Inhaled steroids in addition to systemic steroids in asthma exacerbations ? WHAT !!

Another pulmonary topic ! Please don't get bored of pulm now. Two more weeks of pulm and then I'll be in MICU.

CASE STORY : 

• We were consulted for a basic bread and butter Asthma exacerbation in a middle aged obese African American women. Patient had a history of intermittent asthma at home, taking only prn albuterol. 
• We were doing all the usual right things with nebulizers, IV solumedrol, antibiotics etc. The only difference this time was, I had a new question that didn't occur to me for the last 2.5 yrs of residency. Blame me!
• Prior to admission, the patient was not on inhaled corticosteroid (ICS). She is now on IV solumedrol 80mg TID for the acute exacerbation.

CLINICAL QUESTIONS !

1. DO I START AN INHALED CORTICOSTEROID (ICS) IN ADDITION TO SYSTEMIC CORTICOSTEROID (SCS) ?
2. IS THERE ANY BENEFIT ?
3. WHAT IS THE EVIDENCE BEHIND THIS TOPIC?

REVELATION : 

• For the last 2.5 yrs, I never added an ICS when the patient was being treated with SCS. Makes total sense right ?! Why would the patient need additional ICS when she is getting SCS. I never tried to look up evidence till today.
• Well, turns out that adding ICS to SCS showed improved outcomes in asthma exacerbations.
• There was a well designed RCT by Rowe et al, published in JAMA that looked at this exact clinical question. Adding ICS to SCS during an exacerbation reduced the relapse rates, improved the quality of life, reduced the frequency of rescue albuterol use.

Few limitations that might question the clinical applicability of these results are:

• There are no other studies that looked at this clinical question. These results need to be replicated in future studies to confidently apply the conclusions in clinical practice.
• This study was limited to Asthma patients who were only on prn albuterol prior to admission (patients on ICS or SCS prior to admission were excluded). So results may not be equated to other patient populations. 
• Patients in this study were not treated inpatient. They were discharged from ER on ICS + SCS. So, we aren't sure if this would be applicable to inpatient population. 

WOULD THIS EVIDENCE CHANGE MY PRACTICE?

• Starting today, I will definitely add ICS to SCS when a patient is admitted for asthma exacerbation (specially those who weren't on ICS prior to admission). 
• They should be discharged on ICS along with the SCS burst/taper. At outpatient follow-up, based on the patients clinical status, we could step-down from ICS if necessary. 
• I guess it may also be ok not to start an ICS - due to the above mentioned limitations. 
• Well, there is one good study :) Change has to begin somewhere! 

A MORE COMMON SCENARIO : 

• The asthma exacerbation patients we usually admit are already on ICS prior to admission. 
• When these patients come in for an exacerbation, no one knows whether continuing ICS in addition to SCS would improve outcomes. 
• Pulmonary team attendings at our institution go either ways (Few are ok with holding the ICS while patients are on SCS, while others are very particular about continuing ICS in addition to SCS). 
• Even in this patient group, my personal opinion (extremely weak evidence, Probably Grade B/C recommendation :) is to continue the ICS in addition to SCS. There is no right / wrong answer. 

Pitch in your thoughts.

References:

1. Rowe BH1, Bota GW, Fabris L, et al. Inhaled budesonide in addition to oral corticosteroids to prevent asthma relapse following discharge from the emergency department: a randomized controlled trial. JAMA. 1999 Jun 9;281(22):2119-26.
2. ACP J Club. 2000 Jan-Feb;132(1):13.  

Hoarseness of voice in a patient with aspiration pneumonia.

My UHATS team recently took care of an ICU transfer out 62 y.o male patient. He was initially admitted to ICU for aspiration pneumonia, intubated for 12 days, and transferred to a regular floor post extubation. Family and staff noted that his voice was extremely hoarse and low intensity (almost inaudible) - this was a new finding. His voice was normal prior to intubation.
ENT was consulted immediately, direct laryngoscopy revealed Unilateral Vocal cord paralysis. We got a CT soft tissue of neck to evaluate any pathology related to recurrent laryngeal nerve that might explain the vocal cord paralysis. CT was unremarkable for any mass lesion / compressive etiology. Eventually, patient was managed with speech therapy and ENT follow up on discharge.
 
