April 2018 Critical Care Case of the Month

Clement U. Singarajah, MD

Phoenix VA Medical Center

Phoenix, AZ USA

History of Present Illness

A 70-year-old man was admitted for shortness of breath (SOB) secondary to a “COPD exacerbation/ILD”. A pulmonary consult was placed for possible interstitial lung disease (ILD). A thoracic CT scan for pulmonary embolism showed no embolism and no obvious ILD. He was treated for a COPD exacerbation with the usual therapy of antibiotics, steroids, nebulized bronchodilators and oxygen. He started to improve.

A few days later as he was preparing for discharge, the patient suddenly decompensated becoming more SOB (once more proving that this a dangerous time for patients in hospital). There were reports that this began after he choked and perhaps aspirated on some food and drink. His blood pressure remained stable, but he became tachycardic to 130 beats/min, hypoxic on 100% non-rebreathing mask with saturations of 92%. Obvious clinical acute respiratory failure was present. The patient was started on non-invasive ventilation but continued to deteriorate.  He was deemed too unstable to obtain a CT scan. EKG showed sinus tachycardia. The patient was transferred to the ICU for respiratory failure. A chest x-ray was obtained (Figure 1).

Figure 1. Panel A: Admission chest x-ray which was interpreted as not different from the patient’s previous chest x-ray. Panel B: Portable chest x-ray taken shortly after initiation of non-invasive ventilation just after arrival in the intensive care unit.

The portable chest x-ray taken in the ICU shows a new right-sided consolidation and which of the following? (Click on the correct answer to proceed to the second of six pages)

1. Left pleural effusion and a loculated pneumothorax with tension physiology
2. Left pneumothorax with tension physiology
3. Left pneumothorax without tension physiology
4. Left sided tension hydropneumothorax
5. None of the above

Cite as: Singarajah CU. April 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;16(4):183-91. doi: https://doi.org/10.13175/swjpcc042-18 PDF

Increased Incidence of Eosinophilia in Severe H1N1 Pneumonia during 2015 Influenza Season

Benjamin Deaton MD

Nicholas Villalobos MD

Andrea Mytinger DO

Michel Boivin MD

Department of Internal Medicine

University of New Mexico School of Medicine

Albuquerque, NM USA

Abstract

Background: A portion of patients with influenza develop a severe, life t-threatening illness requiring intensive care. We observed a significant number of critically ill influenza patients with eosinophilia during the 2015 influenza season in New Mexico.

Methods: Patients were identified sequentially by reviewing disposition records of all patients admitted to the University of New Mexico Hospital medical intensive care unit between October 2015 and May 2016 for a diagnosis of influenza.

Results: Eleven patients were identified who developed respiratory failure from influenza. Average age was 43.7 + 11.3 (SD) with an average SAPS-2 score of 52.0 + 13.9 (SD) on admission. All 11 were found to have H1N1 influenza. All 11 required mechanical ventilation vasopressor support. Ten patients survived. Notably, 6 (54.5%) developed peripheral eosinophilia (>300/μL) during their hospitalization and all but one of these did not have peripheral eosinophilia at the time of admission. Bronchoalveolar lavage was performed in 5 patients (45.5%) and none were consistent with eosinophilic pneumonia. Further data analysis revealed exploration revealed no significant differences in multiple parameters and no clear cut cause of drug-induced eosinophilia was identified.

Conclusion: During the 2015 influenza season in New Mexico, a disproportionate number of patients with H1N1 influenza and respiratory failure developed peripheral eosinophilia. Type 2 errors could have occurred due to low sample size. Given the unusual frequency of peripheral eosinophilia further studies regarding the association of influenza A and peripheral eosinophilia is warranted.

Introduction

Influenza pneumonia remains a cause of significant morbidity and mortality (1). The re-emergence of H1N1 influenza in 2009 was associated with particularly severe respiratory illness, acute respiratory distress syndrome (ARDS) and mortality (2). The ARDS associated with H1N1 influenza appeared to disproportionately affect younger individuals, compared to other strains of influenza A (2). During the 2015 influenza season H1N1 circulated relatively late in the southwestern United States (3). Intensivists caring for patients with severe H1N1 pneumonia at the University of New Mexico hospital noticed a series of cases associated with significant peripheral eosinophilia. Eosinophilia with influenza or its treatments has rarely been described (4). We therefore sought to examine all cases of severe influenza pneumonia during the 2015 influenza season for the prevalence of peripheral eosinophilia and to assess for potential associations.

