HCAP Replacement

Healthcare Associated Pneumonia is no longer considered a clinically useful category,[1] there is little guidance about how to treat patients with pneumonia who are nonetheless at higher risk for resistant organisms.

Since vancomycin for MRSA and antipseudomonal beta lactams are the central considerations for treating resistant organisms, it may be helpful to simply review when one would consider

Guidance when considering vancomycin for MRSA:

1- If a patient has received broad spectrum IV antibiotics recently (within the last 90 days is a reasonable cutoff).

2- Severe illness, where any potential therapeutic advantage is warranted.

3- The history suggests an acutely worsening viral infection suggestive of bacterial superinfection.  The classic example is staph aureus causing a highly morbid superinfection in the wake of influenza or other respiratory virus.

4- Presence of a cavitary lesion on imaging. Cavitation is a serious infection that suggests necrosis, which suggests staph aureus.


Guidance when considering antipseudomonal beta lactams (pipercillin-tazobactam, cefepime, ceftazidime.)

1- If a patient has received broad spectrum IV antibiotics recently (within the last 90 days is a reasonable cutoff).

2- Severe illness, where any potential therapeutic advantage is warranted.

3- If a patient has structural lung disease (bronchiectasis, prior cavitary lesion, cystif fibrosis, etc.)


Important caveats:
1- A negative nasal MRSA swab essentially rules out MRSA pneumonia.[2]

2- Sputum culture is low yield, but harmless and potentially very helpful, especially patients with structural lung disease who often have prior respiratory cultures for guidance.






[1] Mortality in patients with HCAP appears more likely due to comorbid conditions in these chronically ill patients than due to resistant organisms. 
Healthcare-associated pneumonia does not accurately identify potentially resistant pathogens: a systematic review and meta-analysis. 
Clin Infect Dis. 2014 Feb;58(3):330-9. doi: 10.1093/cid/cit734. Epub 2013 Nov 22.
https://www.ncbi.nlm.nih.gov/pubmed/24270053

[2] Predictive Value of Methicillin-Resistant Staphylococcus aureus (MRSA) Nasal Swab PCR Assay for MRSA Pneumonia
Antimicrob Agents Chemother. 2014 Feb; 58(2): 859–864.

Shortness of Breath: Quick Decision Making

[DISCLAIMER- This piece is not medical advise. It is intended as teaching for medical residents.]

Let's simplify a very complex problem according to the relatively few quick-acting things you can do for someone who is short of breath in the hospital.

While you're thinking of what to do, pull up the most recent CXR and if it is more than 12 hrs old, consider ordering a second one.

1- Suction. Mucus plugging can happen soon after repositioning and not be evident on imaging. Chest PT and suctioning are rarely harmful.

2- Ipratropium/albuterol nebulizer. Very commonly helpful, sometimes resolves the problem. Wheezes on exam, history of asthma/reactive airways/COPD, hyperinflated chest x-ray make this a sure bet. Duonebs are very well tolerated. 

Potential Harm:

Albuterol can drive rapid afib, delirium and anxiety. If either has been a problem, you can just give ipratropium. Trying to force a delirious patient to keep a mask on their face is a bad idea. For upper airway issues, particularly tracheobronchomalacia, nebs can be an irritant. Lastly, nebs can give false reassurance- a desperate patient wants to believe that all they need is a quick breathing treatment and can be quick to report improvement. Keep in mind that they are a temporary solution, and further work is needed to root out the underlying problem.

3- Lasix. CHF is very common, even in older patients without a formal diagnosis. Take a moment to look for CHF in the history, lasix in the home med list, congestion on the most recent imaging, how much fluid they got recently (especially maintenance fluids), BNP, extremity or sacral edema. Lasix acts quickly, causes lasting improvement, and is relatively harmless. And it provides some diagnostic utility. Don't forget to aggressively treat other drivers of CHF like hypertension in flash pulmonary edema and rapid A fib. 

Potential Harm:

Watch the kidneys (keeping in mind that volume overload can cause AKI as well).

4- Naloxone. If the patient is somnolent, naloxone is almost always a good idea. It is well tolerated, fast acting, and diagnostic. Even if a patient isn't on opioid meds, they sometimes are using their own surreptitiously. 

Potential Harm:

Almost none. In cancer patients with lots of pain, especially if on comfort focused care, naloxone is very uncomfortable.

5- Steroids. Most COPD/asthma patients are already on steroids, but if not, this can be helpful.

Potential Harm:

Hyperactive delirium, possibly fluid retention in CHF, though a few doses overnight is unlikely to cause a problem.

6- Noninvasive ventilation. For alert patients who have failed the above, BIPAP is generally well tolerated. Sometimes it makes sense to trial it on the sooner side so that a patient can get acquainted with having a mask over their face before they start to get frantic or delirious and try to pull the mask off. Checking pH and pCO2 is helpful, and a VBG is less painful than an ABG for this.

Potential Harm:

Hypotension due to increased intrathoracic pressure, aspiration in obtunded patients, unnecessary ICU transfer.

