Pneumocystis jirovecii Pneumonia

Today in morning report we discussed the diagnosis and management of PJP.

Check out this previous blog post on the subject.

Note that workup of a patient with suspected PJP includes an artieral blood gas on room air to determine if criteria are met for treatment with steroids. These are:
- PaO2 less than 70 mmHg
- Aa gradient greater than 35 mmHg

If oxygen saturation is low by pulse oximetry, this would also qualify the patient for steroids.

Vertigo

Today we talked about a patient with vertigo who ended up having something really rare.

It gave us a chance to revisit the often tricky approach to vertigo.

Here are some important points:

1) Key question is distinguishing a peripheral from a central cause of vertigo, as the central causes are the most dangerous. There are some clues on history and physical exam that can help:
History: 
- Stroke risk factors: central
- Presence of other neuro symptoms: central
- Presence of other ear-related symptoms: peripheral

Physical:
- Vertical or gaze-evoked (ie changes direction depending on where patient looks) nystagmus: central
- Nystagmus suppresses with visual fixation: peripheral. Note: would also increase when fixation removed, can test this by using fundoscopy, nystagmus seen with ophthalmoscope to increase when you cover the other eye
- Severe unsteadiness (even with eyes open): central (note in peripheral may tilt to side of lesion, romberg positive)
- Any other neuro findings: central

2) Consider brain imaging even if history and physical suggest a peripheral cause in the following cases:
- older patient
- stroke risk factors
- and acute onset vertigo that persists for more than 48 hours

MRI/MRA are needed in this case since CT is not great for our areas of interest: the brainstem and cerebellum.

 Note that a labyrinthine TIA/stroke will look like a peripheral lesion on history and physical.

3) The image above probably depicts something similar to the Dix-Hallpike maneuver, used to diagnose Benign Paroxysmal Positional Vertigo.

Follow this link to see a video of the nystagmus seen in such patients.

Follow this link for a great NEJM review of acute vertigo. It's an oldie but a goodie.

Infective Endocarditis

Today we had a very high yield morning report on infective endocarditis.

Here is a recap of some important points from the discussion:

1) The Modified Duke's criteria is used to make the diagnosis.
Diagnosis is made by any of the following:
- pathology confirmation
- presence of 2 major criteria
- presence of 1 major and 3 minor criteria
- presence of 5 minor criteria

Possible endocarditis: 1 major and 1 minor OR 3 minor criteria are met.

Major Criteria:
A) Micro criteria (any of the following)
a) Culture of a typical endocarditis organism (in 2/2 cultures)
- Staph Aureus
- Viridans group Strep
- Strep gallolyticus (formerly Bovis) and nutritionally-variant strep
- HACEK organism
- Community-acquired enterococci (no primary focus)

b) Single positive culture of Coxiella Burnetti (Q fever) on culture or serology IgG positive >1:800

c) Persistently positive cultures with another organism: 3/3 positive or 3/4 positive.

B) Evidence of cardiac disease: do TTE first, then TEE if prosthetic valve OR at least possible I.E. by clinical criteria. Any of:
- vegetation
- abscess
- new partial dehiscence of prosthetic valve
- new regurgitant murmur

Minor Criteria: 
- Vascular phenomena: splinter hemorrhages, conjunctival hemorrhages, Janeway lesions,
- Embolic phenomena: Glomerulonephritis, RF positivity, Osler's nodes, Roth spots
- fever of at least 38 degrees
- predisposing condition: IVDU, congenital cardiac disease or prosthetic valve
- positive cultures not meeting descriptions above.

2) When is prophylaxis for endocarditis needed? In a high-risk patient AND a high-risk procedure
High risk patients:
- past IE
- prosthetic valve
- uncorrected cyanotic shunts, or in first 6 months post correction
- heart transplant valvulopathy

High risk procedure:
- dental with gingival manipulation
- transbronchial biopsy
- involving infected GI, GU, skin, muscle

3) When to consult cardiac surgery in endocarditis:
- refractory CHF or shock
- uncontrolled infection: abscess/fistula, ongoing fevers, ongoing culture positivity, or fungal or resistant organism
- very large vegetation (>1cm)
- reucrrent embolic phenomena


Check out this very recent small study published in NEJM which sheds some light on those "debatable" indications for cardiac surgery (ie. size of vegetation and embolic phenomena). In this study, patients randomised to early surgery had significantly fewer embolic events (most of these were strokes) than those who had conventional therapy. Of note, 77% of patients on the conventional therapy group went on to have surgery (just later) and there was no difference in 6 month mortality in the two groups.

