January 2018 Critical Care Case of the Month

Theodore Loftsgard, APRN, ACNP 

Department of Anesthesiology and Critical Care

Mayo Clinic Minnesota

Rochester, MN USA

History of Present Illness

The patient is a 51-year-old woman admitted with a long history of progressive shortness of breath.  She has a long history of “heart problems”. She uses supplemental oxygen at 1 LPM by nasal cannula.

Past Medical History, Social History and Family History

She also has several comorbidities including renal failure with two renal transplants and a history of relatively recent RSV and CMV pneumonia. She is a life-long nonsmoker. Her family history is noncontributory.

Physical Examination

• Vital signs: Blood pressure 145/80 mm Hg, heart rate 59 beats/min, respiratory rate 18, T 37.0º C, SpO2 91% of 1 LPM.
• Lungs: Clear.
• Heart: Regular rhythm with G 3/6 systolic ejection murmur at the base.
• Abdomen: unremarkable.
• Extremities: no edema

Which of the following should be performed? (Click on the correct answer to proceed to the second of seven pages)

1. Brain naturetic peptide (BNP)
2. Chest x-ray
3. Echocardiogram
4. Electrocardiogram
5. All of the above

Cite as: Loftsgard T. January 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;16(1):1-7. doi: https://doi.org/10.13175/swjpcc155-17 PDF

December 2017 Critical Care Case of the Month

Michael B. Gotway, MD

Department of Radiology

Mayo Clinic Arizona

Scottsdale AZ USA

Clinical History: A 57-year-old man with no known previous medical history was brought to the emergency room via ambulance and admitted to the intensive care unit with a compliant of severe chest pain in the substernal region and epigastrium. The patient was awake and alert and did not complain of shortness of breath.

Physical examination was largely unremarkable and the patient’s oxygen saturation was 98% on room air. The patient’s vital signs revealed tachycardia (105 bpm) and his blood pressure was 108 mmHg / 60 mmHg.

Laboratory evaluation showed a slightly elevated white blood cell count (13 x 10⁹ cells/L), but his hemoglobin and hematocrit values were with within normal limits, as was his platelet count. 

Which of the following diagnoses are appropriate considerations for this patient’s condition? (Click on the correct answer to proceed to the second of nine pages)

1. Acute pericarditis
2. Aortic dissection
3. Community-acquired pneumonia
4. Myocardial infarction
5. All of the above

Cite as: Gotway MB. December 2017 critical care case of the month. Southwest J Pulm Crit Care. 2017;15(6):241-52. doi: https://doi.org/10.13175/swjpcc145-17 PDF 

November 2017 Critical Care Case of the Month

Stephanie Fountain, MD

Pulmonary and Critical Care Medicine

Banner University Medical Center Phoenix

Phoenix, AZ USA

History of Present Illness

A 56-year-old man presented with “food stuck in throat” since eating steak 18 hours prior to presentation. He is unable to eat or drink and has a sore throat. He is able to speak but has a “hoarse voice.” He denied drooling.

Past Medical History, Family History, and Social History

• He described himself as “healthy” and had not sought medical care in years.
• Former smoker but quit 2 years ago.
• He uses alcohol daily.
• He denied illicit drug use.

Physical Exam

• Afebrile, blood pressure 137/74 mm HG, heart rate 74 beats/min, SpO2 98% on room air.
• Physical exam was normal

Which of the following should be done next? (Click on the correct answer to proceed to the second of six pages)

1. Esophagogastroduodenoscopy (EGD)
2. Papain (Adolph’s Meat Tenderizer®) administration
3. Tracheostomy
4. 1 and 3
5. All of the above

Cite as: Fountain S. November 2017 critical care case of the month. Southwest J Pulm Crit Care. 2017;15(5):191-8. doi: https://doi.org/10.13175/swjpcc130-17 PDF

A New Interventional Bronchoscopy Technique for the Treatment of Bronchopleural Fistula

Evan Denis Schmitz, MD

Abstract

A patient receiving mechanical ventilation with multiple left hydropneumothoraces had a persistent air leak through the thoracostomy tube. The leak was temporarily resolved by interventional bronchoscopy at the bedside in the ICU. Because of the limited resources available at the hospital, a Swan-Ganz catheter was inserted into the left upper lobe bronchus, inflated and left in place. The air leak ceased and the left upper lobe bronchus was occluded with an autologous blood plug by infusing the patient’s own blood through the distal port of the catheter. The patient’s oxygenation improved significantly. The effects persisted for 2.5 hours until the air leak returned while the patient remained intubated. Such a technique may be useful when managing persistent air leaks.

