January 2025 Critical Care Case of the Month: A 35-Year-Old Admitted After a Fall

Susanna G. Von Essen MD

University of Nebraska Medical Center

Omaha, NE USA

History of Present Illness

A 35-year-old was injured at work earlier that day. He fell approximately 10 feet while power washing a hog confinement pen from inside the bucket of a skid loader. He complained of pain in his left foot. He had struck his head but denied loss of consciousness. He was admitted to an outside hospital ICU for observation.

PMH, SH, and FH

• He has no chronic medical conditions and has never been hospitalized.

• He has never smoked and only drinks socially. He is single.

• His mother died at 55 of heart disease. His father and 6 brothers and sisters are all healthy.

Physical Examination

He is 5’5” and weighs 193 pounds. There is a head laceration and he has tenderness in his left foot. Otherwise, his physical examination is normal.

Radiology

A foot x-ray reveals fractures of the left second and third metatarsals. Head CT was interpreted as normal.

His chest x-ray is shown in Figure 1.

Figure 1. Chest x-ray on the day of injury. To view Figure 1 in a separate enlarged window click here.

Which of the following are true? (Click on the correct answer to be directed to the first of seven pages

1. His chest x-ray is normal.

2. He has fractures of the 9th and 10th right ribs.

3. He can be discharged from the hospital

4. 1 and 3

5. None of the above

Cite as: VonEssen SG. January 2025 Critical Care Case of the Month: A 35-Year-Old Admitted After a Fall. Southwest J Pulm Crit Care Sleep. 2024;30(1):1-4. doi:

https://doi.org/10.13175/swjpccs036-24

PDF

July 2024 Critical Care Case of the Month: Community-Acquired Meningitis

Robert A. Raschke MD

The University of Arizona College of Medicine – Phoenix

Phoenix, AZ USA

History of Present Illness

A 59-year-old man was brought to our emergency department at 0300 with a possible stroke. He was last known well at 2230 the previous evening, when he complained of severe headache and took some acetaminophen before going to bed. His wife (who provided all history) noted that the patient awoke about midnight, vomited and took some naproxen. The wife next heard the patient awake at 0230, and found him back in the bathroom vomiting again, slow to respond, “mumbling” and confused. The wife was able to get the patient into their car with some difficulty and drove him to the ER.

Past Medical History, Social History, Family History

Only minimal past medical history was elicited. There was no known trauma, no fever and no recent illnesses. The patient took no prescription medications. He did not have any history of neurological disease or of substance abuse.

Physical Examination

Vitals from the ER at 0300 included: BP 157/130 mmHg, HR 101 bpm, RR 16 bpm, temperature 97.7°F.

The patient was described as “non-toxic appearing.” His eyes were open, but he was mute and didn’t obey commands. His Glascow Coma Scale was E4, V1, M5. Formal strength testing wasn’t performed, but he was observed to spontaneously move his arms. No facial asymmetry was noted.

Hospital Course

A “Stroke alert” was called based on the clinical presentation. The laboratory evaluation was significant for: WBCC 14.9x10⁹/L, hemoglobin 13.2 g/L, platelets 181x10⁹/L; Na 135 mmol/L, K 4.0 mmol/L, Cl 100 mmol/L, CO2 23 mmol/L, BUN 14 mg/dL, creatinine 0.7 mg/dL, glucose 349 mg/dL and INR 1.0. A procalcitonin was elevated at 0.8 ng/mL. Urinalysis showed >500 mg/dL glucose, moderate leukocyte esterase, WBCC 19/hpf, and no bacteria. A urine drugs of abuse screen was negative. CT head, CTA head/neck and brain perfusion scans were all negative for acute abnormalities. A virtual stroke neurologist recommended against lytics and/or thrombectomy, due to the lack of radiographic evidence of a large vessel occlusion.

The patient was admitted to the family medicine service. Ceftriaxone 1gm was administered for a presumed urinary tract infection. His temperature was retaken at 0630, at which time it had risen to 102.7°F. At 0730 the patient became agitated, diaphoretic and his SpO₂ fell to 79%. His BP was 223/139 mmHg, HR 115 bpm, and RR 53 bpm and he was emergently intubated and transferred to the ICU.

Which of the following is false regarding the clinical findings of community-acquired bacterial meningitis? (Click on the correct answer to be directed to the second of 5 pages)

1. Fifty percent of patients present within 24 hours of symptom onset.
2. The majority of patients have the classic triad of fever, stiff neck and altered mental status.
3. Ninety-five percent of patients have at least two of four findings: (headache, fever, stiff neck and altered mental status).
4. Patients may less commonly present with community-acquired hemiplegia, aphasia, seizure, and cranial nerve deficits.
5. All are true.