Here is a link to the classic NEJM review on endocarditis 

Hepatorenal Syndrome

Today in morning report we heard about a patient with decompensated liver disease. He presented with jaundice and an elevated creatinine.

When patients with cirrhosis present with an AKI, we ask is this Hepatorenal syndrome or something else?

Things that can trigger renal failure in cirrhotic patients:
- Overdiuresis

- NSAIDs (cirrhotic patients very dependent on renal prostaglandin synthesis) and other nephrotoxins
- GI bleed
- Bacterial infections including translocation of bacteria in gut and spontaneous bacterial peritonitis (SBP)
- Any acute decompensation of cirrhosis

Hepatorenal Syndrome is "characterized by functional renal vasoconstriction that leads to a severe reduction in GFR with minimal renal histologic abnormalities" (NEJM, see below). The figure above shows which mechanisms lead to this.

Type 1: Develops rapidly. Creatinine doubling over less than 2 week period
Type 2: More gradual than type 1.

To be labelled hepatorenal syndrome:
- no improvement after 2 days off diuretics and albumin 1gm/kg/day for 2days minimum
- no recent nephrotoxic drugs
- no shock
- no evidence of renal parenchymal disease (significant proteinuria, hematuria, or abnormal looking kidneys on ultrasound)

Initial Management of AKI in patient with ascites:
- Exclude bacterial infection: diagnostic paracentesis + other cultures
- Exclude GI bleed
- Hold diuretics
- Stop nephrotoxic drugs

- give a trial of albumin as above

Distinguishing hepatorenal syndrome from ATN can be tricky as both can cause the presence of heme granular casts in the urine. Once diuretics are held, a FENa (fractional excretion of sodium) less than 1% supports the diagnosis of hepatorenal syndrome.

Specific therapies for hepatorenal syndrome:
- Terlipressin: improves renal function, no effect on survival found so far
- Midodrine and octreotide together: small studies suggest benefit on renal function

- TIPS= transjugular intrahepatic portosystemic shunt: some observational studies show improvement, however many patients with HRS too sick to undergo this procedure

- Liver transplantation- don't forget to consider this

Prognosis of HRS is very poor. Mortality is higher with type 1 hepatorenal syndrome than with type 2 (median survival, 1 month vs. 6 months)

Prevention of HRS in patients with ascites:
- Albumin as part of treatment for SBP: 1.5 gm/kg at initiation and 1gm/kg at 48 hours.
- Prevention of SBP with norfloxacin in selected patients- see this study


Here is a link to the most recent NEJM review on the topic

Flash Pulmonary Edema

Today in morning report we touched on the causes of flash pulmonary edema. We haven't addressed this on the blog previously, so I thought we would go over it:

Flash pulmonary edema is a particularly sudden form of Acute Decompensated CHF (in patient without chronic CHF). Mechanism of flash pulmonary edema is a sudden increased in LV end-diastolic pressure

Classic causes of flash pulmonary Edema:

1) Primary Cardiac Problems
- Mitral stenosis: in setting of tachycardia, atrial fibrillation, or high circulating volume of pregnancy
- Acute mitral or aortic regurgitation
- Arrythmia in a patient with pre-existing diastolic dysfunction
- Sudden Pump failure: acute MI or stress-induced cardiomyopathy

2) Hypertensive Emergency

3) Renovascular
Bilateral renal artery stenosis more commonly than unilateral. Patient with RAS are predisposed to developping flash pulmonary edema because of "(i) defective natriuresis; (ii) increased haemodynamic burden and exacerbation of diastolic dysfunction and (iii) failure of the pulmonary capillary blood–gas barrier" (Messerli FH. Eur Heart J (2011) 32 (18): 2231-2235). 

Acute Treatment is centered around decreasing preload as well as afterload:
- Lasix
- (Morphine) Limiting supporting data. In theory, decreased sympathetic drive, thus leads to veno/arterial vasodilatation
- Nitroglycerin (venodilator thus reduces preload,  weaker arterial vasodilator)
- Oxygen
- P= Position (sitting up) but also Pressure (ie. Non-Invasive Positive Pressure Ventillation aka CPAP or BiPAP)

Have a great day!