Critical Care Scenarios

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We look at the patient with known pulmonary hypertension admitted for new issues like sepsis and pneumonia, and how they differ from our usual bread and butter, with help from Dr. Raymond Foley, director of the medical ICU and the pulmonary/critical care fellowship at UConn Health, as well as director of their pulmonary vascular disease program.

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Takeaway lessons

1. Evaluate for the risk of decompensation in a patient with known PH and acute illness by considering their most recent echocardiogram, and repeating it as soon as possible after admission. Signs of baseline and/or new RV strain, such as reduced TAPSE, septal bowing, etc, as well as pericardial effusion, suggest a poor reserve for the stresses of their new ICU course. Right heart cath or echo PA pressures are less relevant than their cardiac function; pulmonary pressures fluctuate and are much less relevant to the clinical picture.
2. Common causes of decompensation of PH include sepsis, medication issues (such as interruption of continuous PH meds), and polypharmacy (such as introducing an alpha agonist to treat a URI).
3. When admitting the acutely ill patient with known PH, strongly consider early transfer to a PH center, preferably the one that already knows the patient.
4. Typically, continue to administer outpatient PH meds, unless forced to hold or convert them to another agent due to lack of enteral access, absorption issues, or other factors.
5. Avoid intubation if at all possible, as this can easily provoke cardiovascular collapse. Avoid hypoxemia and hypercarbia as well, which can both lead to worsening pulmonary arterial pressures. Maintaining both of these goals may require a thoughtful decision on when a patient should transition from modalities like high-flow nasal cannula to intubation. Non-invasive positive pressure like CPAP/BiPAP may be a reasonable middle ground, but could still provoke some instability due to the positive pressure.
6. Consider targeting a higher MAP than in other patients to maintain perfusion of the RV. A reasonable MAP goal is 65 plus the CVP.
7. Norepinephrine is a reasonable first-line vasopressor, but vasopressin might be even smarter, as it has no effect of increasing on the PVR and at low doses may even reduce it (activating V1/V2 receptors in the pulmonary circulation). Epinephrine at lower doses is a good second line, providing inotropic support for the RV without much impact on PVR.
8. Place an arterial line early. Consider a central one such as in the femoral artery if they’re sick. Place a central line; trending CVP can be helpful. If they’re really hemodynamically unstable, consider floating a PA catheter. Non-invasive cardiac output monitors are of questionable utility.
9. If intubating, induce them thoughtfully, avoiding agents like propofol. Ketamine or etomidate may be wise. Consider pushing the BP higher to avoid episodes of hypotension.
10. On the ventilator, be liberal with oxygen and don’t be in a rush to wean it. While hyperoxia is not needed, avoid hypoxia, even transiently. Oxygen is a potent pulmonary vasodilator, and is much better for these patients than giving them a higher PEEP.
11. If shock and RV failure are progressing, consider a pulmonary vasodilator, such as inhaled nitric oxide (INO) or inhaled epoprostenol. These have similar effects, although INO is more expensive. Drugs like epo can also be given intravenously, but this has the downside of dilating the entire pulmonary circulation, which can worsen VQ matching; nebulizing it improves perfusion to ventilated alveoli while ignoring shunted lung units. A positive response is improved oxygenation, reduced PA and RA pressures, and improved cardiac output.
12. Most patients in RV failure don’t need additional preload, and indeed may benefit from cautious diuresis. A CVP of around 8-12 is usually a good goal.
13. Dobutamine and milrinone are all reasonable options for inotropes, depending on your comfort.
14. Decompensated PH due to CTEPH can potentially be treated, even in the setting of critical illness, via surgical intervention (e.g. pulmonary endartarectomy).
15. Consider mechanical support early, with the best choice probably being VA ECMO.
16. Weaning of support, such as inhaled vasodilators, can be achieved by transitioning to other agents like IV or enteral vasodilators (e.g. sildenafil).

References

1. IBCC on RV failure

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An exploration of clinical documentation and billing/coding with Dr. Robert Oubre (@Dr_Oubre), full-time hospitalist and CDI Medical Director for a community hospital in southern Louisiana.

Takeaway lessons

1. Acute respiratory failure is justified when there is altered gas exchange (SpO2 <90%, PaO2 <60, CO2 >60 with pH <7.35, or P/F <300), clinical signs of increased work of breathing (using accessory muscles, etc), and a patient requiring respiratory support more than 4L O2 by nasal cannula. Requiring additional monitoring is also contributory.
2. Many diagnostic names for pneumonia, such as nosocomial pneumonia or HCAP, end up coding to the same thing. Higher reimbursement comes from billing for “Gram negative pneumonia,” which requires risk factors including being hospitalized and received IV antibiotics in the last 90 days, immunosuppressed (including diabetes, alcoholism, CHF, cirrhosis, chemotherapy, CKD, drug-induced neutropenia, chronic malnutrition), or have structural lung disease such as bronchiectasis. It also requires treating with an antibiotic that covers gram negatives, and treatment for 5 or more days. If you have all of this, you may be able to bill for “gram negative pneumonia.” Treatment can be presumptive and you may state this; actual culture data is not required for this, although it is supportive if available.
3. Diagnoses that are suspected but never fully proven can still be billed, particularly if they end up on a discharge summary.
4. When in doubt, more detail is always better in diagnostic labels.
5. Spell out your findings and reasoning and you’ll get more grace on your diagnoses.
6. Sepsis diagnoses are a mess. Reimbursers tend to like sepsis 3 definitions (qSOFA), core metrics may still use the older definitions. Many facilities may have their own policies on what definition to adopt. From a clinician’s perspective, at this point, you should probably just call it sepsis when you think it’s sepsis and let the billing will work itself out.
7. Document every diagnosis that contributes in any way to their current stay, even if your active management is minimal – it generally contributes to their risks and complexity.
8. In 2023, the whole billing paradigm is expected to change, with less emphasis on billing based on number of categories in the HPI, ROS, PE, etc, and complexity being instead based mainly on time and acuity.
9. Various providers can document diagnoses and all will count, but if there is dispute it will usually fall to the attending of record to make a final call.
10. The “case mix index” is an amalgamate of the overall complexity of your patient population, which is reviewed regularly and modifies overall reimbursement; this help capture complexities and costs of care beyond what’s shown by the specific DRGs. This is based on other diagnoses and factors; hence, document everything.
11. At the end of the day, you may not like the requirements for documentation and how it’s linked to reimbursement, but it is the way it is, and doing a poor job doesn’t mean the system will change – it just means your employer will be under-reimbursed, which in the end does affect you and your patients.

References

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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