Cite as: Raschke RA.  2024 Critical Care Case of the Month: Community-Acquired Meningitis. Southwest J Pulm Crit Care Sleep. 2024;29(1):1-5. doi: https://doi.org/10.13175/swjpccs027-24 PDF

March 2023 Critical Care Case of the Month: A Bad Egg

Richard A. Robbins, MD

Phoenix Pulmonary and Critical Research and Education Foundation

Gilbert, AZ

History of Present Illness

You are asked to see a 35-year-old man who was admitted to the ICU from the ER the previous night with an exacerbation of his chronic obstructive pulmonary disease (COPD). He has a long history of COPD and came to the ER for COVID-19 testing because he was at a party where a friend was later found to COVID-19. He denies any change in his chronic respiratory symptoms but his spirometry was significantly worse than his baseline in the ER and despite his protests he was admitted. He was treated with empiric antibiotics (amoxicillin and clavulanic acid), corticosteroids (methylprednisolone 125 mg every 6 hours), bronchodilators (albuterol/ipratropium every 4 hours) and oxygen. He says his breathing has not improved and he wants to go home. He has had gradually increasing shortness of breath for the past 8-10 years. He has minimal cough but denied any fevers, systemic symptoms, or wheezing.  

PMH, FH, and SH

He had a history of multiple pneumothoraces which eventually led to bilateral pleurodesis. He has had not pneumothoraces since. He had a benign bone tumor removed about 25 years ago and a history of manic-depression. There is no FH of any similar type of problems. He does smoke about 3/4 pack of cigarettes per day and has more than occasional marijuana use.

Physical Exam

Physical examination was unremarkable expect for a well-healed scar on the left thigh.

Spirometry

Previous spirometry performed as an outpatient showed his FVC 2.54 L (53% of predicted) with an FEV1 1.25 L (31% of predicted). These improved to 2.99 L and 1.52 L after a bronchodilator. His spirometry last night in the ER was FVC 1.63 L (29 % predicted) and FEV1 0.80 L (18 % predicted).

Radiography

A chest radiograph was performed (Figure 1).

Figure 1. PA (panel A) and lateral (panel B) chest x-ray.

What should be done at this time? (Click on the correct answer to be directed to the second of five pages)

1. Continue his antibiotics, corticosteroids and bronchodilators
2. Order an alpha-1 antitrypsin level
3. Transfer to the floor
4. 1 and 3
5. All of the above

Cite as: Robbins RA. March 2023 Critical Care Case of the Month: A Bad Egg. Southwest J Pulm Crit Care Sleep. 2023;26(3):28-30. doi: https://doi.org/10.13175/swjpccs009-23 PDF 

October 2022 Critical Care Case of the Month: A Middle-Aged Couple “Not Acting Right”

Richard A. Robbins, MD

Pulmonary and Critical Care Research and Education Foundation

Gilbert, AZ USA

History of Present Illness

A 62-year-old man and his 61-year-old wife were brought to Emergency Department by family who reported “they’re not acting right”. Both complain of headache, weakness, tiredness, trouble with daily activities and memory difficulties.

PMH, SH, and FH

• They live in a log cabin in a rural area near Payson.
• The man had a history of myocardial infarction and was post-op percutaneous intervention with stenting 3 years ago.
• There was no significant PMH in the woman.
• Both are retired. Neither drank alcohol to excess or smoked.

Meds (man only):

• Enteric-coated aspirin
• Metoprolol
• Atorvostatin

Physical Examination

• Vital signs in both are normal
• Both are oriented X 3 but sluggish and slow to answer.
• Physical examination is otherwise unremarkable in both.

What should be done at this time? (click on the correct answer to be directed to the second of seven pages)

1. CBC, BMP, ABGs
2. CXR
3. EKG
4. 1 and 3
5. All of the above

Cite as: Robbins RA. October 2022 Critical Care Case of the Month: A Middle-Aged Couple “Not Acting Right”. Southwest J Pulm Crit Care Sleep. 2022;25(4):43-46. doi: https://doi.org/10.13175/swjpccs042-22 PDF

Point-of-Care Ultrasound and Right Ventricular Strain: Utility in the Diagnosis of Pulmonary Embolism

Ramzi Ibrahim MD, João Paulo Ferreira MD

Department of Medicine, University of Arizona – Tucson and Banner University Medical Center

Tucson AZ USA

Abstract

Pulmonary emboli are associated with high morbidity and mortality, prompting early diagnostic and therapeutic considerations. Utilization of rapid point-of-care ultrasound (POCUS) to assess for signs of pulmonary emboli can provide valuable information to support immediate treatment. We present a case of suspected pulmonary embolism in the setting of pharmacological prophylaxis for venous thromboembolism with identification of right heart strain on bedside POCUS exam. Early treatment with anticoagulation was initiated considering the clinical presentation and POCUS findings. CT angiogram of the chest revealed bilateral pulmonary emboli, confirming our suspicion. Utilizing POCUS in a case of suspected pulmonary emboli can aid in clinical decision making.

