Tag: pulmonary

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Case 78: Seizure-Associated Takotsubo Syndrome Complicated by Suspected Left Ventricular Thrombus and Multifocal Ischemic Stroke

Matthew Van Ligten, Bryan Merte

A 52-year-old woman with epilepsy treated with levetiracetam and lamotrigine, hypertension, and non-Hodgkin lymphoma previously treated with chemotherapy and in remission presented after being found confused and incontinent of urine. Her daughter found her staring blankly after being unable to reach her by phone for approximately one hour.

As the patient remained postictal and was a limited historian, additional history was obtained from emergency medical services. Paramedics had been called for what appeared to be one of her typical seizures with prolonged confusion. They subsequently witnessed a second episode of blank staring in the ambulance followed by extensor posturing, which resolved prior to medication administration after approximately two minutes.

There was no reported head trauma or infectious prodrome and no known cardiopulmonary disease. Chart review showed an outside hospitalization several months earlier for sepsis secondary to pneumonia; her prior lymphoma treatment regimen was not available in the records, though a recent formal echocardiogram was unremarkable.

The patient was comfortable appearing and in no acute distress. Respiratory effort and breath sounds were normal, as were heart rate and rhythm. She was alert and oriented to person and place but not year, with impaired attention. She was drowsy but demonstrated no focal cranial nerve, motor, sensory, or coordination deficits.

TestResult
White blood cell count20.4 × 10³/µL
Absolute neutrophil count17.3 × 10³/µL
Hemoglobin14.1 g/dL
Platelets512 × 10³/µL
Sodium134 mmol/L
Creatinine1.01 mg/dL
Glucose299 mg/dL
Lactate2.5 mmol/L
Image 1. Initial chest radiograph showing patchy and hazy left-lung opacities, interpreted as possible pneumonia or asymmetric pulmonary edema.

Approximately 60 minutes after ED arrival, the patient had another staring spell concerning for recurrent seizure. During the episode, her oxygen saturation fell into the low 70s with a reliable waveform and associated lip cyanosis. The episode resolved before benzodiazepine administration. Serial reassessments over the next 30 minutes showed progressive tachycardia, hypertension, and hypoxemia.

Vital signValue
Blood pressure205/145 mm Hg
Heart rate146 beats/min
Respiratory rate26 breaths/min
Temperature36.7°C
Oxygen saturation93% on 2 L/min nasal cannula

She appeared ill and agitated with mildly increased work of breathing. Electrocardiography demonstrated sinus tachycardia without ST-segment elevation or other acute ischemic changes. Initial troponin was 424 ng/L (reference <51 ng/L).

A bedside ultrasound of the heart and lungs was performed.

Video 1. Cardiac POCUS demonstrating severe left ventricular systolic dysfunction with relative basal hyperkinesis.
Video 2. Additional cardiac POCUS demonstrating left ventricular systolic dysfunction, a normal-sized right ventricle, and no interventricular septal flattening.
Video 3. Lung POCUS demonstrating multiple B-lines consistent with pulmonary interstitial syndrome.
Image 2. Chest radiograph obtained after deterioration showing progression to bilateral interstitial and alveolar pulmonary edema.

Emergency Department Course

The patient received intravenous levetiracetam while CT of the head, CT angiography of the head and neck, and CT pulmonary angiography were obtained to investigate structural, vascular, and cardiopulmonary causes. Because the history remained limited and the differential included recurrent pneumonia, aspiration, and central nervous system infection, a broad infectious and metabolic evaluation was initiated. Lumbar puncture was deferred because of clinical instability, and empiric vancomycin, ampicillin, and ceftriaxone were administered. Before cardiopulmonary decompensation, while her vital signs were normal, she received a total of 1 L of intravenous crystalloid.

