Flash pulmonary edema

Acute onset shortness of breath is a common reason for referral to GIM and congestive heart failure is in the top three admission diagnoses in most hospitals. Flash pulmonary edema is a rapid development of pulmonary congestion, usually secondary to the development of increased left ventricular diastolic pressure. It can present quite dramatically, as the name suggests, having impressive pulmonary infiltrates, dyspnea and hypoxemia.

Risk factors for flash pulmonary edema are similar to other risk factors for heart failure, including:

HTN
ischemic heart disease
valvular heart disease
diastolic dysfunction
bilateral renal arterty stenosis

The diastolic dysfunction that leads to high pressures may be suggested on echocardiography. First, we should review the phases of diastole, which include:

Isovolumetric phase
early atrial empyting
stasis phase
atrial contraction

On echo, the early (E) to atrial contraction (A) phase should be relatively high, where E >75% of the interval. As diastolic dysfunction develops this ratio will decrease <1 .="" a="" additional="" and="" can="" changes="" eventually="" occur="" over="" pseudonormalization="" ratio="" see="" time="" where="" you="">2 suggesting restricted filling. 
This can be seen in patients with chronic diastolic dysfunction.

Mitral regurgitation is another cause of flash pulmonary edema. If there is ischemia to the papillary muscles they can rupture or become dysfunctional. This would be evident by a loud regurgitant holosystolic murmur best heard at the apex. Ischemia can be related to anterolateral papillary muscle dysfunction or posteromedial dysfunction. The anterolateral muscle is supplied the LAD and Cx artery, while the posteromedial tends to be only supplied by the posterior descending artery (PDA). As a result the collateral circulation of the anterolateral muscle makes it less susceptible to rupture. The PDA can stem from several possible arteries, which determines the dominance of the coronary circulation:

A "right dominant" circulation occurs when the PDA stems from the RCA.
A " left dominant" circulation occurs when the PDA stems from the Cx.
A "codominant"circulation occurs when the PDA stems from the Cx and RCA.

In the setting of acute MR from ischemia, cardiovascular surgery may be required. Surgery should also be considered in patient with severe MR (regurg fraction >50%, orifice >0.4cm, volume of regurgitation >60%

Approximately 70% of the population is right dominant, where only 10% are left dominant.

Renal artery stenosis, whether artherosclerotic or fibromuscular dysplasia can result in flash pulmonary edema (formerly known as pickering syndrome). Overall it may cause up to 5% of HTN in adults. Patient with refractory HTN or flash pulmonary edema may be considered for renal artery stenting, however there another recent trial that suggested this intervention is no better than medical therapy alone. Think about RAS in the following settings:

1. Worsening kidney function of 30% in started and ACEi
2. Systolic/Diastolic renal bruit
3. Onset HTN after 55
4. Flash pulmonary edema
5. Asymmetry in renal size >1.5 cm (see previous RAS blog post)

Here is the latest NEJM article on RAS stenting efficacy

NEJM RAS stent vs medical managment

Pyogenic liver abscess

Discussion today surrounded an atypical presentation of a pyogenic liver abscess. Typically, this condition will present with fever, sweats, abdominal pain (usually RUQ) and occasionally symptoms of systemic infection. Todays case was a bit strange, given the only consistent features were constitutional symptoms, and atypical chest and abdominal pain were misleading. As a result, one must have a high index of suspicion for a liver abscess with fever of unknown origin (FUO). Following negative preliminary testing in the evaluation of FUO abdominal imaging should be considered, especially when there are abnormal liver enzymes. This approach led to a diagnosis in 19% of cases where first line tests were unrevealing.

Pyogenic liver abscess is the most common visceral location for focal infection. That being said, its really not that common, where some studies quote 2-3 cases per 100,000. Most studies on epidemiology of liver abscess have been performed in South East Asia, and may even be more uncommon in our population.

These infections can develop through several mechanisms:

1. Hematologic bacteremia leading to seeding
2. Biliary obstruction and reflux of bacteria into liver parenchyma
3. Direct invasion through adjacent structures (gastric perforation) or contact through bowel leakage/perforation

Most often these infections involve the right side of the liver given the blood supply tends to be larger for this lobe.

Many micro-organisms can cause liver abscess formation. Some of these include:

Strep. anginosis, staph. aureus and strep pyogenes are amongst the most common pathogens involved. Klebsiella sp., as in our patient, which is a gram negative abscess forming bacteria is also well described. There was a large case series from Taiwan which found that Klebsiella was a common cause of liver abscess (nearly 70%), most often developed in the community, and was associated with DMII and hyperglycemia.

The treatment of these patients is antibiotic therapy, with a strong focus on source control. Abscess drainage can be both therapeutic and diagnostic and is a required part of therapy unless the abscess are too small for drainage. Antibiotic therapy should be targeted towards the identified infection, and duration consist of at least 4 weeks of IV antimicrobials.

One case series of Klebsiella liver abscess patients found an overall mortality rate of nearly 10%, and a relapse rate of 4%. Sepsis was the cause of death in all of those who died. This organism can be aggressive and patients should be evaluated for additional metastatic sites of infection.