Case Presentation

Our patient is a 50-year-old man with a history of morbid obesity, obstructive sleep apnea, and poorly controlled diabetes mellitus type 2 who was admitted to the hospital for sepsis secondary to left foot cellulitis and found to have left foot osteomyelitis with necrosis of the calcaneus. The patient was started on intravenous antimicrobials, underwent incision and debridement, and completed a partial calcanectomy of the left foot. During the hospital course, he remained on subcutaneous unfractionated heparin at 7,500 units three times a day for prevention of deep vein thrombosis. On post-operative day 12, he developed acute onset of dyspnea requiring 2 liters of supplemental oxygen and was slightly tachycardic in the low 100s. He complained of chest tightness without pain, however, he denied lower extremity discomfort, palpitations, orthopnea, or diaphoresis. Electrocardiogram was remarkable for sinus tachycardia without significant ST changes, T-wave inversions, conduction defects, or QTc prolongation. Rapid point-of-care ultrasound (POCUS) at bedside revealed interventricular septal bowing, hypokinesia of the mid free right ventricular wall, and increased right ventricle to left ventricle size ratio (>1:1 respectively) (Figures 1 and 2).

Figure 1. A: Static apical 4-chamber view showing interventricular bowing into the left ventricle (blue arrow), significantly enlarged right ventricle, and right ventricular free wall hypokinesia (green arrow). B: Video of apical 4-chamber view.

Figure 2. A: Static parasternal short axis view showing interventricular septal bowing in the left ventricle (green arrow). B: Video of parasternal short axis view.

With these findings, the patient was started on therapeutic anticoagulation. CT angiogram of the chest revealed a large burden of bilateral pulmonary emboli (PE). The pulmonary embolism severity index (PESI) score was 130 points which is associated with a 10%-24.5% mortality rate in the following 30 days. Formal echocardiogram showed a severely dilated right ventricle with reduced systolic function, paradoxical septal movement, and a D-shaped left ventricle. Patient remained hemodynamically stable and was discharged home after transition from heparin to rivaroxaban.

Discussion

Pulmonary emboli remain a commonly encountered pathological phenomenon in the hospital setting with a mortality rate ranging from <5% to 50% (1). Venous thromboembolism prophylaxis has been shown to reduce the risk of VTE in hospitalized patients, however, this does not eliminate the risk completely. Prompt diagnosis allows earlier treatment and improved outcomes however this is often challenging given the lack of specificity associated with its characteristic clinical symptoms (2). In the proper context, utilization of POCUS can aid the diagnosis of PE by assessing for signs of right ventricular strain. Characteristic findings seen on a cardiac-focused POCUS that represent right ventricular strain include McConnell’s sign (defined as right ventricular free wall akinesis/hypokinesis with sparing of the apex), septal flattening, right ventricular enlargement, tricuspid regurgitation, and tricuspid annular plane systolic excursion under 1.6 cm (3). Their respective sensitivities and specificities are highly dependent on the pre-test probability. For example, a prospective cohort study completed by Daley et al. (4) in 2019 showed that for patients with a clinical suspicion of PE, sensitivity of right ventricular strain was 100% for a PE in patients with a heart rate (HR) >110 beats per minute, and a sensitivity of 92% if HR >100 BPM. This study provides evidence to support the use of cardiac focused POCUS in ruling out pulmonary emboli in patients with signs of right ventricular strain and abnormal hemodynamic parameters such as tachycardia. Additionally, in settings where hemodynamic instability is present and the patient cannot be taken to the CT scanner for fear of decompensation, rapid POCUS assessment can be helpful. In our patient, given the acute need for supplemental oxygenation and dyspnea, along with his risk factors for a thromboembolic event, the use of POCUS aided in our clinical decision making. The yield of information that can be provided by POCUS is vital for early diagnostic and therapeutic decision making for patients with a clinical suspicion of pulmonary emboli.

References

1. Torbicki A, Perrier A, Konstantinides S, et al. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J. 2008 Sep;29(18):2276-315. [CrossRef][PubMed]
2. Roy PM, Meyer G, Vielle B, et al. Appropriateness of diagnostic management and outcomes of suspected pulmonary embolism. Ann Intern Med. 2006 Feb 7;144(3):157-64. [CrossRef][PubMed]
3. Alerhand S, Sundaram T, Gottlieb M. What are the echocardiographic findings of acute right ventricular strain that suggest pulmonary embolism? Anaesth Crit Care Pain Med. 2021 Apr;40(2):100852. [CrossRef] [PubMed]
4. Daley JI, Dwyer KH, Grunwald Z, et al. Increased Sensitivity of Focused Cardiac Ultrasound for Pulmonary Embolism in Emergency Department Patients With Abnormal Vital Signs. Acad Emerg Med. 2019 Nov;26(11):1211-1220. [CrossRef][PubMed]