After cardiac and lung POCUS raised concern for Takotsubo syndrome with cardiogenic pulmonary edema, no additional large-volume crystalloid was administered. Treatment included intravenous furosemide, nitroglycerin, supplemental oxygen, and metoprolol 5 mg IV ×2. Metoprolol was used for severe-range hypertension and tachycardia after clinically significant LV outflow tract obstruction was considered unlikely on POCUS. Heart rate and blood pressure improved without observed hypotension, bradycardia, or another adverse effect. Because nitroglycerin and other interventions were given concurrently, the improvement cannot be attributed to metoprolol alone.

Noninvasive positive-pressure ventilation was deferred because the oxygen requirement remained modest and airway protection was a concern during the postictal period. The patient was admitted to the intensive care unit for recurrent seizure or possible nonconvulsive status epilepticus, acute hypoxemic respiratory failure, and severe left ventricular systolic dysfunction.

Hospital Course and Outcome

During admission, NT-proBNP resulted at 19,459 pg/mL, and troponin peaked at 2,259 ng/L. Formal transthoracic echocardiography demonstrated an LVEF of 19%, regional wall-motion abnormalities consistent with Takotsubo syndrome, and a possible apical LV thrombus. Therapeutic anticoagulation was started empirically.

Coronary CT angiography showed moderate stenosis of the first diagonal branch with otherwise mild plaque burden. Lesion-specific CT-derived fractional flow reserve indicated a low likelihood of flow limitation.  No LV thrombus was visualized on coronary CT angiography or subsequent contrast-enhanced echocardiography.

Serial imaging showed rapid recovery of systolic function: LVEF improved from 19% to 54% on early repeat echocardiography and to 66% within 48 hours. The characteristic wall-motion pattern, prior documentation of normal systolic function, absence of a flow-limiting coronary lesion, and rapid recovery strongly supported Takotsubo syndrome. Invasive coronary angiography was therefore deferred.

Video 4: Repeat echocardiogram showing improvement of LV systolic function.

The neurologic presentation was characterized as possible nonconvulsive status epilepticus. EEG showed possible epileptiform discharges, although no further clinical seizure-like episodes occurred. Brain MRI demonstrated acute left parietal and left paramedian frontal infarcts. The stroke service considered the multifocal distribution most consistent with a cardioembolic mechanism in the setting of the suspected apical thrombus and initial LVEF of 19%.

Because the patient had recovery of her systolic function and neither contrast-enhanced echocardiography nor coronary CT angiography confirmed a persistent thrombus, therapeutic anticoagulation was discontinued in favor of antiplatelet therapy. The patient was discharged home on aspirin with family support at her neurologic baseline.

Discussion

Takotsubo syndrome is an acute heart failure syndrome characterized by transient regional LV dysfunction. The classic pattern consists of apical and midventricular hypokinesis or akinesis with relative basal hyperkinesis, though other variants occur.  While regional dysfunction generally extends beyond a single coronary artery distribution, alternative causes of myocardial injury such as culprit coronary lesions must still be excluded before formal diagnosis.1,2

Acute neurologic disease is a recognized physical trigger, and seizures are among the most frequently reported neurologic precipitants. These patients may not report chest pain or dyspnea, so the diagnosis can be overlooked when the initial evaluation is dominated by altered mental status or seizure activity.3 In this case, the causation between seizure activity, multifocal ischemic stroke, and cardiac dysfunction could not be definitively established; therefore, the diagnosis is most accurately represented by seizure-associated Takotsubo syndrome.

POCUS cannot independently distinguish Takotsubo syndrome from acute coronary occlusion, and B-lines are not specific to cardiogenic edema. However, immediate recognition of severe LV dysfunction with a characteristic regional pattern, combined with diffuse B-lines, rapidly shifted the working diagnosis toward cardiogenic pulmonary edema. This led the team to withhold additional crystalloid, begin diuresis and afterload reduction, and advocate for the appropriate level of care for stabilization and definitive cardiac testing. The case does not establish that the initial liter of crystalloid caused the deterioration or that additional fluid would necessarily have caused harm.