This patient also got a Pulmonary function test incidentally for evaluation of his restrictive lung disease that showed the following :
 

 
This is a classic flow volume loop for vocal cord paralysis (variable extra thoracic obstruction) where the inspiratory loop is flattened. Please compare it to the text book picture below.
 

 
 
 
1. How common is vocal cord palsy post extubation?

• No one knows, but there are ample number of case reports that we must know about it.
• Unilateral vocal cord paralysis typically manifests as hoarseness immediately after extubation.

 
2. Patho-physiology?

• Caused by compression of the anterior branch of the recurrent laryngeal nerve between the ETT cuff and the thyroid cartilage in the subglottic larynx.
• The paralyzed cord becomes fixed in the adducted position.
• Bilateral vocal cord injury is less common, but its clinical manifestations are more severe (eg: extubation failure).

 
3. What are the risk factors?

• Prolonged intubation (variably defined as ≥36 hours to ≥3 days)
• Traumatic intubation
• Not using a myorelaxant drug during intubation.
• Large ETT (>8 mm in men, >7 mm in women)
• Aspiration
• Presence of a nasogastric tube

 
4. How to treat ?

• Early ENT referral is important in these patients to rule out potentially serious causes such as malignancy.
• Once bad stuff is ruled out, there is no magic treatment for ETT trauma related vocal cord paralysis !!
• Speech therapy is key for functional improvement.

 
5. Is the damage permanent?

• Usually resolves over days to months. Only time will tell :)

 
6. Can we prevent it? 

• We can definitely try!
• Avoiding the following:
• An oversized ETT
• Overinflated ETT cuff [As a general guideline, cuff pressure should be maintained between 18 and 25mm Hg. Above 18 mmHg to prevent an air leak (air escaping around the ETT cuff) and reduce aspiration around the cuff. Below 25 mmHg to reduce the risk of pressure necrosis]
• Excessive ETT movement
• Prolonged intubation if possible.  

Reexpansion pulmonary edema following thoracentesis

Another pulmonary case! This time around it is a case report about what didn't happen...reexpansion pulmonary edema.

We had a pleasant 39 year old female with a PMH of RA on adalimumab and recurrent metastatic breast cancer presenting with dyspnea due to a large right sided pleural effusion. We're talking the entire right lung opacified on the CXR. We knew the etiology of the effusion to be malignant so we were mainly performing a therapeutic thoracentesis. The post-thora CXR showed a small improvement in aeration in the apex of the right lung. That's it. WHY DIDN'T WE TAKE MORE OFF? We actually removed 2 whole liters.

Important points to address here:

1.  What is reexpansion pulmonary edema?

• After thoracentesis the lung can quickly fill back up with fluid - in an alveolar filling pattern (hence reexpansion pulmonary edema, not reexpansion pleural effusion). 
• The pulmonary edema can range from radiographic changes only to full on ARDS requiring intubation.
• This typically comes on quickly, within 1 hour after the procedure. 
• Presentation includes dyspnea, tachypnea, cough, hypoxia, chest pain and hypotension

2.  Is it bad?

• MORTALITY UP TO 20%

3.  Pathophys?

• There are several postulated mechanisms, all of which likely contribute, including:
• Reperfusion and oxidative stress/oxygen free radicals
• Histologic changes and vascular permeability from lung expansion and damage
• Increased hydrostatic pressure from reperfusion with negative pleural pressure

4.  How can we prevent it?

• This is where the evidence gets dicey...there have been multiple small studies to try and predict how negative the pleural pressure can get, how much can be taken off, etc. but there is no consensus
• Most authors agree that taking off no more than 1.5 - 1.8 liters reduces the risk to acceptable levels
• One sign of potential early edema and lung reexpansion/friction of the visceral and parietal pleura is coughing and chest pain, so some authors suggest that if they haven't had these signs you are ok to continue
• In our patient we removed 2 liters as she had no symptoms of coughing or pain until that point
• In our institution generally we stick to 1.5 - 1.8 liters from what I have seen, IR and Pulm will both go up to 2 liters occasionally but NEVER more than 2 liters