Cite as: Ibrahim R, Ferreira JP. Point-of-Care Ultrasound and Right Ventricular Strain: Utility in the Diagnosis of Pulmonary Embolism. Southwest J Pulm Crit Care Sleep. 2022;25(2):34-36. doi: https://doi.org/10.13175/swjpccs040-22 PDF

Point of Care Ultrasound Utility in the Setting of Chest Pain: A Case of Takotsubo Cardiomyopathy

Ramzi Ibrahim MD, Chelsea Takamatsu MD, João Paulo Ferreira MD

Department of Medicine, University of Arizona - Tucson and Banner University MedicalCenter, Tucson

Tucson, AZ USA

Abstract 

Chest pain is a frequently encountered chief complaint in the Emergency Department and entails a broad differential. Point-of-care ultrasound (POCUS) can be utilized to guide diagnostic decision making and initial triaging. Takotsubo cardiomyopathy presents similarly to acute coronary syndrome and has characteristic findings on echocardiogram. This case presentation details a scenario of ST segment elevation on electrocardiogram and elevated high sensitivity troponin levels, worrisome for a ST elevation myocardial infarction (STEMI). Apical hypokinesis to akinesis and apical ballooning were appreciated on echocardiogram, raising suspicion for Takotsubo cardiomyopathy, subsequently confirmed by coronary angiogram. A cardiac focused point-of-care ultrasound assessment can provide valuable information to aid in diagnostic accuracy. 

Case Presentation 

A 72-year-old woman with a known history of chronic obstructive pulmonary disease (COPD) presented to the hospital for progressively worsening dyspnea in the previous few days along with new onset chest discomfort in the past one day. Patient was found to have an oxygen saturation of 87% on room air, pH of 7.25 and a pCO2 of 98 on venous blood gas, and was admitted for acute on chronic hypoxic and hypercapnic respiratory failure in the setting of a COPD exacerbation. Patient was intubated for respiratory distress and worsening acuteencephalopathy. Chest radiograph was grossly unremarkable for consolidations or

opacities. A bedside point-of-care ultrasound (POCUS) assessment revealed clear lung zones bilaterally without apparent B lines; however, minimal pleural sliding was appreciated on the left anterior lung zones. Cardiac focused assessment identified marked hypokinesis to akinesis of the entire mid-distal left ventricle with apical ballooning, raising the suspicion of Takotsubo cardiomyopathy (Videos 1-2).

 

Video 1. Subcostal view with identification of a hyperkinetic basal segment and hypokinetic apex. Apical ballooning is also clearly identifiable in this view. (Click here to view the video in a separate window)

Video 2. Parasternal short axis identifying a hyperkinetic basal segment near the level of the mitral valve with subsequent hypokinetic apical view. The image plane is being panned from base to apex and back. (Click here to view the video in a separate window).

High sensitivity troponin level was elevated at 42 ng/L with an increase to 540 ng/L on repeat testing. Electrocardiogram (ECG) was initially grossly unremarkable for signs of acute ischemic changes, however, repeat ECG revealed ST elevation in the anterior leads. The patient was taken urgently to the catheterization lab where intervention identified mild non-obstructive disease in a right dominant circulation and the diagnosis of Takotsubo cardiomyopathy was confirmed. 

Discussion 

Chest pain is among the most common chief complaints of patients presenting to the Emergency Department. The differential diagnoses of chest pain remain broad which includes a variety of pathological processes. POCUS has emerged as an indispensable tool for diagnostic accuracy and for aid with initial triaging before considering further confirmatory testing. An emerging consideration is its utility in the acute setting, specifically when trying to differentiate between cardiac and non-cardiac chest pain. Comprehensive echocardiography, usually completed in a formal setting upon request, provides valuable information that can be indicative of ischemic states, including regional wall motion abnormalities, decreased systolic movement, decreased myocardial thickening, valvular function abnormalities, inter-ventricular shunts, and acute papillary muscle dysfunction (1). Alternatively, bedside POCUS in acute settings for assessment of cardiac function and structural abnormalities provides timely objective data but holds greater limitations mainly due to inferior ultrasound quality, variable operator skillsets, and time constraints. of

In our case, we utilized POCUS in an unresponsive, intubated patient, noting discrete regions of hypokinesis-akinesis the left ventricle with apical ballooning, prior to ECG showing elevated ST segments in the anterior leads and a rising troponin level on serial lab tests. Our initial impression based on the POCUS findings was concerning for Takotsubo cardiomyopathy. Given the urgency of the troponin and ECG abnormalities, a Code STEMI was called. Cardiology urgently took the patient to the catheterization lab which confirmed the diagnosis of Takotsubo cardiomyopathy after identifying no obstructive coronary artery disease.