Introduction

An air leak during mechanical ventilation despite the insertion of a thoracostomy tube can be detected by the bubbling of air through the air seal in the chest drainage system (1). A persistent air leak (PAL) is often defined as persistence of the air leak beyond 24 hours, which can hinder ventilation and inhibit lung expansion. Furthermore, the leak may inhibit healing of the fistula between the lung and the pleural space. Recommendations for the management of PALs include surgical repair as the gold standard for treatment (1,2). However, published anecdotal reports describe successful treatment of PALs with endobronchial insertion of fibrin sealants, ethanol injection, metal coils, Watanabe spigots and endobronchial valves. Success is also reported with chemical and autologous blood patch pleurodesis (1). We report a bedside interventional bronchoscopy technique using a Swan-Ganz catheter for the treatment of PALs while intubated and ventilated. A Swan-Ganz catheter is inserted into a lobar bronchus using direct visualization with a bronchoscope, the balloon is inflated and left in place while an autologous blood plug is created utilizing the distal port of the catheter.

Case Presentation

A 69-year-old man with no prior medical contact presented to the emergency department with severe shortness of breath and altered mental status. He was intubated in the emergency department for hypoxia. On arrival to the ICU he was in hypoxic respiratory failure and septic shock with a PaO₂ in the 40s. His ventilator plateau pressures were 40-50 cm H₂O. Chest radiography revealed moderate pneumomediastinum and multiple loculated hydropneumothoraces involving the left lung with suspected necrotic left upper lobe (Figure 1).

Figure 1. Portable AP chest x-ray showing left lung loculated hydropneumothoraces in the apex, medial and lateral walls of the left chest, subcutaneous emphysema, mediastinal emphysema and very low lung volumes. There are right apical and lower lobe areas of consolidation. A left thoracostomy tube is in place.

A 32 Fr thoracostomy tube was placed in the left intercostal space lateral to the nipple in the mid-axillary. The larger thoracostomy tube was chosen because of concern that the smaller pig-tailed catheters might not be adequate to control the leak. Plateau pressure improved to 30 cm H2O.

Despite a low tidal volume ventilator strategy and -40 cm H₂O suction through the thoracostomy tube, the patient had an air leak through the thoracostomy tube which continued to bubble in the water seal chamber during both inspiration and expiration. The air leak did not improve over the ensuing 24 hours and subcutaneous emphysema worsened when attempts were made to decrease suction which was confirmed by physical exam and chest x-ray. Selective right lung ventilation led to inadequate ventilation as evidenced by increasing end-tidal CO_2.

To determine and attempt to control the source of the persistent air leak, an interventional bronchoscopy was performed at bedside. Because other devices to such as metal coils, endobronchial valves, fibrin glue and a YAG laser were unavailable, a 6 Fr Swan-Ganz catheter was used. The Swan-Ganz catheter was threaded through the opening of the bronchoscope adaptor down the endotracheal tube to 3 cm above the carina. A flexible bronchoscope was then advanced along the side of the catheter through the bronchoscope adaptor and down the endotracheal tube. The catheter was not inside the working channel of the bronchoscope. The catheter was manipulated along with the bronchoscope, taking advantage of the inherent bend in the catheter, into the left mainstem bronchus and into the left upper lobe bronchus just distal to the lingular bronchus and inflated (Figure 2).

Figure 2. Panel A: Bronchoscopic view showing the Swan-Ganz catheter in the left upper lobe bronchus. Panel B: Chest x-ray confirming the Swan-Ganz catheter in the left upper lobe with the balloon inflated (arrow).

The massive air leak stopped completely. A blood plug was then created by instilling 20 ml of the patient’s own blood into the distal port of the catheter distal to the balloon along with 5 ml of 1:1000 epinephrine. The bronchoscope was used to hold the balloon in place for 10 minutes while the blood clotted. The bronchoscope was carefully removed and the catheter with the balloon inflated was left in place (Figure 3).

Figure 3. Bronchoscopic view showing the catheter passing into the left upper lobe bronchus with the surrounding blood plug.