5.  Let's say we didn't prevent it...

• Oops! Happens in less than 1% of cases but happens nonetheless
• Treatment is supportive - oxygen, occasionally PEEP in the form of CPAP/BiPAP or intubation and mechanical ventilation
• Diuretics vs IVF vs pressors - this just depends on the hemodynamics and overall clinical picture

Key Points

• This is a rare, preventable and potentially fatal complication of thoracentesis
• Our best guess - stick to 1.5 - 1.8 liters off at one time
• They deserve close monitoring the first hour after the procedure - watch out for dyspnea, tachypnea, hypoxia, cough, chest pain and hypotension

To find out more:

http://www.respiratorycasereports.com/article/S2213-0071(14)00046-X/fulltext

http://www.uptodate.com/contents/noncardiogenic-pulmonary-edema#H14

http://www.nejm.org/doi/full/10.1056/NEJMicm1309844

WTH IS THIS BLOG ! WHY SHOULD I READ IT ? IS IT USEFUL ?

FOOD FOR THOUGHT . . .


How much new stuff (obviously I'm taking about medical stuff) do each of us learn every day? (both individually and everyone put together) - A LOT - ACTUALLY AN INSANE AMOUNT (Imagine close to 60 IM residents and 10 IM attendings - learning one new medical fact per person every day, in a hospital that offers an even broader spectrum of physio-pathology.

Do you ever discuss with your colleagues the new things you learnt today or over the last one week ?

Have you ever wondered - if every resident learnt one new medical fact every day, and you could get a peek into all of 'em on a daily basis - you would know close to 70 new medical facts by the end of the day - wouldn't you become extra smart pretty soon :)

Do you think you can focus for an entire hour reading a review article / listening to a lecture / morning report / conferences? How much of it do you retain?. No disrespect to structured reading, but I think it is more applicable to med school days where you had to get a sense of the entire playground. 
Residency ain't a perfect place to sit down and go through tons of pages and hours of lectures. When you are on the run all day, the only sensible thing for you to do is adapt to learn stuff on the run.

• Read while on the move - You don't have to sit in a room with 30 other colleagues on a auspicious day / time to learn stuff. I want to learn stuff while I wait to pick up my Chinese (of course only if I feel like reading)!
• Read in bits and pieces - Fragment the topic - No one told you to listen to a 2 hour long lecture on CHF and fall asleep while doing it. Instead learn on day one that there are 3 beta blockers that improve mortality (Metoprolol succinate, carvedilol, bisoprolol), on day 2 learn that adding a touch of thiazide to Lasix would augment the diuresis in a CHF exacerbation - and goes on to day 3,4 and ...)

These were all the thoughts and questions that made me feel that what ever we are currently learning on a daily basis is absolutely inadequate. We try our best to keep up with the day to day work commitments, attend morning reports, noon conferences, grand rounds, once in a while feel frustrated that I don't know s*** and try to eat through an entire book overnight and not retain most of it. Formal education via above mentioned methods is just not cutting the deal for us. We need something more easy, comfy, cozy and non-formal.

We all agree that there is ample amount of medical knowledge exposure among each of us - we just need a better platform to share this information in an effective, short, flexible and interesting way. I want to learn what my co-residents currently doing their Cardiology and GI rotations learnt today. I want to be able to do it when ever and where ever I want to, in 10-15 mins.

On your way home everyday after work, think of one thing you learnt that day / one interesting case scenario ---- that's it -- Now share it with UICOMP -- imagine how helpful this would be to every one and you as an author. Your colleagues get the luxury of absorbing the essence of your medical experiences - all credit to you.

Go on to www.chroniclesofmyresidency.com or uicompim.blogspot.com and write / contribute your 2 cents. Teach us and get taught. 
If you do not have access to write a post:

• Email me at hmoole@uic.edu to gain author privileges. 
• Also, excuse me for not sending an invite to you already ;)

Writer's / author's rules:

1. HIPAA, HIPAA and HIPAA!!! NO patient information (name, MRN, room number, bed number, any other identifiers).
2. Content should be as short and to the point as possible. I don't want people falling asleep reading the chronicles. We have enough resources to teach review articles / total topic revisions; so please - ONLY SPECIFIC FOCUSSED (END BRANCH) TOPIC CENTERED DISCUSSION. 
3. Content should be related to patient care that has happened at OSF/SFMC or ongoing at OSF-SFMC/ UICOMP. I don't want to write here about a super-interesting case that someone has heard about at an other facility, I have Dr.Google for it. I want readers to get a feeling of personalization and belongingness when they write or read the chronicles.

