Ultrasound for Critical Care Physicians: Sometimes It’s Better to Be Lucky than Smart

Robert A. Raschke MD and Randy Weisman MD

Critical Care Medicine

HonorHealth Scottsdale Osborn Medical Center

Scottsdale, AZ USA

We recently responded to a code arrest alert in the rehabilitation ward of our hospital. The patient was a 47-year-old man who experienced nausea and diaphoresis during physical therapy. Shortly after the therapists helped him sit down in bed, he became unconsciousness and pulseless. The initial code rhythm was a narrow-complex pulseless electrical activity (PEA). He was intubated, received three rounds of epinephrine during approximately 10 minutes of ACLS/CPR before return of spontaneous circulation (ROSC), and was subsequently transferred to the ICU.

Shortly after arriving, a 12-lead EKG was performed (Figure 1), and PEA recurred.

Figure 1. EKG performed just prior to second cardiopulmonary arrest showing S1 Q3 T3 pattern (arrows).

Approximately ten-minutes into this second episode of ACLS, a cardiology consultant informed the code team of an S1,Q3,T3 pattern on the EKG. A point-of-care (POC) echocardiogram performed during rhythm checks was technically-limited, but showed a dilated hypokinetic right ventricle (see video 1).

Video 1. Echocardiogram performed during ACLS rhythm check: Four-chamber view is poor quality, but shows massive RV dilation and systolic dysfunction.

Approximately twenty-minutes into the arrest, 50mg tissue plasminogen activator (tPA) was administered, and return of spontaneous circulation (ROSC) achieved two minutes later. A tPA infusion was started. The patient’s chart was reviewed. He had received care in our ICU previously, but this wasn’t immediately recognized because he had subsequently changed his name of record to the pseudonym “John Doe” (not the real pseduonym), creating two separate and distinct EMR records for the single current hospital stay. Review of the first of these two records, identified by his legal name, revealed he had been admitted to our ICU one month previously for a 5.4 x 3.6 x 2.9 cm left basal ganglia hemorrhage. We stopped the tPA infusion.

On further review of his original EMR is was noted that two weeks after admission for intracranial hemorrhage, (and two weeks prior to cardiopulmonary arrest), he had experienced right leg swelling and an ultrasound demonstrated extensive DVT of the right superficial femoral, saphenous, popliteal and peroneal veins. An IVC filter had been due to anticoagulant contraindication. The patient’s subsequent rehabilitation had been progressing well over the subsequent two weeks and discharge was being discussed on the day cardiopulmonary arrest occurred.

On post-arrest neurological examination, the patient gave a left-sided, thumbs-up to verbal request. Ongoing hypotension was treated with a norepinephrine infusion and inhaled epoprostenol. An emergent head CT was performed and compared to a head CT from four weeks previously (Figure 2), showing normal evolution of the previous intracranial hemorrhage without any new bleeding. 

Figure 2. CT brain four weeks prior to (Panel A), and immediately after cardiopulmonary arrest and administration of tPA (Panel B), showing substantial resolution of the previous intracranial hemorrhage.

A therapeutic-dose heparin infusion was started. An official echo confirmed the findings of our POC echo performed during the code, with the additional finding of McConnell’s sign. McConnell’s sign is a distinct echocardiographic finding described in patients with acute pulmonary embolism with regional pattern of right ventricular dysfunction, with akinesia of the mid free wall but normal motion at the apex (1). A CT angiogram showed bilateral pulmonary emboli, and interventional radiology performed bilateral thrombectomies. Hypotension resolved immediately thereafter. The patient was transferred out of the ICU a few days later and resumed his rehabilitation.

A few points of interest:

• IVC filters do not absolutely prevent life-threatening pulmonary embolism (2,3).
• Sometimes, serendipity smiles, as when the cardiologist happened into the room during the code, and provided an essential bit of information.
• Emergent POC ultrasonography is an essential tool in the management of PEA arrest of uncertain etiology.
• Barriers to access of prior medical records can lead to poorly-informed decisions. But in this case, ignorance likely helped us make the right decision.
• Giving lytic therapy one month after an intracranial hemorrhage is not absolutely contra-indicated when in dire need.
• As the late great intensivist, Jay Blum MD used to say: “Sometimes it’s better to be lucky than smart.”

References

1. Ogbonnah U, Tawil I, Wray TC, Boivin M. Ultrasound for critical care physicians: Caught in the act. Southwest J Pulm Crit Care. 2018;17(1):36-8. [CrossRef]
2. Urban MK, Jules-Elysee K, MacKenzie CR. Pulmonary embolism after IVC filter. HSS J. 2008 Feb;4(1):74-5. [CrossRef] [PubMed]
3. PREPIC Study Group. Eight-year follow-up of patients with permanent vena cava filters in the prevention of pulmonary embolism: the PREPIC (Prevention du Risque d'Embolie Pulmonaire par Interruption Cave) randomized study. Circulation. 2005 Jul 19;112(3):416-22. doi: [CrossRef] [PubMed]

Cite as: Raschke RA, Weisman R. Ultrasound for Critical Care Physicians: Sometimes It’s Better to Be Lucky than Smart. Southwest J Pulm Crit Care. 2021;22(6):116-8. doi: https://doi.org/10.13175/swjpcc016-21 PDF 

Ultrasound for Critical Care Physicians: Caught in the Act

Uzoamaka Ogbonnah MD¹

Isaac Tawil MD²

Trenton C. Wray MD²

Michel Boivin MD¹

¹Department of Internal Medicine

²Department of Emergency Medicine

University of New Mexico School of Medicine

Albuquerque, NM USA

A 16-year-old man was brought to the Emergency Department via ambulance after a fall from significant height. On arrival to the trauma bay, the patient was found to be comatose and hypotensive with a blood pressure of 72/41 mm/Hg. He was immediately intubated, started on norepinephrine drip with intermittent dosing of phenylephrine, and transfused with 3 units of packed red blood cells. He was subsequently found to have extensive fractures involving the skull and vertebrae at cervical and thoracic levels, multi-compartmental intracranial hemorrhages and dissection of the right cervical internal carotid and vertebral arteries. He was transferred to the intensive care unit for further management of hypoxic respiratory failure, neurogenic shock and severe traumatic brain injury. Following admission, the patient continued to deteriorate and was ultimately declared brain dead 3 days later. The patient’s family opted to make him an organ donor

On ICU day 4, one day after declaration of brain death, while awaiting organ procurement, the patient suddenly developed sudden onset of hypoxemia and hypotension while being ventilated. The patient had a previous trans-esophageal echo (TEE) the day prior (Video 1). A repeat bedside TEE was performed revealing the following image (Video 2).

Video 1. Mid-esophageal four chamber view of the right and left ventricle PRIOR to onset of hypoxemia.

Video 2. Mid-esophageal four chamber view of the right and left ventricle AFTER deterioration.

What is the cause of the patient’s sudden respiratory deterioration? (Click on the correct answer to be directed to an explanation)

1. Atrial Myxoma
2. Fat emboli syndrome
3. Thrombus in-transit and pulmonary emboli
4. Tricuspid valve endocarditis

Cite as: Ogbonnah U, Tawil I, Wray TC, Boivin M. Ultrasound for critical care physicians: Caught in the act. Southwest J Pulm Crit Care. 2018;17(1):36-8. doi: https://doi.org/10.13175/swjpcc091-18 PDF