Methods

This study was reviewed and approved by the Institutional Review Board of the University of New Mexico Health Sciences Center. Patients from the University of New Mexico Hospital (UNMH) adult Medical Intensive Care Unit (MICU) admitted between October 2015 through May 2016 were retrospectively screened for inclusion. Inclusion criteria included a diagnosis of influenza (using a PCR based assay of nasal swab), admission to the UNMH MICU and age ≥ 18 years. Exclusion criteria included patients admitted to the MICU where influenza did not lead to significant respiratory failure.

In this retrospective cohort chart review, data was collected for demographics, clinical parameters at presentation and throughout their hospital course, and interventions received. Patients were assessed for the presence of eosinophilia at any point during their hospital course. Eosinophilia was defined as a serum eosinophil count that exceeded the upper limit of normal on a complete blood count (0.3x10³ cells/microliter). Values are reported with their standard deviation. Statistical analysis was performed using Stata 14 for Mac. The data was explored using two-sided t-tests, Fisher’s exact and Chi-squared tests between the 2 groups with and without eosinophilia. The paper was partially presented in poster form at the 2017 American Thoracic Society International Congress in Washington, DC (5).

Results

Thirteen patients with influenza were identified. Two patients were excluded from further analysis as they did not meet the criteria of having respiratory failure, the remaining eleven were included in this study. The average age of patients in the study was 43.7 ±11.3 years with an average SAPS-2 score of 52.0 ± 13.9 on admission. All eleven patients in the study admitted with severe influenza A leading to respiratory failure during the 2015-2016 influenza season were found to be infected by the H1N1 strain of influenza. See Table 1 for further descriptors of the cohort.

Table 1. Baseline and treatment characteristics by group.

The peak eosinophil count of the group with normal eosinophil count was 0.1(+0.1) X10³ cells/µl compared to 1.9 (+ 2.1) X10³ cells/µl in the group with significant peripheral eosinophilia (p=0.06). The range of eosinophilia in the group with normal eosinophil count was 0.0-0.3 X10³ cells/µl, and 0.5-4.8 X10³ cells/µl in the group with eosinophilia. The group with normal eosinophil count reached a “peak” count after an average of 4.6 days, and the group with an elevated eosinophil count after 17.1 days (p<0.02).None of the patients who underwent bronchoscopy had a significant elevation in the bronchoalveolar lavage eosinophil count.

Discussion

During the 2015-2016 influenza season in New Mexico, critically ill patients at UNM hospital admitted with influenza pneumonia were infected with the H1N1 subtype. Over 50 percent of these patients developed peripheral eosinophilia at some point of their hospital course. Among those who underwent bronchoscopy, significant alveolar eosinophilia was not observed, suggesting against a pulmonary cause of eosinophilia, such as acute or chronic eosinophilic pneumonia. All patients were treated with oseltamivir, so an association with this treatment could not be determined. No demographic differences were noted between patients who vashad peripheral eosinophilia and those that did not. The patients with significant peripheral eosinophilia trended to have a longer ICU and hospital length of stay (LOS) but this did not reach statistical significance in this small cohort.

Type 2 errors (failure to detect a true difference between groups due to small numbers of subjects) could have occurred due to low sample size while exploring etiologies. Potential etiologies that could have explained the observed eosinophilia included drug effect, possibly due to oseltamivir, antibiotics, diuretics or other medications. A review of the literature reveals case reports of associations between eosinophilia and influenza vaccine (6,7). Acute eosinophilic pneumonia has also been associated with H1N1 infection, but eosinophilia was not demonstrated on broncho-alveolar lavage in our series (8.9). Potentially this could have been a reaction to epitopes of this particular strain of H1N1 influenza. However, there have yet to be reports of eosinophilia during the 2015-2016 influenza season in the literature. Perhaps local factors could have contributed to an increased incidence of significant peripheral eosinophilia. Anecdotally, the authors do not however recall an increased incidence of eosinophilia in patients admitted for diagnoses other than H1N1. Patients were screened for other causes of viral pneumonia, and there was no clear co-infection that was associated with influenza associated eosinophilia. It was also noted the time to peak eosinophil count was much later in the elevated eosinophil group, and in most it took 14 days for the count to peak. This suggests the stimulus for the eosinophilia was ongoing for considerable time during the admission.

In conclusion, we describe an unusually high incidence of peripheral eosinophilia in patients with severe H1N1 influenza during the 2015 flu season. This eosinophilia was not associated with alveolar eosinophilia. Further observation for the recurrence of this association of H1N1 influenza A and peripheral eosinophilia is warranted during future influenza seasons.

