Crashing Asthmatic POD

We treat asthma on a daily basis, especially in the peds ED. But what if duonebs x3, steroids, and mag isn’t doing the trick?

THE CRASHING ASTHMATIC

• Nebulized epinephrine may help.

• If no improvement, start dosing IM epi as if it were anaphylaxis: 0.5 mg (0.01 mg/kg) q 10 min, or start a drip at 5 mcg/min and titrate to effect.

• Keep going with continuous albuterol nebs.

• If pharmacy isn’t around to make an epi drip, consider a “dirty” epi drip: 1 mg epi (an entire vial of code cart epi) added to 1 L NS or LR, start at 2 drops per second and titrate up.

• Alternatively, terbutaline IV can be started: 10 mcg/kg bolus over 10 min and then drip starting at 0.4 mcg/kg/min and titrate up. Terbutaline is a systemic beta agonist. Perhaps they’re so tight that the albuterol you’re nebulizing is not getting where it needs to go due to profound bronchoconstriction. The main adverse effect is here is vasodilation-related hypotension.

By this point, your intubation stuff should be ready and the patient should be in resus.

They also will be having insensible losses so should get as 20 cc/kg IVF bolus.

Still getting worse.

Now this gets interesting.

We are really trying to avoid intubating any asthmatic because of historically poor outcomes with intubation, but sometimes it is unavoidable.

Next step is to try BiPAP. BiPAP could also be started simultaneously with epi. If they can’t tolerate BiPAP, consider ketamine to help them tolerate BiPAP. Ketamine can be dosed numerous ways. If sub-dissociative dosing is pursued, you risk them freaking out. If dissociative dosing, there’s a higher risk of laryngospasm. But consider this, they’re on the brink of getting intubated anyway. If your last-ditch-effort-ketamine gives them laryngospasm, that might be your cue to push a paralytic.

Ketamine and BiPAP has failed.

Time to intubate. Preoxygenate as much as possible. Use the largest ETT possible. First pass success is key. Induce with ketamine 2 mg/kg if they’re not already in the K-Hole. Roc or Sux.

Now they’re intubated

• They have OBSTRUCTIVE LUNG PHYSIOLOGY. It will take them way longer than usual to exhale. Thus:

• Low respiratory rate! 8 breaths/min

• Lung protective tidal volume: 7 cc/kg ideal body weight

• Minimal PEEP: 0 (ZEEP) - 2 cc H2O

• High inspiratory flow rate: 90 LPM or I:E 1:5

• FiO2 100%

• The ventilator will alarm due to high PEAK pressures. This is OK. Have the respiratory therapist fix it to raise the alarm threshold. The high peak pressures are a consequence of their tight bronchioles.

• If running into issues with ventilator dyssynchrony, consider paralyzing with cisatracuium

• Relative hypoxia (sat mid 80s, goal >90%) and hypercarbia (goal >7.15) is OK

• Aggressive airway suctioning

• If they begin crashing, disconnect from vent and push on chest to ensure breath stacking is not the issue; rule out pneumothorax; rule out displaced/clogged/kinked ETT

Still doing poorly

• Call the ECMO team for VV ECMO

• Anesthesia to set up inhaled anesthetics! e.g. desflurane, sevoflurane. Not tons of evidence, but in case series' and anecdotally, this works really well.

• Fun fact, CO2 can be dialyzed out of someone rather than ventilated out of someone. However, you need to be in a center where ECMO is also done, because it’s basically putting a piece of the ECMO circuit into a CVVHD circuit. Yes. Blew my mind too.

See Reuben’s algorithm on this at https://emupdates.com/when-the-patient-cant-breathe-and-you-cant-think-the-emergency-departement-life-threatening-asthma-flowsheet/

Nephrotic Syndrome Pearl of the Day

Nephrotic Syndrome

Pathophysiology

Think about it like this: Glomerular basement membrane problem, you spill all your protein (albumin) from your plasma into your urine, leading to high urine protein, low serum protein, and edema. It may help to simply think of it as decreased oncotic pressure causing movement of fluid from the intravascular space to the interstitial space; in reality the pathophysiology of edema in nephrotic syndrome is a little more complicated - has to do with a combination of primary (due to renal disease) and secondary (via RAS pathway) sodium retention.

Thus,

nephrotic syndrome is defined by:

1. Heavy proteinuria

(protein excretion > 3.5 g/24 hours; UPEE>3.5; >2 in children)

2. Hypoalbuminemia

(< 3 g/dL; <2.5 in children)

3. Peripheral edema

(Hyperlipidemia and thrombotic disease are frequently observed with nephrotic syndrome but not required for the diagnosis, may also be immunosuppressed)

(UA should have no significant hematuria, casts, or RBCs which would suggest a nephritic picture)

Measuring Proteinuria 

The most convenient way is to calculate a 

Urinary Protein Excretion Estimation (UPEE)

(insert infantile bathroom humor here)

UPEE (g/day) = (urine protein (mg/dL)) / (urine creatinine (mg/dL))

This works because a random urine protein to urine creatinine ratio very closely approximates the true 24 hour urine protein excretion, as shown below.

Interpretation:

UPEE <2.0 g/day —> Within normal limits

UPEE 2.0–3.5 g/day —> Above normal limit - investigate further

UPEE >3.5 g/day —>Nephrotic range

Nephrotic vs Nephritic

Remember to always think of nephrotic syndrome in contrast to nephritic syndrome! I love this image:

Workup

1.