7- Foley or straight cath. Particularly in patients with multifactorial dyspnea (some CHF, some COPD, some anxiety), you are looking for every little bit that can help. Urinary retention is common, and some patients can have more than 1.5L of urine in their bladder.

Potential Harm:

Catheter associated UTI.

8- Thoracentesis (or paracentesis). Check the x-ray and breath sounds for signs of pleural effusion, pneumothorax, hemothorax. If it's easy to visualize fluid, then it'll probably feel a lot better when it's drained. Urinary retention or ascites with distended abdomen can cause a restrictive deficit.

Potential Harm:

All the harms of an invasive procedure. 

9- Morphine. 0.5 mg IV morphine, or 0.5mg IV lorazepam can be very helpful for patients in distress. We worry about respiratory suppression, but a small dose is unlikely to tip someone over the edge. For the occasional patient whose anxiety is compromising ventilation, a small dose of sedation can break a feedback loop. Remember that pure anxiety is a diagnosis of exclusion (but some anxiety always accompanies dyspnea.)

Potential Harm:

Respiratory depression, delirium.

10- Pain. Shallow breathing with atelectasis from splinting can cause tachypnea and/or hypoxia (as well as fever and look like pneumonia on chest x-ray). Patients are not usually dyspneic. Treating pain can help, though keep in mind that PE's and pericarditis hurt.

Important considerations, though unlikely to improve quickly

- Broaden antibiotics. Patients with worsening symptoms and pneumonia deserve broader coverage. Think of fungi, legionella, and multi drug resistant organisms. 

- Acute coronary syndrome. Dyspnea is often an angina equivalent, and patients with lung disease often have comorbid coronary disease. An EKG and troponin are almost never a mistake.

- Pulmonary embolism. PE is very common in COPD exacerbations. Use the Wells criteria to identify high risk patients, apply the PERC rule, and correct D-dimer for age [upper limit of normal = age/50 in mg/L FEU, age x 10 in mcg/L DDU].

- Pericardial effusion. Review CT chest, echocardiogram. Check pulsus paradoxus.


Please email criticism/questions/suggestions to astupple at gmail so I can update this post.

Trying to Diagnose TB in the Hospital

When you suspect active TB when admitting a patient to the hospital, it turns out it is quite difficult to rule someone in or out. Here is a brief look at how you can get tricked trying to diagnose TB, and some recommendations for workup up these patients.

Skin test and quantiferon gold assay are bad at diagnosing active TB:
- Quant gold cannot exclude active (or latent) TB because 10-35% of patients with active TB will have a negative quant gold assay.
- The skin test will be negative in 50% of patients with disseminated disease and 5-40% of patients with pulmonary disease.
- This online latent test interpreter is excellent: http://www.tstin3d.com/en/calc.html

You really can't RULE OUT active TB with sputum tests. All you can do is have a certain degree of confidence about how many TB organisms are present in the patient's airways. If you have a negative sputum smear, you have detected down to a minimum of 5 thousand colony forming units (CFU)/mL. A negative sputum PCR detects down to 150 CFU/mL. A negative culture detects down to 10 CFU/mL.

Unfortunately, the culture takes weeks, so it's not helpful in the short term when admitting. Many hospitals don't have sputum PCR or Gene Expert testing. That usually leaves us with sputum smear. This will tell you something if the airways are teaming with organisms, but can be falsely negative for disseminated TB or for a lower burden of respiratory disease. The main thing that the negative sputum gives you is confidence that the patient is not contagious to the rest of the hospital.

Imaging is helpful, but also doesn't rule out TB. 5-15% of active pulm TB have negative CXR, CT is better but not absolute.

Takeaways:
- If you have even a low suspicion for pulm TB (A respiratory complaint in a patient from an endemic area, HIV, homeless/incarcerated, unexplained wt loss, etc), they need to be on airborne precautions.
- If the sputum smears are negative x3 (you can order them 12 hrs apart), you can be reasonably confident that they're not contagious.
- The skin test and quant gold assays can be negative, but still have pulm or disseminated TB, so they're not very helpful in the inpatient setting. It's worth testing because if positive, they will need TB clinic and likely treatment for at least latent TB and further workup for disseminated disease.
- Your main job in working up active TB is to protect the hospital, patients, their families and staff. An exposure affects hundreds of people, causes lots of hassle, and costs lots of money.

How urgent is hypertensive urgency?

How quickly do I have to lower blood pressure in “hypertensive urgency”?

The term hypertensive urgency was established in 1974 as SBP >180, DBP >110 without evidence of end organ damage, and recommended to “lower MAP by 20 over 24-48 hours."[1] However, there has never been data to quantify the short term cardiovascular risk of hypertensive urgency, let alone the benefit of BP reduction in the short term.

Until now:

Characteristics and Outcomes of Patients Presenting with Hypertensive Urgency in the Office Setting. Patel et al. JAMA IM. 2016;176(7) [2]

Bottom line:

There was no significant difference in stroke or MI (Major Adverse Cardiac Events, MACE) between those admitted to the hospital for urgent management and observation vs. those sent home with uptitrated oral meds for patients with SBP >200.