Evidence for beta-blockers in Takotsubo syndrome remains observational and conflicting. Expert consensus considers beta-blockade reasonable in selected hemodynamically stable patients until LV recovery, with cautious use in acute severe heart failure, hypotension, bradycardia, and marked QTc prolongation.4 A recent registry analysis associated beta-blocker therapy at discharge with lower long-term mortality but not reduced recurrence or faster LVEF recovery.5 There is no randomized evidence establishing benefit from acute IV beta-blockade. The observed improvement after metoprolol in this case should therefore be reported as a clinical course observation rather than evidence of efficacy.

Severe apical dysfunction can promote LV thrombus formation and systemic embolization.6 The first formal echocardiogram raised concern for an apical thrombus and prompted empiric anticoagulation, while MRI showed multifocal cerebral infarcts. However, neither contrast echocardiography nor coronary CT angiography later confirmed the thrombus. The case therefore illustrates a suspected cardioembolic complication rather than a definitively demonstrated LV thrombus.

The rapid recovery from an LVEF of 19% to 66% within 48 hours, together with prior normal systolic function, favored the diagnosis of transient stress cardiomyopathy. Initial severe systolic dysfunction identified a high-risk phenotype, even though ventricular function recovered quickly.7,8

Bottom Line

In patients with seizure or altered mental status who develop unexplained tachycardia, hypoxemia, elevated cardiac biomarkers, or pulmonary edema, combined cardiac and lung POCUS can rapidly identify severe ventricular dysfunction and pulmonary congestion. The examination can guide early stabilization and level-of-care decisions while definitive coronary and cardiac evaluation proceeds. Severe transient apical dysfunction should also prompt evaluation for LV thrombus and systemic embolic complications.

References

1. Medina de Chazal H, Del Buono MG, Keyser-Marcus L, et al. Stress cardiomyopathy diagnosis and treatment: JACC state-of-the-art review. J Am Coll Cardiol. 2018;72(16):1955-1971. doi:10.1016/j.jacc.2018.07.072

2. Singh T, Khan H, Gamble DT, et al. Takotsubo syndrome: pathophysiology, emerging concepts, and clinical implications. Circulation. 2022;145(13):1002-1019. doi:10.1161/CIRCULATIONAHA.121.055854

3. Cammann VL, Scheitz JF, von Rennenberg R, et al. Clinical correlates and prognostic impact of neurologic disorders in Takotsubo syndrome. Sci Rep. 2021;11(1):23555. doi:10.1038/s41598-021-01496-9

4. Ghadri JR, Wittstein IS, Prasad A, et al. International expert consensus document on Takotsubo syndrome (part II): diagnostic workup, outcome, and management. Eur Heart J. 2018;39(22):2047-2062. doi:10.1093/eurheartj/ehy077

5. Raposeiras-Roubin S, Santoro F, Arcari L, et al. Beta-blockers and long-term mortality in Takotsubo syndrome: results of the multicenter GEIST Registry. JACC Heart Fail. 2025;13(5):815-825. doi:10.1016/j.jchf.2024.11.015

6. Ding KJ, Cammann VL, Szawan KA, et al. Intraventricular thrombus formation and embolism in Takotsubo syndrome: insights from the International Takotsubo Registry. Arterioscler Thromb Vasc Biol. 2020;40(1):279-287. doi:10.1161/ATVBAHA.119.313491

7. Citro R, Radano I, Parodi G, et al. Long-term outcome in patients with Takotsubo syndrome presenting with severely reduced left ventricular ejection fraction. Eur J Heart Fail. 2019;21(6):781-789. doi:10.1002/ejhf.1373

8. Almendro-Delia M, Lopez-Flores L, Uribarri A, et al. Recovery of left ventricular function and long-term outcomes in patients with Takotsubo syndrome. J Am Coll Cardiol. 2024;84(13):1163-1174. doi:10.1016/j.jacc.2024.05.075

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Case 51: Utility of the Spine Sign in Detecting Pleural Effusion on POCUS