Takotsubo cardiomyopathy often presents very similarly to acute coronary syndrome with elevated markers of myocardial ischemia and ST changes on ECG (2). Hallmarks of this clinical entity include apical hypokinesia and basal segment hyperkinesia on echocardiogram and no obstructive coronary artery disease on coronary angiography. Given the acuity of these findings, this case presentation portrays the importance of utilizing a cardiac focused POCUS assessment to help tailor differential diagnoses and raise index of suspicion not only to acute coronary syndromes, but also to mimicking clinical diseases. 

References

1. Leischik R, Dworrak B, Sanchis-Gomar F, Lucia A, Buck T, Erbel R. Echocardiographic assessment of myocardial ischemia. Ann Transl Med. 2016 Jul;4(13):259. [CrossRef] [PubMed]
2. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J. 2008 Mar;155(3):408-17. [CrossRef] [PubMed]

Cite as: Ibrahim R, Takamatsu C, Ferreira JP. Point of Care Ultrasound Utility in the Setting of Chest Pain: A Case of Takotsubo Cardiomyopathy. Southwest J Pulm Crit Care Sleep. 2022;25(2):30-33. doi: https://doi.org/10.13175/swjpccs035-22 PDF  

October 2021 Critical Care Case of the Month: Unexpected Post-Operative Shock

Sharanyah Srinivasan MBBS

Sooraj Kumar MBBS

Benjamin Jarrett MD

Janet Campion MD

University of Arizona College of Medicine, Department of Internal Medicine and Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Tucson, AZ USA

History of Present Illness 

A 55-year-old man with a past medical history significant for endocarditis secondary to intravenous drug use, osteomyelitis of the right lower extremity was admitted for ankle debridement. Pre-operative assessment revealed no acute illness complaints and no significant findings on physical examination except for the ongoing right lower extremity wound. He did well during the approximate one-hour “incision and drainage of the right lower extremity wound”, but became severely hypotensive just after the removal of the tourniquet placed on his right lower extremity. Soon thereafter he experienced pulseless electrical activity (PEA) cardiac arrest and was intubated with return of spontaneous circulation being achieved rapidly after the addition of vasopressors. He remained intubated and on pressors when transferred to the intensive care unit for further management.

PMH, PSH, SH, and FH

• S/P Right lower extremity incision and drainage for suspected osteomyelitis as above
• Distant history of endocarditis related to IVDA
• Not taking any prescription medications
• Current smoker, occasional alcohol use
• Former IVDA
• No pertinent family history including heart disease

Physical Exam

• Vitals: 100/60, 86, 16, afebrile, 100% on ACVC 420, 15, 5, 100% FiO2
• Sedated well appearing male, intubated on fentanyl and norepinephrine
• Pupils reactive, nonicteric, no oral lesions or elevated JVP
• CTA, normal chest rise, not overbreathing the ventilator
• Heart: Regular, normal rate, no murmur or rubs
• Abdomen: Soft, nondistended, bowel sounds present
• No left lower extremity edema, right calf dressed with wound vac draining serosanguious fluid, feet warm with palpable pedal pulses
• No cranial nerve abnormality, normal muscle bulk and tone

Clinically, the patient is presenting with post-operative shock with PEA cardiac arrest and has now been resuscitated with 2 liters emergent infusion and norepinephrine at 70 mcg/minute.

What type of shock is most likely with this clinical presentation?

1. Cardiogenic shock
2. Hemorrhagic shock
3. Hypovolemic shock
4. Obstructive shock
5. Septic / distributive shock

Cite as: Srinivasan S, Kumar S, Jarrett B, Campion J. October 2021 Critical Care Case of the Month: Unexpected Post-Operative Shock. Southwest J Pulm Crit Care. 2021;23(4):93-7. doi: https://doi.org/10.13175/swjpcc041-21 PDF 

Acute Type A Aortic Dissection in a Young Weightlifter: A Case Study with an In-Depth Literature Review

Stella C. Pak, MD¹

Edinen Asuka, MD²

¹Department of Medicine,

Orange Regional Medical Center

Middletown, NY USA

²All Saints University School of Medicine

Dominica

Abstract

In spite of the continuing efforts of researchers and practitioners, the mortality rate for acute type A aortic dissection remains relatively high at about 20-50%. Conventional risk factors associated with acute type A aortic dissection include a family history or prior history of aortic disease, connective tissue disease, smoking, alcohol use, substance abuse, diabetes mellitus type II, and age of 40 or greater. With the growing awareness for fitness in our society, vigorous exercise is emerging as a novel risk factor for acute type A Aortic dissection. Herein, we present a non-trauma related acute type A aortic dissection secondary to weight-lifting in a young man. We also reviewed several articles in order to provide a comprehensive literature overview for readers, clinicians and future researchers.

