Critical Care Scenarios

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Discussing pleural effusions in the critically ill, including how and when to drain them, methods of drainage, interpreting laboratory studies, and managing complications, with Dr. Emily Fridenmaker (@emily_fri), pulmonologist and intensivist at Charleston Area Medical Center in West Virginia.

Continuing education for this episode

CME credit provided courtesy of Academic CME. To claim your CME credit for this episode, click here to complete a short quiz.

Takeaway lessons

1. IMAGING
   1. CXR – underestimate
      1. Lateral – 75mL (5-15 mL is normal)
      2. AP – 175mL
         iii. 500mL for 100% sensitivity
   2. CT – overestimate
      1. Contrast can help delineate pleural surface
   3. Ultrasound – goldilocks
      1. Can see 5-50mL fluid
      2. > 1cm generally safe to sample
2. INITIAL WORKUP
   1. Thora – no absolute contraindications
      1. Should tap an effusion if you don’t know what’s causing it
         1. Diagnostic or therapeutic
         2. Does little to change hypoxia—can impact dyspnea though due to diaphragm length-tension relationships
         3. Complication rate = ??
      2. Differential
         1. Nucleated cells – greater than 50k usually paraPNA/empyema
         2. Lymphocytosis – TB, lymphoma, sarcoid, RA, yellow nail syndrome, chylothorax, cancer
         3. Eosinophilia – >10%; pneumo, hemo, infarction, asbestos, parasites, fungus, drugs, catamenial, malignancy, TB, CEP
         4. Mesothelial – normal in pleural fluid
      3. Light’s Criteria—protein and LDH (serum and pleural), albumin, cholesterol
         1. Aim was to have a high sensitivity, since shouldn’t miss an exudate
         2. The criteria—any one of them gives you an exudate
         3. Pleural protein/serum protein > 0.5—can be elevated by diuresis
         4. Serum albumin/pleural > 1.2
         5. Pleural LDH/serum LDH > 0.6
         6. Pleural fluid LDH > 2/3 ULN
         7. Cholesterol >45 can also help to indicate an exudate
         8. Glucose
            1. Low: complicated effusion/empyema, malignant, TB, lupus, rheumatoid pleurisy, esophageal rupture
         9. pH – normal is 7.6 due to bicarb gradient
            1. <7.3 – same conditions as low glucose ii. If low, higher yield on cytology for malignancy, less response to chemical pleurodesis
            2. Parapneumonic <7.15 – needs pleural space drainage
            3. Lidocaine will falsely drop the pH
         10. Amylase – pancreatic or esophageal etiologies
         11. ADA – TB; usually >40
         12. Cytology – malignant; sensitivity is 60%, 85% with second sample
3. TRANSUDATIVE VS EXUDATIVE
   1. Transudative
      1. Atelectasis, CHF, hepatic hydrothorax, low albumin, iatrogenic, nephrotic syndrome, PD, urinothorax
   2. Exudative
      1. Infectious, drug induced, trauma, malignancy (stage 4), CTD (RA, lupus, EGPA, GPA), hypothyroid/ovarian hyperstimulation syndrome, chylothorax, pancreatitis, sarcoid, post cardiac injury syndrome, radiation, PE, BAPE
4. PARAPNEUMONIC CLASSIFICATIONS
   1. Simple – resolve with abx (1-2 weeks), don’t require drainage or special abx considerations
      1. Free flowing, sterile
      2. Exudative – neutrophilic predominance, normal pH and glucose level
   2. Complicated – evidence of infection of the space
      1. Exudative, high white count, pH <7.2, glucose <40 (or 60?), LDH >1000, + gram stain
      2. Large, loculated, thickened pleura, air bubbles in effusion
   3. Empyema (subset of complicated)
      1. Pus in the pleural space
      2. Longer clinical course, possibly subacute
         D. Complex
         i. Internal loculations
5. MANAGEMENT OF COMPLICATED PARAPNEUMONIC EFFUSIONS
   1. Drainage usually required for source control—poorer prognosis without it
      1. Particularly if pH <7.15, low glucose, or LDH>1000
   2. Empyema
      1. Loculated
      2. + gram stain or culture
      3. Thickened parietal pleura
   3. Approach to drainage: Tube thoracostomy
      1. Small bore (10-14) similar efficacy to large
      2. MIST 1 – no difference in mortality or need for VATS between large, medium, or small bore tubes
         1. Retrospective—small bore noninferior
         2. Flush q6 to keep patent
      3. Suction is typical but not necessary
      4. Reimage after placement, when drainage slows
      5. Remove when less than 50-100mL for a couple of days, imaging is improved, clinically improving
      6. Reimage in about 2 weeks
   4. Failure of drainage – Repeat imaging 24hrs after completion of chosen intervention
      1. Lytics, multiple tubes preferred before VATS
         1. Probably best for early, multiloculated effusions
         2. DNAse breaks down DNA, reducing viscosity. tPA is fibrinolytics, busts up loculations
         3. MIST 2 – less need for VATS (30-80%) with tpa (10)/dornase (5) BID x 3 days
         4. New data shows simultaneous admin may be as efficacious
      2. VATS if significant organization, trapped lung (can be elective)
         1. No mortality benefit shown
         2. Pleural hemorrhage – 1-7%, indication for VATS
         3. Indicated when abx, tube, lytics have failed
         4. Also indicated up front if there is significant organization, fibrothorax, trap
         5. May need to be converted to open thoracotomy
         6. Maybe reduced LOS? MIST 3 looking at early VATS vs early lytics
      3. Window thoracostomy/eloesser flap
6. ANTIMICROBIAL THERAPY
   1. i. CAP – Rocephin + flagyl or unasyn
   2. Lots of clinda resistance now
   3. Atypicals rarely cause complicated effusions
   4. MDRO risk factors – MRSA, pseudomonas, and anaerobes
   5. Optimal duration unknown
      1. usually 2-3 weeks for complicated
      2. 4-6 weeks for empyema
      3. Can switch to PO when clinically improving
      4. Radiographic resolution can take weeks to months; this is not the goal
7. COMPLICATIONS OF PLEURAL SPACE INFECTIONS
   1. Fibrothorax, pleural fibrosis
   2. Restriction, unexpandable lung
   3. Decortication not considered unless restriction/limitation present 6 months later

