial therapeutic paracenteses.


2. Postparacentesis albumin infusion may not be necessary for a single paracentesis of less than 4 to 5 L.


3. For large-volume paracenteses, an albumin infusion of 6 to 8 g/L of fluid removed can be considered.


4. Transjugular intrahepatic portasystemic stent-shunt (TIPS) may be considered in appropriately selected patients who meet criteria similar to those of published randomized trials.

Who Needs SBP Prophylaxis?

1. Anyone who has had SBP before.


2. Anyone with cirrhosis admitted with a variceal bleed. See the NEJM paper


3. Anyone with cirrhosis, ascites ascitic protein less than 1.5, creatinine greater than 106 mmol/L OR BUN greater than 8.9 mmol/L), serum Na less than 130, MELD greater than 9 points with bilirubin greater than 3 mg/dL.

One question that came up was whether prophylaxis should be daily or intermittently. Both regiments have been shown to be of benefit in clinical trials, but there is concern that intermittent dosing will lead to bacterial resistance and therefore the preferred regimen according to the AASLD is daily.

Renal Failure in Ascites

Erik mentioned using albumin in patients with SBP. The major evidence supporting this practice is from an article published in the NEJM in 1999 which randomized patients with SBP to either antibiotics alone or antibiotics with albumin. The investigators found a statistically significant reduction in renal dsyfunction and mortality with this regimen.

There was aslo a recent review article on renal failure and cirrhosis in the NEJM.

See the AASLD Guidelines for more information on the management of ascites.

Graves' Disease

Here is a NEJM review on Graves.

We also discussed anti-NMDA receptor encephalitis - there is a case presentation here. A discussion of paraneoplastic syndromes involving the CNS is posted here.

Back in Business

Articles from yesterday's morning report:

NEJM article on acute pericarditis here:

The classic Art of Pimping article here:

Today at morning report we discussed Wegener's Granulomatosis. An older NEJM review of small vessel vasculitis that I like is here

Hyponatremia - no it's Hyperhydroemia

CLINICAL PEARLS WHEN TREATING HYPONATERMIA?

1. In patients on diuretics, the fractional excretion of urea can be used to help determine if patient is hypovolemic. FeUrea= (Uurea/Purea)/(UCr/Pcr)
FeUrea <35% suggests prerenal state.

2. Before accusing someone of having SIADH, you must check TSH and adrenal function (ACTH stim).

3. Acute recognition of a chronic problem (chronic hyponatremia) does not require acute treatment.

4. To prevent overly rapid correction of hyponatremia, consider the role for DDAVP (often given as 1-2mcg SC/IV). If you do correct too quickly (want to correct 0.5 mmol/h at the absolute most) also consider giving D5W in addition to DDAVP - see the article below.

5. If volume repletion is required, give fluid that is isotonic to the patient by using a combination of NS and D5W.

6. Attach the foley catheter to the IV (figuratively) - be sure to monitor urine osm and output - and consider calculating a tonicity balance

Extras:
When seeing hyponatremia in the ER:

First rule out acute hyponatremia that needs acute correction.

Recheck the lytes as they were often done a while ago and the patient has possibly received intravenous fluids that may have significantly altered the sodium concentration - especially if the stimulus (often ECF volume depletion) for ADH secretion has been removed. Following the urine output may help to identify this (although recording can be an issue outside of the ICU) as a brisk, dilute diuresis can be bad sign.



An article on DDAVP to prevent rapid correction is posted here.

Familial Mediterranean Fever

Doctor, There's a Hole in my Heart!?

An interesting article published by one of our staff and residents on morning report can be found here.

A prior blog on the causes of platypnea and orthodeoxia can be found here.

Review of PFO formation:

• The endocardial cushions fuse, separating the heart into R and L sides.

• Early in utero the septum primum grows and fuses with the endocardial cushion, closing the formaen primum, however perorations have developed in the septum primum to fuse, forming the foramen secundum (still allowing right to left shunting)

• A second membrane, the septum secundum, grows on the right atrial side of the septum primum. The septum secundum overlaps the foramen secundum, forming an incomplete septal partition that becomes the foramen ovale. The remaining septum primum forms a flap-like valve over the foramen ovale.
• After birth, normal circulation is established (left sided pressures>right sided) and the flap fuses in 75% of people by age 2. The remainder have a PFO.
• The PFO is completed covered, but not sealed and shunting can occur if there is a reversal in intracardiac pressures (i.e. right to left shunt).
  
• If an open communication exits (no flap) this is an ASD.
  

In studies, PFO prevalance is as high as 25%

A debate on PFO closure (with respect to cryptogenic stroke) can be found in these two Circulation articles: Close v. Don't Close (or at least do an RCT).

SIGNOVER SAFETY

An effective handover is critical to safe and efficient patient care.

The mneumonic "SIGNOUT?" was developed as part of a signover curriculum discussed in this article.

S - Is the patient sick? Stable? Code Status?
I- ID
G - General Hospital Course
N - New events of the day
O - Overall clinical condition
U - Upcoming possibilities (those that can reasonably anticipated) with plan/rationale
T - Tasks to complete overnight (explicit instructions) and rationale
? - Any questions?