Case Report

A 45-year-old man who was otherwise healthy presented to the Emergency Department after having a “popping” sensation in his chest while weight-lifting with an 80-lbs (36.3 kg) dumbbell at a gym. He is an avid weight-lifter. This chest discomfort was immediately followed by a sensation of electric shock from his chest down to his legs and a transient loss of bilateral vision. He then developed an acute episode of lightheadedness, diaphoresis, throbbing headache, and a heavy-pressure in his neck, chest, and back. He denied any recent trauma or injury. He denied the use of tobacco, recreational drugs, or anabolic steroid. He denied the history of connective tissue diseases or cardiovascular diseases.

He was hypotensive with blood pressure of 99/45 mmHg. However other vital signs were within the normal limit: a temperature of 98.2 °F, a heart rate of 74/min, and a respiration rate of 15/min, an oxygen saturation of 97% at room air. His physical examination was remarkable for diminished pulses on his right upper and lower extremities. He did not have any marfanoid traits, such as tall stature, elongated face, or dolichostenomelia. His height and weight measured at the time of admission were 181cm and 95.7kg respectively (BMI 29.2).

His white blood count was elevated at 12.1 x 10⁹/L, but his hemoglobin remained stable at 15.6 g/dL. His troponin I was 0.26. He was found to have acute renal injury with BUN of 26 and creatinine of 1.7. His ECG, Chest X-ray, and CT of head and neck were unremarkable. He subsequently underwent a diagnostic cardiac catheterization, which revealed a swirling pattern and delayed washout of the contrast, findings suggestive of a false lumen. CT angiography displayed type A aortic dissection from the aortic root all the way down to the abdomen (Figure 1).

Figure 1.  CT angiography demonstrating ascending aortic dissection (arrow). The area with the arrow is the ascending portion of the aorta.

TEE visualized a rupture in the left coronary cusp at the aortic valve was visualized with the ejection fraction of 40% to 45%. Histopathological examination of the aortic wall and the aortic valve cusps revealed myxoid degeneration. There was no evidence of cystic medial necrosis.

He underwent an emergent repair of aorta with aortic root replacement, using a Dacron aortic graft and a mechanical aortic valve (25-On-X). Heparin bridging was initiated once his post surgically bleeding risk was low. Warfarin was later started with therapeutic INR goal of 2.0 to 3.0. On postoperative day 10, he was discharged on Aspirin 81 mg, warfarin and metoprolol 50 mg daily. 

At 1 month post-discharge follow-up, his distal pulse was strong and equal in all four extremities. He was asymptomatic with no complaints of chest pain, dyspnea, headache, or lightheadedness.

Literature Review

Aortic dissection occurs when the tunica intima of the aorta develops a tear that extends into the inner two-third layer of its tunica media which consists of collagen, smooth muscle and elastic fibers. The above pathological changes lead to the formation of a true lumen and a false lumen separated by an intimal flab (1-14). This causes blood to escape into the false lumen and incite a cascade of events. The external elastic lamina separates the tunica media from the adventitial layer, which serves as an external scaffolding. The tunica adventitia consists of fibroblast cells, collagen and elastic fibers. On the other hand, the tunica intima is made of endothelial cells on basement membrane; separated from the tunica media by the internal elastic lamina (2-14). As blood enters the false lumen, retrograde or anterograde propagation of blood occurs due to pressure changes. If a retrograde propagation takes place within the false lumen, it can extend into the aortic root through the sinotubular junction, eventually causing damage to the aortic root and its content or escape into the pericardial space; consequently leading to aortic insufficiency, acute coronary syndrome or cardiac tamponade (10-34). The contents of the aortic root in question include sinuses of Valsalva where the coronary sinuses and the orifices of the coronary arteries are located, or other structures such as aortic annulus, commissures, leaflets (cusps) and ventriculo-aortic junction. In the case of an anterograde propagation, the blood collection within the false lumen can extend distally from the site of initial tear to the branches of the aorta such as brachiocephalic trunk (innominate artery), left subclavian artery, renal arteries and mesenteric arteries thereby leading to stroke, limb ischemia, renal insufficiency and bowel ischemia. Involvement of the brachiocephalic trunk or the left subclavian artery can also cause pseudohypotension (35-41). In some cases, distal extension can reach the site of aortic bifurcation and recanalize into the intravascular compartment; thereby, creating a double barrel aorta. This in effect, reduces the risk of aortic rupture (10,34-44). In a clinical scenario where there is no preceding intimal tear, the most likely causes are always connective tissue diseases such as Marfan syndrome (FBN1 gene mutation), Ehlers-Danlos syndrome (vascular type-COL3A1 gene mutation), familial thoracic aortic aneurysm and dissection (TGFBR1 and TGFBR2, FBN1, MYH11, and ACTA 2 genetic mutations), and Leoys-Dietz aneurysm syndrome (TGFBR1 or TFGBR2 gene mutations) (12,14,34-44). In such cases, there is an initial formation of intramural hematoma, which may occur secondary to rupture of the aortic vasa vasorum. Disruption of the vaso vasorum can also occur due inflammatory response generated from vasculitides or infectious causes like syphilis.