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We explore the controversial area of using hypertonic saline to support hemodynamics, protect the kidneys, and facilitate diuresis in the critically ill patient. Our guest is Dr. Sean Barnett, hypertonic aficionado and nephrologist with a focus in critical care.

Takeaway lessons

1. The furosemide stress test in the shocked patient is a useful means to assess renal prognosis and determine whether oliguria is due to a prerenal state or ATN. 1mg/kg for the diuretic-naive or 1.5mg/kg for those with previous loop diuretic exposure, then monitor urine for the first 2 hours. If they make 200ml of urine, chances are good that the kidneys are still working to some extent, and the patient is less likely to proceed to needing dialysis.
2. In the case of prerenal azotemia, massive ongoing fluid overload via crystalloids can be mitigated by instead giving small boluses of hypertonic saline. A 100ml 3% saline bolus has a third of the sodium and a ninth of the volume of a 1000ml normal saline bolus, but because of the concentrated sodium load, still increases flow to the kidneys and effectively shuts off the patient’s RAAS axis that’s been activated by the shock. There are few tools that can suppress renin as potently as a hypertonic saline bolus, even a small one.
3. Angiotensin II is a key driver of capillary permeability: high RAAS = high capillary leak states. Downregulating this feedback loop with hypertonic helps to escape the shock-fluid cycle.
4. Combine the 3% bolus with furosemide and you’ve increased renal perfusion at the same time as you’ve stimulated diuresis. It’s a great approach for diuresing the patient who’s still in shock.
5. Albumin is less effective on its own, although albumin combined with hypertonic saline seems to have excellent synergy, outperforming each alone, allowing the preservation of intravascular volume that many believe they’re getting from albumin alone. Concentrated (e.g. 25%) albumin is not as good, does not reduce capillary permeability, and may be nephrotoxic.
6. Anything you can do to increase renal perfusion will help protect the kidneys during shock, and this is exactly what concentrated hypertonic saline can do.
7. With the small hypertonic boluses used here (rarely more than ~300ml in a day), the serum sodium usually does not rise by much. Just monitor it and ensure you’re giving adequate free water, especially if diuresis occurs.
8. Scheduled 3% boluses of ~100 ml every 8 hours or so, combined with scheduled furosemide boluses, is an effective diuretic strategy in the shocked, overloaded patient with heart failure.
9. Hypertonic saline stimulates ANP and nitric oxide by both stretching and creating hypertonicity in the right atrium; this helps decrease PVR and supports both sides of the heart.
10. A 3% saline infusion can work brilliantly to facilitate ultrafiltration during CRRT. Overloaded patients may be intolerant of volume removal because it’s being pulled straight out of the RV, which can be a tough stimulus in an unstable heart; hypotension and arrhythmias can occur. Hypertonic saline can support preload without adding much volume; it pulls volume into the vascular space for CRRT to filter out. Trending ScvO2 from the tip of the dialysis catheter can be a good guide as to whether UF is helping or hurting the heart as well.
11. The best evidence for hypertonic saline is to support diuresis. The next best evidence base is for cirrhosis with volume overload. As an IV fluid, the best data is in the surgical literature, generally showing it as equal or better to other fluids. Using it during CRRT has weaker evidence, although many nephrologists will use it during regular dialysis.
12. 3% saline is certainly safe and causes no issues with increases blood viscosity. It is safe through peripheral IVs as well.
13. The effect can be proven by checking the urine sodium and urine osmolality. The former is generally low and the latter high in the patient whose kidneys are conserving due to shock. Give them 3%, and the urine sodium shoots up while the urine osms decrease, as the RAAS axis and ADH become attenuated.