Reader's rules:

1. My favorite announcement in a Grey hound bus - "Please sit-back, relax and enjoy the ride" 
2. If you fall asleep reading the chronicles - please stop reading it. This website is definitely not working for you. Please go back to reading Harrisons and good luck staying awake. 
3. If you have any questions and additions to the topic you are reading - please mention so in the comments section of the post. 
4. Don't read the chronicles while you drive. Staying alive is worth more than being educated (well, at least for me !!). 
5. You agree or not, restroom is a perfect place to dedicate yourself some self-teaching time. All you need is a cell phone to open the chronicles. 
6. If you think this website is helping you, get your friends hooked up to it.

Uncomplicated parapneumonic effusion vs Comlicated parapneumonic effusion vs Empyema

As a part of Pulmonary team, we were consulted by ER to evaluate a 72 y.o male with no significant PMH, presented to ER with cough, green sputum, fevers, chills, exertional dyspnea.  He was diagnosed with HCAP and severe sepsis in ER. CXR showed a moderate sized pleural effusion. Appropriate IVF and antibiotics were initiated. 

1. Does the patient need a diagnostic thoracentesis?
2. Does he need a chest tube?
3. What is the difference between Uncomplicated parapneumonic effusion vs Comlicated parapneumonic effusion vs Empyema?

This patient ended up getting diagnostic thoracentesis - we were unsuccessful as we could not get any fluid for diagnostic eval due to loculated effusion and septations (visible on ultrasound lung). Patient was referred to IR team for Fluoro guided Chest tube placement. Fluid revealed frank pus. However first day drainage was <100ml purulent effusion. So, the patient received tPA and DNAase via the chest tube to break down the septations and improve drainage. We requested the IR docs not to manage the fibronylitics. We preferred to do it ourselves. 

What is the difference between Uncomplicated parapneumonic effusion vs Comlicated parapneumonic effusion vs Empyema?

• An uncomplicated parapneumonic effusion has "exudative" chemistries, normal pH and glucose, and negative cultures. 
• A complicated parapneumonic effusion typically has "exudative" chemistries, a low pleural pH (pH <7.20), a low glucose, and is often loculated. 
• Empyema fluid typically looks like pus and organisms are visible on Gram stain, although cultures may be negative

Who would qualify for a diagnostic thoracentesis?

• In general, all parapneumonic effusions, EXCEPT those that are free flowing and layer less than 10 mm on a lateral decubitus film, should be sampled (diagnostic) by thoracentesis. 

Who would qualify for a Chest tube placement?

• In patients with a large, loculated, or complicated parapneumonic effusion or empyema. 

Pearls:

• CT or ultrasound-guided placement of multiple tubes may be needed when pleural loculations prevent adequate drainage by a single tube. 
• In patients with a thoracic empyema - tube thoracostomy and video-assisted thoracoscopic surgery (VATS) with debridement are acceptable. The latter may be preferred in patients with multiple loculations and a thick pleural peel. 
• When tube thoracostomy is used for initial drainage of an empyema, a chest CT scan should be obtained within 24 hours after chest tube placement to document appropriate placement of the tube and assess drainage. 
• For patients who do not have good drainage of empyema fluid from a well-placed chest tube, administer a combination of TPA 10 mg and deoxyribonuclease (DNase) 5 mg, twice daily for three days. IR team does a different regimen that is not effective and not evidence based. So do not let IR team manage the fibrinolytics. 

Trivia: 

• The only pleural effusion with a trasudative chemistry but low pH : URINOTHORAX. 
• Red tinged effusion is likely a hemothorax when the pleural fluid hematocrit / blood hematocrit ratio is >50%
• Chylothorax  - triglyceride level >110. 
• Lights criteria can be false positive when a patient with transudative effusion gets lasix. 

Uptodate reference