The bronchoscope adaptor was taped post-bronchoscopy at the opening with an occlusive dressing so no air could leak around the catheter. The patient tolerated the procedure well. The air leak was successfully stopped with no evidence of worsening pneumothoraces. After PaO₂ increased from the 40s on admission to the 170s after the PAL was stopped. Chest x-ray at 1 and 3 hours showed no evidence of worsening pneumothorax with the Swan-Ganz catheter still in place and inflated in the left upper lobe bronchus. After 2.5 hours, a smaller air leak did return but was present only during inspiration.

Discussion

A PAL during mechanical ventilation can be a serious complication of ventilator therapy. It can lead to poor lung expansion, ventilation/perfusion mismatch, direct extension of airway infection into the pleural space, and an inability to maintain positive end-expiratory pressure. Patients with a PAL have increased complications, including ICU readmission, pneumonia, and a longer hospital stay (3,4). Fortunately, it appears to be relatively rare. In a retrospective study only 39 out of 1,700 mechanically ventilated patients had a PAL defined as lasting for greater than 24 hours (5).

The American College of Chest Physicians guidelines published in 2001 and the 2010 British Thoracic Society guidelines on pleural disease recommend waiting for about 4 days and then seeking surgical evaluation for a PAL (2,6). It was recommended that consideration should be given to placing the thoracostomy tube to water seal rather than to suction. However, this may not be possible in patients with a large persistent air leak that complicates ventilation. In those instances, a variety of endobronchial and pleural interventions have been attempted. Although the reports are anecdotal, most achieved success with either none or minimal complications (1). There have been two basic approaches to treat PALs; sealing the air leak from the bronchial side or from the pleural side. Those therapies administered through the bronchoscope include fibrin sealant, metal coils, Watanabe spigots, synthetic hydrogel, platelet gel, endobronchial valves and YAG laser (1). Complications were infrequent and minor. Ethanolamine and ethanol have also been used but there appear to be more complications with those treatments. From the pleural side, blood patch and chemical pleurodesis have been used successfully (1). However, chemical pleurodesis might result in a trapped lung.

The technique reported here can be performed with materials available in the ICU. A torqueable guidewire can be inserted if needed to help increase the catheter stiffness and help with advancement of the catheter into the individual bronchus to identify the source of the bronchopleural fistula. Alternatives to a blood patch might include occlusion of the culprit bronchus with the patient’s own mucus and argon plasma coagulation to form a clot. A blood patch can be used to determine the potential success of a more permanent material to occlude the bronchus, such as a fibrin seal, synthetic hydrogel, laser, or before attempting endobronchial valve placement.

Conclusion

Bedside endobronchial management of PAL is feasible using a flexible bronchoscope and Swan-Ganz catheter for localization, tamponade and delivery of a blood plug.

References

1. Dugan KC, Laxmanan B, Murgu S, Hogarth DK. Management of persistent air leaks. Chest. 2017;152(2):417-23. [CrossRef] [PubMed]
2. Baumann MH, Strange C, Heffner JE. Management of spontaneous pneumothorax: an American College of Chest Physicians Delphi consensus statement. Chest. 2001;119(2):590-602. [CrossRef] [PubMed]
3. Liberman M, Muzikansky A, Wright CD, et al. Incidence and risk factors of persistent air leak after major pulmonary resection and use of chemical pleurodesis. Ann Thorac Surg. 2010;89(3):891-897. [CrossRef] [PubMed]
4. DeCamp MM, Blackstone EH, Naunheim KS, et al. Patient and surgical factors influencing air leak after lung volume reduction surgery: lessons learned from the National Emphysema Treatment Trial. Ann Thorac Surg. 2006;82(1):197-206. [CrossRef] [PubMed]
5. Pierson DJ, Horton CA, Bates PW. Persistent bronchopleural air leak during mechanical ventilation. A review of 39 cases. Chest. 1986;90(3):321-3. [CrossRef] [PubMed]
6. Havelock T, Teoh R, Laws D, et al. Pleural procedures and thoracic ultrasound: British Thoracic Society Pleural Disease Guideline 2010. Thorax. 2010;65(suppl 2):ii61-ii76. [CrossRef] [PubMed]

Cite as: Schmitz ED. A new interventional bronchoscopy technique for the treatment of bronchopleural fistula. Southwest J Pulm Crit Care. 2017;15(4):174-8. doi: https://doi.org/10.13175/swjpcc120-17 PDF 

ACE Inhibitor Related Angioedema: A Case Report and Brief Review

F. Brian Boudi, J. L. Rush, Cameron Farsar, Connie S. Chan

Carl T. Hayden VA Medical Center

University of Arizona, College of Medicine Phoenix Campus

Phoenix, AZ USA

Abstract

We present a case report of angiotensin converting enzyme (ACE) inhibitor angioedema successfully treated with icatibant (Firazyr®). The pathophysiology and treatment of ACE inhibitor angioedema is reviewed.