Aortic dissection is relatively rare when compared to other cardiovascular diseases such as ruptured aortic aneurysm, acute coronary syndrome and abdominal aortic aneurysm. The true incidence of aortic dissection is hard to determine because most case approximations are made from autopsy reports (34,39,40-45). Although, the estimated incidence is 5 to 30 cases per million people yearly. Aortic dissections are known to occur more in males compared to females with men constituting about 65% of cases. Peak age of onset is between 50-65 years. In a population-based study of all Olmsted County, Minnesota, residents with aortic dissection between 1995 to 2015, it was noted that age- and sex-adjusted incidence of aortic dissection for men was 10.2 per 100,000 person-years versus 5.7 per 100,000 person-years for women (1,11-14,46). Aortic dissection is commonly classified based on time of presentation and structural variations. With regards to time of presentation, it can be acute (less than 2 weeks) or chronic (greater than 2 weeks) (1,46). Chronic aortic dissections tend to have better prognosis.

There are two main anatomic classifications, DeBakey (Figure 2) and Stanford (Figure 3). Most aortic dissections originate mainly from the ascending aorta with the rest emanating from the aortic arch and the descending aorta (1,46).

The DeBakey classification is divided into three main types:

• Type I- emerges from the ascending aorta, extends to the aortic arch and often involving the distal segment of the aorta. Most common in the younger population (less than 40 years). It is also the most serious form of aortic dissection.
• Type II- Emerges from the ascending aorta and is restricted to this section of the aorta.
• Type III- Emerges from the descending aorta extending distally above the diaphragm (Type IIIa) or beyond the diaphragm into the abdominal aorta (Type IIIb) (34,46).

Figure 2. Illustrations of DeBakey classification (Type I, II, and III). T Paul Tran and Ali Khoynezhad. Dove Medical Press Limited. 2009. Available at: https://www.dovepress.com/articles.php?article_id=2444 (accessed 8/7/20).

The Stanford classification is broken down into:

• Type A- Involvement of the ascending aorta irrespective of the origin of intimal tear. A composite of DeBakey Type I and II.
• Type B- Involvement of the descending aorta (distal to the origin of the left subclavian artery) and its distal component. An analogy of type III DeBakey (1,34,46).

Figure 3. Stanford classification of aortic dissection (Type A and B). T Paul Tran and Ali Khoynezhad. Dove Medical Press Limited. 2009. Available at: https://www.dovepress.com/articles.php?article_id=2444 (accessed 8/7/20).

Etiology. There are several risk factors for aortic dissection. The main predisposing risk factors most commonly reported include:

• Hypertension (Associated with about 70%-80% of cases).
• Connective tissue diseases and genetic disorders such as Marfan syndrome, Ehlers-Danlos syndrome, Familial thoracic aortic aneurysm and dissection, Leoys-Dietz aneurysm syndrome, Turner syndrome, and bicuspid aortic valve (5% likelihood of aortic dissection).
• Age greater than 40 years (75% of cases occur in patients between 40-70 years)
• Use of illicit substances such as cocaine, and ecstasy.
• Pre-existing aortic aneurysm
• Previous history of aortic dissection
• Family history of aortic dissection
• Pregnancy
• Vasculitides and autoimmune diseases such as Giant cell arteritis, Takayasu’s arteritis, polyarteritis nodosa, and Behcet’s disease.
• Iatrogenic causes such as cardiac catheterization, aortic valve replacement, coronary artery bypass graft and intra-aortic balloon pump.
• Tertiary syphilis
• Use of anabolic steroids
• Penetrating atherosclerotic ulcer secondary to infiltration of the tunica media by an atherosclerotic plaque. Meaning, risk factors for atherosclerosis such as smoking, hypercholesterolemia, and diabetes are implicated in aortic dissection.
• Penetrating chest trauma
• Chronic alcohol use
• Weight-lifting is a novel risk factor for aortic dissection even in individuals without connective tissue diseases or cardiovascular risk factors. The existence of other risk factors only makes it more likely to occur (17-20, 40-46).