References

Improved overall fluid balance / UOP / hemodynamics in diverse settings. 

https://link.springer.com/article/10.1007/s00134-020-06132-0

https://journals.lww.com/annalsofsurgery/fulltext/2014/09000/the_hyslar_trial__a_prospective_randomized.5.aspx?casa_token=B1zfybqWhEYAAAAA:2QEHFpXKGY8dUDSqJpN4hrI8jz1K6_A75t5pSpbAUn5YLmZXFBisetKuRO50q6HGAXfTaL_KA0PAlo6lXM58I2xl6wXF-

https://journals.lww.com/shockjournal/FullText/2015/03000/Comparison_of_3__and_7_5__Hypertonic_Saline_in.7.aspx?casa_token=yGinfDHpavQAAAAA:ynzZ5fHTZkSRlkBiFoz_DHl0EhmdO7HG0gbonrlOJljz1l8kxW-Ur6xqGwiC5A8dew3IiwhAi8la22puhq3aAPrfi0-E

https://www.ahajournals.org/doi/abs/10.1161/01.CIR.41.1.97

Diuresis

https://www.ingentaconnect.com/content/wk/ccm/2021/00000049/00000011/art00005

https://link.springer.com/article/10.1007/s00059-013-4041-6

https://www.sciencedirect.com/science/article/abs/pii/S0270929511001355

https://link.springer.com/article/10.1007/s00059-010-3394-3

https://journals.physiology.org/doi/full/10.1152/ajprenal.00686.2020

COVID

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9253300/

https://link.springer.com/article/10.1186/s13063-020-04634-2

https://www.researchgate.net/profile/Paola-Rosati/publication/345765160_Hypertonic_saline_nasal_irrigation_and_gargling_as_an_inexpensive_practical_adjunctive_weapon_to_combat_asymptomatic_SARS-CoV-2_infections_A_case_report/links/5fad195a299bf18c5b6a1aa6/Hypertonic-saline-nasal-irrigation-and-gargling-as-an-inexpensive-practical-adjunctive-weapon-to-combat-asymptomatic-SARS-CoV-2-infections-A-case-report.pdf

Anti-Inflammatory

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1449974/

https://journals.lww.com/jtrauma/Fulltext/2000/10000/Hypertonicity_Prevents.2.aspx?casa_token=usB9uYwpcS0AAAAA:4IwYxvh4E2Tm5NjcbkEwr3C-r0FwkKyVOVhLlSewPABY85zrx5gedIHmoDcw2MA1sDx5_6T5Qb-6XPe0blmHBIwe2Nya

https://journals.lww.com/jtrauma/Fulltext/1997/04000/Hypertonic_Saline_Resuscitation_Decreases.4.aspx?casa_token=c_TsE2LFt_kAAAAA:LiaOb-JeONa3wo26fO1_-M3Ayx3rc7kpXOzWXDkDrOIxuV_2Wwwm-HhbddHOp22io7H7AvPIXMcqVNm0_dxKaO1uLVTW