Introduction

Angioedema, swelling caused by a rapid increase in permeability of submucosal or subcutaneous capillaries and post-capillary venules with localized plasma extravasation, is associated with random, highly variable and often unpredictable clinical manifestations (1). Attacks are associated with significant decreased quality of life both during and between attacks, significant functional impairment and a high risk of morbidity and mortality. Angioedema can be caused by either mast cell degranulation or activation of the kallikrein-kinin cascade. ACE inhibitor-related angioedema is one the leading causes of drug-induced angioedema. While ACE inhibitor-induced angioedema is rare, awareness of this serious and potentially life-threatening complication is of great importance because of the extensive use of this class of drugs in clinical practice. Cases presenting into the emergency department because ACE inhibitors, one of the most widely prescribed medications prescribed in the United States, account for about 20-40 percent of emergency room admissions related to angioedema (1,2).

Approximately 50% of patients with ACE inhibitor-induced angioedema arise within the first week of treatment. The remainder can become symptomatic weeks, months, or even years later. The estimated incidence is likely underestimated. The actual incidence can be far higher because of poorly recognized presentation of angioedema and its sometimes-late onset. The incidence can be even higher (up to 3-fold) in certain risk groups, for instance Afro-Americans (3). It seems to have a predilection for the head, neck, lips, mouth, tongue, larynx, pharynx, and subglottal areas without urticaria (4).

Case Presentation

A 55-year-old veteran presented to the Emergency Department for the Carl T. Hayden Veterans Administration Medical Center in Phoenix Arizona with impressive angioedema. The Veteran had been taking lisinopril for 6 years and had another similar episode two months prior. The prior episode presented with facial swelling that resolved within a couple of hours. However, the present episode was accompanied by difficulty breathing and swallowing. He was begun on an allergic reaction protocol which included establishing and making sure the veteran had a patent airway, nasal trumpet, placing a peripheral intravenous catheter and starting iv fluid of sodium chloride 0.9% to keep vein open, medications of diphenhydramine 50 mg, famotidine 20 mg, methylprednisolone 125mg and 0.3 mg epinephrine subcutaneously. He was also given racemic epinephrine mixed via nebulizer and 30 mg subcutaneously of icatibant (Firazyr®), a bradykinin B2 receptor antagonist used to treat hereditary angioedema. He improved and was subsequently admitted to the intensive care unit for continued observation. The following day he was discharged with prescriptions for prednisone and orders to discontinue the use of lisinopril.

Discussion

Despite newer therapies, there are no currently approved guidelines for the treatment of ACE inhibitor-induced angioedema in the United States. It is difficult to tell whether icatibant was truly effective in this case presentation as it was one of multiple therapies administered. Many causes of angioedema result from release of histamine (1). However, ACE inhibitor angioedema results from other inflammatory mediators, especially bradykinin (2) (Figure 1).

Figure 1. Simplified pathway for bradykinin-mediated angioedema showing the sites of drug activity (5).

Mast cells are not believed to be involved in this form of angioedema, and pruritus and urticaria are absent. Bradykinin-mediated angioedema, unlike histamine-mediated angioedema, frequently affects the gastrointestinal mucosa, leading to bowel wall edema and presenting with episodes of abdominal pain, nausea, vomiting, and/or diarrhea. While antihistamines and corticosteroids are often administered for treatment of angioedema, they are unlikely to have effect in ACE inhibitor induced angioedema. Epinephrine may slow (or stop) the rate of swelling. ACE inhibitor angioedema may be treated with additional drugs that act on the bradykinin pathway (e.g., icatibant, ecallantide). The recommended dose of icatibant is 30 mg administered by subcutaneous (SC) injection in the abdominal area. Additional doses may be administered in 6 hours if response is inadequate. Icatibant may decrease the time of recovery from ACE inhibitor related angioedema (6). Another ACE inhibitor should not be prescribed as the reaction is a class, not a drug specific reaction (7). Checking the complement C4 may be helpful. Patients with preexisting angioedema, including hereditary angioedema caused by C1 esterase inhibitor deficiency, are predisposed to develop angioedema in response to ACE inhibitors (8).