John Hermez

A 74 year-old male with a past medical history of metastatic castration-resistant prostate cancer complicated by cauda equina necessitating laminectomy decompression, chronic RLE DVT on apixaban and chronic hypotension presented to the emergency department accompanied by his spouse for altered mental status. Per the patient’s wife, he experienced cognitive decline and increasing weakness for one week prior to presentation. Two days prior to his arrival in the ED, the patient became more confused and agitated with his wife reporting that he appeared to be hallucinating intermittently. While he typically ambulates without assistance and straight-catheterizes himself, he has been unable to care for himself independently.

Vitals: BP 91/53 | Pulse 85 | Temp 98.1 °F (36.7 °C) | Resp 12 | Wt 92.3 kg (203 lb 7.7 oz) | SpO2 98% | BMI 29.1 kg/m²

Physical Exam:

On exam, the patient is in no acute distress and is oriented only to his name. He has diffuse anasarca with 2+ right lower extremity edema and 1+ left lower extremity edema. He is not pale or cyanotic and has shallow respirations on room air with diminished lung sounds and a flat JVP.

Labs: WBC 25.7 and initial lactate 2.2. Hb 9.5 PLT 98, Urine cloudy and orange, growth pending

ECG: NSR at 82 bpm with occasional PVCs, no evidence of ST changes

CXR: Compared to prior, there are new heterogenous bibasilar lung opacities and atelectasis possibly representing pneumonia. No definite pleural effusion or pneumothorax. Stable cardiac silhouette.

To clarify cardiac function and better characterize pulmonary status, a bedside point of care echocardiography was performed.

Figure 1: Trace pericardial effusion seen on parasternal short axis view.

Figure 2: Sagittal right sview demonstrating the thoracic spine sign

Discussion:

Radiographic imaging of the thorax is routinely performed in the ED to aid in the diagnosis of a wide range of cardiopulmonary manifestations. While upright chest x-rays are the Gold Standard for detecting pneumonia in patients, the detection of pleural effusion may be less clearly visualized. Meta-analysis has shown that the screening sensitivity of ultrasound may be 94% as compared to 51% for chest x-ray, in spite of having similar specificity.1 In this case, we rapidly obtained a point-of-care echocardiogram and pulmonary ultrasound to guide medical decision making in a patient with advanced metastatic disease and anasarca with equivocal radiograph.

A parasternal short axis view was obtained (figure 1) and demonstrated a trace pericardial effusion estimated to be 3mm without evidence of gross systolic dysfunction. Although the right ventricle was poorly visualized during diastole, the small volume of effusion and history of chronic hypotension was reassuring against tamponade physiology. Acquisition of a right subcostal view (figure 2) demonstrated the thoracic spine sign which is a reliable indicator of pleural effusion or hemothorax.2

Figure 3: Subcostal view labelled to identify anechoic pleural effusion (image courtesy of Stanford Medicine 25)5

The spine sign is a sonographic description of the visualization of vertebral bodies above the level of the diaphragm, which indirectly indicates that a thoracic fluid collection is present. When there is no thoracic free fluid present, an abrupt loss of the vertebral bodies occurs at the diaphragm due to air in the lungs impeding transmission.2 Pleural effusions and traumatic hemothorax can both represent fluid collections, hence the utility of subcostal imaging in the eFAST exam to evaluate thoracic trauma. One study on closed chest trauma has shown the absence of the spine sign to have a negative predictive value of 97.8% in assessing pleural effusion.3 The focused use of ultrasonography in the emergency department is regarded of high value in the early detection and diagnosis of multiple pathologies. Algorithmic exams such as the RUSH protocol provide rapid feedback on the physiology of a critically ill patient which can guide management and are recommended both by the American College of Emergency Physicians and Critical Care Societies.4 The potential applications of ultrasonography in resource-limited, austere environments by prehospital personnel are also of particular interest given novel advancements in AI-technology and focused training protocols.