Make the diagnosis: urinalysis, urine protein, urine creatinine, serum albumin, a lipid panel, basic metabolic panel

2. Consider further testing to differentiate primary vs secondary on a case-by-case basis: HIV, ANA, complement (C3/C4 and total hemolytic complement), serum free light chains and urine protein electrophoresis and immunofixation, syphilis serology, hepatitis B and hepatitis C serologies, and the measurement of cryoglobulins; when in doubt, run it by nephrology

3. Consider testing for complications: POCUS for pleural effusion/ascites; CXR for pleural effusion, dopplers or CTA for venous thromboembolism; antithrombin III, plasminogen, protein S (hyper coagulability); immunoglobulins; 

3. Usually renal biopsy is required for definitive diagnosis

Etiology/Treatment/Dispo

In children 10 years or younger, it is minimal change disease (MCD) 90% of the time. Most MCD responds to corticosteroids.

In children >10 years, it is MCD >50% of the time.

In adults focal segmental glomerulosclerosis (FSGS) is the most common etiology (35%). It can be primary/idiopathic, or associated with other disease processes, most commonly HIV or massive obesity.

In most cases, a biopsy will be needed in order to confirm diagnosis.

Admit patients with severe edema, pulmonary effusions or respiratory symptoms, or signs and symptoms suggestive of systemic infection or thrombotic complications to the hospital.

Discharge with nephrology follow up ASAP and low salt diet if only mild-moderate edema.

In kids age 1-10, may consider starting a course of steroids (

Prednisone 2 mg/kg/day x 6 wks then 1.5 mg/kg every other day x 6 wks) only if:

• Age 1-10

• No renal insuficiency

• No macroscopic hematuria

• No sx systemic disease

• No HTN

• Normal C3 levels

Special scenarios

Nephrotic syndrome + chest pain?

DDX: PE and myocardial ischemia because hyperthrombotic, pneumonia (immunosuppressed), pleural effusion

Consider POCUS, CXR, CTA, EKG, cardiac enzymes

Severe edema:

Requires lasix

May need albumin infusion prior to lasix if anasarca or signs of intravascular depletion

Hopefully you’ve already consulted ICU if you’re having to do this

Significant hypertension:

ACEi or ARB

SBP/Empyema:

Pleural effusions/ascites are common in severe fluid overload

Both are extra susceptible to infection in this state

Low threshold for diagnostic paracentesis/thoracentesis

References

Uptodate: Overview of heavy proteinuria and the nephrotic syndrome

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e: Chapter 134: Renal Emergencies in Children

Michael Mojica, MD. “PEM Guides.” NYU Langone Medical Center, 2015. iBooks. 

https://itunes.apple.com/us/book/pem-guides/id1039923332?mt=11

Google Image Search

Hemoptysis Pearl

Let’s Talk Hemoptysis

So your patient thinks they’re coughing up blood...

Initial questions:

• Are they actually coughing up blood?

• Or are they having hematemesis?

• Or epistaxis?

Seems like they actually are. So what could they have? What should you ask in your history?

• Infectious/inflammatory causes are very common:

  • Acute bronchitis - if you cough enough, you will get some inflammation of your airways and BOOM, hemoptysis)

  • COPD can cause neoangiogenesis to enhance alveolar blood delivery, new fragile blood vessels can rupture

  • In immunosuppressed patients, consider aspergillus and of course TB causing necrotic badness, thus also ask travel history

  • Lung parasites! paragonimiasis, echinococcus, schistosomiasis - ask about travel

  • Neoplastic

    • Bronchogenic carcinoma, bronchial adenoma, squamous cell carcinoma — ask about weight loss and constitutional sx, but know that tumors can also cause massive hemoptysis

    • Structural

      • Aortobronchial fistula — good point, if their giant thoracic aortic aneurysm eroded into one of their bronchi, they would be in extremis to say the least and you wouldn’t be taking this detailed history…

      • Tracheo-innominate fistula — usually 3d-6w after tracheostomy placement, life-threatening and scary, we’ll save management of TIF for another POD

      • Other chronic lung diseases leading to bronchiectasis —> chronic inflammation —>destruction of cartellagenous support —> ruptured blood vessels

      • Vasculitides and collagen-vascular diseases

        • Goodpastures - remember this? Me neither. Autoimmune disease where antibodies attack the basement membrane of the kidneys and lungs — so if known renal failure or hematuria + hemoptysis, think about this

        • Granulomatosis with polyangiitis, SLE, and Behçet’s can all do similar things — h/o autoimmune disorders, family history…

        • Cardiovascular

          • PE can cause a pulmonary infarction —> ischemia/necrosis of lung tissue—> bleeding — ask about PE risk factors!

          • Pulmonary hypertension — ?CHF ?mitral stenosis

OK, enough of that. Let’s break down management.

Are they bleeding a lot? Coughing up large amounts of copious bright red frothy blood in front of you and in respiratory distress? 

Massive Hemoptysis

They need

airway management (often emergent intubation), STAT labs/portable CXR, bronchoscopy, CT surgery/IR/ICU consults, CT scan if stable enough

. Also,

position them on their side with the bleeding lung down

so that gravity doesn’t wash all the blood into their ventilated lung. I like this algorithm from Tinti’s below. The only confusing acronyms are MDCT (multidetector computed tomography) and BAE (bronchial artery embolization).

You may be able to intubate the healthy mainstream

as shown below in order to protect the side you’re able to ventilate. As another option pulmonology/IR may help with placement of a Fogarty catheter to tamponade the bleeding side.

If it’s

mild hemoptysis

, think about whether quarantine and TB workup is needed. If not, they most likely have bronchitis, and may only need a CXR, but refer to this simpler algorithm to tell you when you need a little more. It’s unlikely that they’ll have a diagnosis by the time they leave, but they will continue their workup with PCP or pulmonology for definitive diagnosis and management.