ACE inhibitor induced angioedema remains a disorder without a clear treatment modality for reduction of symptoms. The primary therapeutic interventions remain removal of the offending agent and airway management when indicated. The use of icatibant may be effective in the management of ACE inhibitor related angioedema; however, its efficacy and benefits have not been clear in the small studies published thus far. There have been three randomized trials evaluating the use of icatibant in ACE inhibitor angioedema. Interestingly, the first study found icatibant to be effective while the more recent and larger studies found no significant difference in time to recovery (3, 6, 9-12). Icatibant is costly with a wholesale price of $9,000-$11,000 and may not be available at all hospitals. Given its questionable outcomes data, icatibant may not appropriate in all medical centers. This is especially important since off-label use may not be covered by insurers. 

References

1. Stone C Jr, Brown NJ. Angiotensin-converting enzyme inhibitor and other drug-associated angioedema. Immunol Allergy Clin North Am. 2017 Aug;37(3):483-495. [CrossRef] [PubMed]
2. Guyer AC, Banerji A. ACE inhibitor-induced angioedema. UpToDate. June 27, 2017. Available at: https://www.uptodate.com/contents/an-overview-of-angioedema-clinical-features-diagnosis-and-management#H30 (requires subscription, accessed 9/18/17).
3. Straka BT, Ramirez CE, Byrd JB, et al. Effect of bradykinin receptor antagonism on ACE inhibitor-associated angioedema. J Allergy Clin Immunol. 2017;140:242-248.e2. [CrossRef] [PubMed]
4. Sabroe R, Black A. Angiotensin-converting enzyme (ACE) inhibitors and angio-oedema. Br J Dermatol. 1997;1:153–8. [CrossRef] [PubMed]
5. Shenvi C, Serrano K. New treatments for angioedema. Emergency Physicians Monthly. 9/12/16. Available at: http://epmonthly.com/article/new-treatments-angioedema/ (accessed 10/20/17).
6. Baş M, Greve J, Stelter K, et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med. 2015 Jan 29;372(5):418-25. [CrossRef] [PubMed]
7. Johnsen SP, Jacobsen J, Monster TB, Friis S, McLaughlin JK, Sørensen HT.Risk of first-time hospitalization for angioedema among users of ACE inhibitors and angiotensin receptor antagonists. Am J Med. 2005;1:1428-9. [CrossRef] [PubMed]
8. Orfan N, Patterson R, Dykewicz M. Severe angioedema related to ACE inhibitors in patients with a history of idiopathic angioedema. JAMA. 1990;1:1287-9. [CrossRef] [PubMed]
9. Sinert R, Levy P, Bernstein JA, et al.Randomized trial of icatibant for angiotensin-converting enzyme inhibitor-induced upper airway angioedema. J Allergy Clin Immunol Pract. 2017 Sep-Oct;5(5):1402-9.e3. [CrossRef] [PubMed]
10. Culley CM, DiBridge JN, Wilson GL Jr. Off-label use of agents for management of serious or life-threatening angiotensin converting enzyme inhibitor-induced angioedema. Ann Pharmacother. 2016 Jan;50(1):47-59 [CrossRef] [PubMed]
11. Fok JS, Katelaris CH, Brown AF, Smith WB. Icatibant in angiotensin-converting enzyme (ACE) inhibitor-associated angioedema. Intern Med J. 2015 Aug;45(8):821-7. [CrossRef] [PubMed]
12. Riha HM, Summers BB, Rivera JV, Van Berkel MA. Novel therapies for angiotensin-converting enzyme inhibitor-induced angioedema: a systematic review of current evidence. J Emerg Med. 2017 Sep 19. pii: S0736-4679(17)30489-4. [CrossRef] [PubMed]

Cite as: Boudi FB, Rush JL, Farsar C, Chan CS. ACE inhibitor related angioedema: a case report and brief review. Southwest J Pulm Crit Care. 2017;15(4):165-8. doi: https://doi.org/10.13175/swjpcc114-17 PDF