In spite of a technically challenging exam, this case was an excellent example of the utility of multimodal imaging to clarify cardiopulmonary status in the ED. The patient was treated with broad antibiotic therapy for suspected urosepsis and admitted to the hospital for multidisciplinary care. He later was scheduled for therapeutic thoracentesis and surgical evaluation for a scapular fluid collection. 

References:

  1. Yousefifard M, Baikpour M, Ghelichkhani P, Asady H, Shahsavari Nia K, Moghadas Jafari A, Hosseini M, Safari S. Screening Performance Characteristic of Ultrasonography and Radiography in Detection of Pleural Effusion; a Meta-Analysis. Emerg (Tehran). 2016 Winter;4(1):1-10. PMID: 26862542; PMCID: PMC4744606.
  2. Dickman, E., Terentiev, V., Likourezos, A., Derman, A. and Haines, L., 2015. Extension of the Thoracic Spine Sign: A New Sonographic Marker of Pleural Effusion. Journal of Ultrasound in Medicine, 34(9), pp.1555-1561.
  3. Vargas CA, Quintero J, Figueroa R, Castro A, Watts FA. Extension of the thoracic spine sign as a diagnostic marker for thoracic trauma. Eur J Trauma Emerg Surg. 2021 Jun;47(3):749-755. doi: 10.1007/s00068-020-01459-1. Epub 2020 Aug 17. PMID: 32803497.
  4. Seif D, Perera P, Mailhot T, Riley D, Mandavia D. Bedside ultrasound in resuscitation and the rapid ultrasound in shock protocol. Crit Care Res Pract. 2012;2012:503254. doi: 10.1155/2012/503254. Epub 2012 Oct 24. PMID: 23133747; PMCID: PMC3485910.
  5. “The Spine Sign.” Edited by Stanford Medicine 25 Bedside Medicine Symposium, Stanford Medicine 25, Stanford Medicine 25 Bedside Medicine Symposium, stanfordmedicine25.stanford.edu/blog/archive/2018/thespinesign1.html. Accessed 25 May 2025.
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Case 49: ARDS

Kayhon Rabbani

A 22 year old male who has no past medical history presented with a 3 day history of viral URI-like symptoms with sore throat, dry cough, shortness of breath, and dyspnea on exertion. The patient was an active marine recruit with many other members in his company being sick during this time. Shortly prior to arrival, the patient became unable to walk short flights of steps without becoming short of breath. The patient otherwise had no respiratory or cardiac history. He had no family history of sudden cardiac death or early MI. The patient denied fevers, chills, chest pain, pleuritic chest pain, positional chest pain, abdominal pain, flank pain, dysuria, hematuria, diarrhea, or any other associated symptoms.

Vitals: BP 87/56 | Pulse 96  | Temp 98.6 °F (37 °C)  | Resp 28 | SpO2 92%

On physical examination, the patient was alert and in acute distress. Patient presented with tachycardia, hypotension, hypoxia, and tachypnea. Mucous membranes were dry. Respiratory exam revealed decreased air movement, breath sounds, and faint crackles in the right lower lung field.

A bedside echocardiogram was performed.

Figure 1: POCUS echocardiogram in 4 chamber apical view demonstrating a small pericardial effusion.

Figure 2: POCUS lung exam revealed bilateral B lines anterosuperior aspects of the lungs.

Figure 3: Lung consolidation and pleural effusion demonstrating positive "spine sign."

The patient was initially stable but desaturated upon position change. The patient was persistently hypoxic with significant work of breathing on BiPAP before escalating to intubation, remaining persistently hypoxic in the mid 80s post intubation on a ventilator.