References

1. Rotrosen ET, Neuzil KM, Influenza: a global perspective. Pediatr Clin North Am. 2017;64:911-36. [CrossRef] [PubMed]
2. Davlin SL, Blanton L, Kniss K, et al. Influenza Activity - United States, 2015-16 Season and Composition of the 2016-17 Influenza Vaccine.MMWR Morb Mortal Wkly Rep. 2016 Jun 10;65(22):567-75. [CrossRef] [PubMed]
3. Uyeki TM. Influenza. Ann Intern Med. 2017 Sep 5;167(5):ITC33-ITC48. [CrossRef] [PubMed]
4. Deaton, BR., Mytinger, AK, Ahmed, S, et al. Peripheral eosinophilia associated with 2016 H1N1 influenza. Am J Resp Crit Care. 2017;195:A5787 [Abstract],
5. Hayashi R, Shimomura N, Hosojima M, et al. A case of non-episodic angioedema with eosinophilia induced by influenza vaccine. Eur J Dermatol. 2017;27:554-5. [CrossRef] [PubMed]
6. Solak B, Dikicier BS, Kara RO, Erdem T. DRESS syndrome potentially induced by allopurinol and triggered by influenza vaccine. BMJ Case Rep. 2016 Mar 30;2016. [CrossRef] [PubMed]
7. Larrañaga JM, Marcos PJ, Pombo F, Otero-González I. Acute eosinophilic pneumonia as a complication of influenza A (H1N1) pulmonary infection. Sarcoidosis Vasc Diffuse Lung Dis. 2016 Mar 29;33(1):95-7. [PubMed]
8. Jeon EJ, Kim KH, Min KH. Acute eosinophilic pneumonia associated with 2009 influenza A (H1N1). Thorax. 2010;65:268-70. [CrossRef] [PubMed]

Cite as: Deaton B, Villalobos N, Mytinger A, Boivin M. Increased incidence of eosinophilia in severe H1N1 pneumonia during 2015 influenza season. Southwest J Pulm Crit Care. 2018;16(3):146-9. doi: https://doi.org/10.13175/swjpcc021-18 PDF 

March 2018 Critical Care Case of the Month

Babitha Bijin MD

Jonathan Callaway MD

Janet Campion MD

University of Arizona

Department of Medicine

Tucson, AZ USA

Chief Complaints

• Shortness of breath
• Worsening bilateral LE edema

History of Present Illness

A 53-year-old man with history of multiple myeloma and congestive heart failure presented to the emergency department with complaints of worsening shortness of breath and bilateral lower extremity edema for last 24 hours. In the last week, he has had dyspnea at rest as well as a productive cough with yellow sputum. He describes generalized malaise, loss of appetite, possible fever and notes new bilateral pitting edema below his knees. Per patient, he had flu-like symptoms one week ago and was treated empirically with oseltamivir.

Past Medical History

• Multiple myeloma-IgG kappa with calvarial and humeral metastases, ongoing treatment with cyclophosphamide, bortezomib and dexamethasone
• Community acquired pneumonia 2016, treated with oral antibiotics
• Heart failure with echo 10/2017 showing moderate concentric left ventricular hypertrophy, left ventricular ejection fraction 63%, borderline left atrial and right atrial dilatation, diastolic dysfunction, right ventricular systolic pressure estimated 25 mm Hg
• Hyperlipidemia
• Chronic kidney disease, stage III

Home Medications: Aspirin 81mg daily, atorvastatin 80mg daily, furosemide 10mg daily, calcium / Vitamin D supplement daily, oxycodone 5mg PRN, chemotherapy as above

Allergies: No known drug allergies

Social History:

• Construction worker, not currently working due to recent myeloma diagnosis
• Smoked one pack per day since age 16, recently quit with 30 pack-year history
• Drinks beer socially on weekends
• Married with 3 children

Family History: Mother with hypertension, uncle with multiple myeloma, daughter with rheumatoid arthritis

Review of Systems: Negative except per HPI

Physical Exam

• Vitals: T 39.3º C, BP 80/52, P121, R16, SpO2 93% on 2L
• General: Alert man, mildly dyspneic with speech
• Mouth: Nonicteric, moist oral mucosa, no oral erythema or exudates
• Neck: No cervical neck LAD but JVP to angle of jaw at 45 degrees
• Lungs: Bibasilar crackles with right basilar rhonchi, no wheezing
• Heart: Regular S1 and S2, tachycardic, no appreciable murmur or right ventricular heave
• Abdomen: Soft, normal active bowel sounds, no tendernesses, no hepatosplenomegaly
• Ext: Pitting edema to knees bilaterally, no cyanosis or clubbing, normal muscle bulk
• Neurologic: No focal abnormalities on neurologic exam