Discussion

Acute respiratory distress syndrome (ARDS) is a severe form of acute respiratory failure characterized by rapid onset of widespread inflammation in the lungs. It is defined by the Berlin criteria, which include acute onset within one week of a known clinical insult, bilateral opacities on chest imaging not fully explained by cardiac failure or fluid overload, and severe hypoxemia with a PaO2/FiO2 ratio of less than 300 mmHg.[1-3]

Common differential diagnoses for ARDS include cardiogenic pulmonary edema, pneumonia, and pulmonary embolism. Cardiogenic pulmonary edema can be differentiated by the presence of signs of fluid overload and cardiac dysfunction, often confirmed by echocardiography. Pneumonia may present with localized infiltrates and clinical signs of infection, while pulmonary embolism typically presents with sudden onset dyspnea, pleuritic chest pain, and may be confirmed by imaging studies such as CT pulmonary angiography.[1][4-5]

On physical examination, patients with ARDS often present with tachypnea, dyspnea, and diffuse crackles on auscultation. Hypoxemia is a hallmark, and patients may exhibit signs of respiratory distress such as use of accessory muscles and cyanosis. Imaging studies, particularly chest radiography, typically reveal bilateral alveolar infiltrates. Computed tomography (CT) scans can provide more detailed images, showing patchy or diffuse ground-glass opacities and consolidations.[1-2][6]

Point-of-care ultrasound (POCUS) is a valuable tool in the diagnosis and management of ARDS. Lung ultrasound findings in ARDS include the presence of multiple B-lines (indicating interstitial syndrome), spared areas, pleural line thickening, and subpleural consolidations. Cardiac ultrasound can help differentiate ARDS from cardiogenic pulmonary edema by assessing left ventricular function and the presence of pleural effusions.[7] Combining lung and cardiac ultrasound can enhance diagnostic accuracy and guide management decisions in critically ill patients with acute hypoxemic respiratory failure.[7]

References

  1. Saguil, A., & Fargo, M. V. (2020). Acute Respiratory Distress Syndrome: Diagnosis and Management. American family physician, 101(12), 730–738.
  2. Meyer, N. J., Gattinoni, L., & Calfee, C. S. (2021). Acute respiratory distress syndrome. Lancet (London, England), 398(10300), 622–637. https://doi.org/10.1016/S0140-6736(21)00439-6
  3. Matthay, M. A., Zemans, R. L., Zimmerman, G. A., Arabi, Y. M., Beitler, J. R., Mercat, A., Herridge, M., Randolph, A. G., & Calfee, C. S. (2019). Acute respiratory distress syndrome. Nature reviews. Disease primers, 5(1), 18. https://doi.org/10.1038/s41572-019-0069-0
  4. Papazian, L., Calfee, C. S., Chiumello, D., Luyt, C. E., Meyer, N. J., Sekiguchi, H., Matthay, M. A., & Meduri, G. U. (2016). Diagnostic workup for ARDS patients. Intensive care medicine, 42(5), 674–685. https://doi.org/10.1007/s00134-016-4324-5
  5. Sekiguchi, H., Schenck, L. A., Horie, R., Suzuki, J., Lee, E. H., McMenomy, B. P., Chen, T. E., Lekah, A., Mankad, S. V., & Gajic, O. (2015). Critical care ultrasonography differentiates ARDS, pulmonary edema, and other causes in the early course of acute hypoxemic respiratory failure. Chest, 148(4), 912–918. https://doi.org/10.1378/chest.15-0341
  6. Zompatori, M., Ciccarese, F., & Fasano, L. (2014). Overview of current lung imaging in acute respiratory distress syndrome. European respiratory review : an official journal of the European Respiratory Society, 23(134), 519–530. https://doi.org/10.1183/09059180.00001314
  7. Corradi, F., Brusasco, C., & Pelosi, P. (2014). Chest ultrasound in acute respiratory distress syndrome. Current opinion in critical care, 20(1), 98–103. https://doi.org/10.1097/MCC.0000000000000042
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Case 43: Shortness of Breath

Molly Chou

An 83-year-old male presented to our emergency department with shortness of breath. He woke up that morning with symptoms and called EMS. On arrival, the patient was alert and oriented with SpO2 90% on room air. The patient had a recent admission for right middle and lower lobe pneumonia. He also reported a history of heart failure with mildly reduced ejection fraction, coronary artery disease, and chronic kidney disease.

Vitals: BP 122/71, HR 92, RR 30, T 98.8F, spO2 90% on room air, 99% on 4LNC

Exam: Normal heart sounds, tachypnea, rhonchi in bilateral lower lobes, non-tender abdomen, >4mm pitting lower extremity edema

Labs: Cr 2.23 (from 1.98), BNPP 34,591 (from 19,366), WBC 31

EKG: new left bundle branch block

CXR: pulmonary edema, bilateral pleural effusions, and opacities that may represent atelectasis, though cannot rule out pneumonia or aspiration.

A bedside ultrasound was performed:

Figure 1: Right-sided pleural effusion, atelectasis, and pneumonia in seen right lower lobe

Figure 2A: During exhalation. Left-sided pleural effusion, atelectasis. 2B: During inhalation. Pneumonia becomes more visible as air fills alveoli adjacent to consolidated lung tissue (also known as “dynamic air bronchogram”)

Discussion: Bedside ultrasound demonstrated persistent pneumonia as a likely contributor to his shortness of breath. While other clinical indicators directed the diagnosis toward acute on chronic heart failure, POCUS was instrumental in also identifying persistent pneumonia. The patient was ultimately started on antibiotics and admitted to Cardiology for pneumonia and diuresis.

Learning points:

  • Pneumonia is among the leading causes of hospitalization, and it can be detected on ultrasound if the pleural line is involved, which is in about 99% of cases.
  • Ultrasound can detect inflammation and lung-tissue thickening of lobar pneumonias and consolidations. Interstitial pneumonias more often manifest as B-lines or white lung areas. Complications such as empyema and lung abscess can also be detected [1].
  • POCUS is highly sensitive (estimated around 93%) and specific (estimated around 98%) for pneumonia, particularly if done by a skilled sonographer [2,3].
  • Classic ultrasound findings:
    • “Hepatization” of lung parenchyma, when multiple hypoechoic areas give the tissue a “liver-like” or “spleen-like” appearance.
    • “Shred sign” (Figure 1), when a clear margin can be detected separating a consolidation with aerated parenchyma.
    • Air bronchograms (hyperechoic, linear punctate spots) can be detected within a consolidation in over 90% of pneumonia patients, though they are non-specific, as they may indicate any form of airway obstruction [1].
      • However, “dynamic air bronchograms” (Figure 2) where air-filled bronchograms move with respiration, are highly specific (94%) to pneumonia and have a high positive predictive value (97%) when seen [4]. An example can be seen below [5]:

References:

  1. Boccatonda A, Cocco G, D'Ardes D, et al. Infectious Pneumonia and Lung Ultrasound: A Review. J Clin Med. 2023;12(4):1402. Published 2023 Feb 10. doi:10.3390/jcm12041402
  2. Reissig A, Copetti R, Mathis G, et al. Lung ultrasound in the diagnosis and follow-up of community-acquired pneumonia: a prospective, multicenter, diagnostic accuracy study. Chest. 2012;142(4):965-972. doi:10.1378/chest.12-0364
  3. Chavez MA, Shams N, Ellington LE, et al. Lung ultrasound for the diagnosis of pneumonia in adults: a systematic review and meta-analysis. Respir Res. 2014;15(1):50. Published 2014 Apr 23. doi:10.1186/1465-9921-15-50
  4. Lichtenstein D, Meziere G, Seitz J. The Dynamic Air Bronchogram: A Lung Ultrasound Sign of Alveolar Consolidation Ruling Out Atelectasis. Chest. 2009;135(6):1421-1425. Published 2009 Jan 8. doi:10.1378/chest.08-2281
  5. Hailey Hobbs, MD. Dynamic Air Bronchograms. NephroPOCUS. Published 2019 Jul 1. Accessed 2024 Dec 13.
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