Laboratory Evaluation

• Complete blood count: WBC 15.9 (92% neutrophils), Hgb/Hct 8.8/27.1, Platelets 227
• Electrolytes: Na⁺ 129, K⁺ 4.0, Cl^- 100, CO2 18, blood urea nitrogen 42, creatinine 1.99 (baseline Cr 1.55)
• Liver: AST 35, ALT 46, total bilirubin1.7, alkaline phosphatase 237, total protein 7.4, albumin 2.
• Others: troponin 0.64, brain naturetic peptide 4569, venous lactate 2.6

Chest X-ray

Figure 1. Admission chest x-ray.

Thoracic CT (2 views)

Figure 2. Representative images from the thoracic CT scan in lung windows.

What is most likely etiology of CXR and thoracic CT findings? (Click on the correct answer to proceed to the second of seven pages)

1. Coccidioidomycosis pneumonia
2. Pulmonary edema
3. Pulmonary embolism with infarcts
4. Staphylococcus aureus pneumonia
5. Streptococcus pneumoniae infection 

Cite as: Bijin B, Callaway J, Campion J. March 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;16(3):117-25. doi: https://doi.org/10.13175/swjpcc035-18 PDF 

Ultrasound for Critical Care Physicians: Ghost in the Machine

Ross Davidson, DO

Michel Boivin, MD 

Division of Pulmonary, Critical Care and Sleep Medicine

University of New Mexico School of Medicine

Albuquerque, NM USA

A 53-year-old woman presented to the emergency department after a sudden cardiac arrest at home. The patient had a history of asthma and tracheal stenosis and had progressive shortness of breath over the previous days. The patient’s family noticed a “thump” sound from the patient’s room, and found her apneic. They called 911 and began cardiopulmonary resuscitation. Paramedics arrived on the scene, found an initial rhythm of pulseless electrical activity. The patient eventually achieved return of spontaneous circulation and was transported to the hospital. On arrival the patient was in normal sinus rhythm, with a heart rate of 110 beats per minute. Blood pressure was 80/45 mmHg, on an epinephrine infusion. The patient was afebrile, endotracheally intubated, unresponsive and ventilated at 30 breaths per minute. An initial chest radiograph was compatible with aspiration pneumonitis and a small pneumothorax. Initial electrocardiogram on arrival had 1mm ST-segment depressions in leads V4 to V6. Transthoracic echocardiography was unsuccessful due to patient’s habitus and mechanical ventilation. Because of the patient’s hemodynamic instability and unknown cause of cardiac arrest, an urgent trans-esophageal echocardiogram (TEE) was performed (Videos 1-3).

Video 1. Mid-esophageal 4-chamber view of the heart.

Video 2. Upper esophageal long-axis view of the pulmonary artery and short axis view of the ascending aorta.

Video 3. Upper esophageal short axis view of the pulmonary artery with the ascending aorta in long axis. 

Based on the images presented what do you suspect is the etiology of the patient’s cardiac arrest? (Click on the correct answer for an explanation-no penalty for guessing, you can go back and try again)

1. Massive Pulmonary Embolism
2. Myocardial infarction
3. Pericardial Tamponade
4. Unable to determine

Cite as: Davidson R, Boivin M. Ultrasound for critical care physicians: ghost in the machine. Southwest J Pulm Crit Care. 2018;16(2):76-80. doi: https://doi.org/10.13175/swjpcc027-18 PDF 

February 2018 Critical Care Case of the Month

Robert A. Raschke, MD

University of Arizona College of Medicine-Phoenix

Phoenix, AZ

History of Present Illness

A 25-year-old was admitted to an outside hospital with an acute episode of nausea and vomiting and chronic progressive weakness.  He smoked 2 cigarettes per day and drank a 12-pack of beer per month.  He had a history of undefined chronic liver disease.

Physician Examination

Physical examination was reported as showing a chronically ill appearing man who was “weak” using crutches to ambulate.

The patient was made NPO and was rehydrated with intravenous normal saline.

Which of the following are indicated at this time? (Click on the correct answer to proceed to the second of four pages)

1. Creatinine phosphokinase (CPK)
2. Serum potassium
3. Thyroid studies
4. 1 and 3
5. All of the above

Cite as: Raschke RA. February 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;16(2):62-6. doi: https://doi.org/10.13175/swjpcc009-18 PDF