Signs and Symptoms: The diagnosis of aortic dissection is greatly missed by most physicians in the emergency department upon presentation. Delay in treatment can lead to an increase in mortality to about 50% within the first 48 hours. It is highly crucial the diagnosis is made quickly and treatment is initiated promptly to decrease the risk of mortality (1,41-46). With respect to clinical presentation, patients present with following symptoms:

• Severe tearing chest pain of sudden onset. Pain may be located in the anterior chest wall, interscapular region and in the abdomen. Anterior chest wall pain is often due to involvement of the ascending aorta while interscapular back pain and abdominal pain are associated with involvement of the distal segments of the aorta due to anterograde extension of the false lumen. Note that about 10% of patients present with painless aortic dissection; which is more common in patients with connective tissue diseases such as Marfan syndrome. Some patients present with pleuritic chest pain secondary to pericardial involvement.  Overall, chest pain is the most common symptom; occurring in about 80-96% of patients, with anterior chest pain being the most reported. About 71.4% of painless aortic dissection present with a normal ECG reading. Coronary malperfusion may result in cardiac arrest (1,14,26-46).
• Sweating, nausea and vomiting (may occur due to autonomic changes)
• Headache
• Lightheadedness
• Back pain
• Abdominal pain
• Neck or jaw pain (aortic arch involvement)
• Neurologic deficits (hemiparesis, hemiplegia hemianesthesis and loss of vision) and syncope as a result of hypovolemia, arrhythmia, acute coronary syndrome, increase vagal tone or involvement of the innominate artery and its branches (such as the internal carotid artery) (1,40-46).
• Horner syndrome (Ptosis, miosis and anhidrosis) secondary to obstruction of sympathetic outflow tract.
• Hoarseness due to vagus nerve compression.
• Exertional leg and gluteal pain may occur if the iliac artery is involved.
• Paresthesia, and extremity pain may occur due to limb ischemia.
• Dyspnea
• Dysphagia
• Hemoptysis
• Anxiety and palpitations

Common signs observed in patients with aortic dissection include:

• Differential blood pressure measurements in the upper extremities
• High blood pressure (More common in Type B aortic dissection)
• Hypotension (More common in Type A aortic dissection)
• Wide pulse pressure measurement (signifying aortic valve involvement)
• Diastolic murmur (secondary to aortic insufficiency)
• Muffled heart sounds
• Weak peripheral pulses
• ECG changes indicating acute coronary syndrome
• Decreased breath sounds, dullness to percussion if pleural effusion is present. Pleural effusion may be as result of inflammatory response, aneurysm leakage or eventual rupture of the dissected aorta. 
• Horner syndrome
• Changes in mental status

Patients may experience a wide range of complications if they are not managed early. Some of which include stroke, paraplegia, life threatening arrhythmia with cardiac arrest, paraplegia, limb amputation, multiple organ failure, severe cardiac tamponade, renal failure, bowel ischemia, myocardial infarction, aortic regurgitation, superior vena cava syndrome and even death (1,22,14,46).  

Diagnostic modalities and findings.

• ECG and cardiac enzyme (troponin) level must be checked to exclude myocardial involvement. ECG findings are usually non-specific with nearly 1-2% showing ST-elevation (1,39,41-46).
• Baseline blood work such as CBC, electrolytes, Blood urea nitrogen (BUN), and creatinine level must be established. D-dimer may be used it low risk patients to exclude diagnosis. Although, due to lack of evidence to validate its use, it is not strongly recommended (40,46).
• Chest x-ray- findings on may include widened mediastinum (present in greater than 80%), calcium sign, apical cap (left); loss of paratracheal stripe; involution of mainstem bronchus; pleural effusion, tracheal and esophageal deviation. Normal x-ray findings occur in about 20% cases (1,41,46).
• Computed Tomography (CT)-chest and abdomen with iodinated contrast- fast, noninvasive and available in most emergency departments. It is used to detect the region of tear and aids surgical planning. Not recommended for patients with contrast allergy, older patients (greater than 65 years), poor renal function and history of renal insufficiency.
• Transesophageal echocardiography (TEE): It is relatively available, noninvasive and best for ascending aortic dissections to detect changes or damages structures within the aortic root. It can be done at bedside and does not require contrast media. Although, it is operator dependent and discouraged in patients with esophageal varices, masses or strictures (14,39,46).
• Magnetic resonance Imaging (MRI): It is used for detection of site of tear, assessment of dissection and involvement of branches of aorta, ascertain the presence and degree of aortic insufficiency. Iodinated contrast is not needed. It also aids surgical planning but it is time consuming, expensive, not readily available in some hospitals and not advisable for use in patients with metallic implants such as pacemakers and implantable cardioverter defibrillator.
• Doppler ultrasound: This can be useful in patients presenting with signs of limb hypoperfusion to assess for diminished blood flow on the extremities involved (22,46).

Management: Aortic dissection can be managed surgically or conservatively with medications. Type A aortic dissections often require surgical management while type B aortic dissection can be managed conservatively with medications. Medical management is necessary at presentation to help stabilize patient’s vitals. The mean arterial blood pressure goal is often between 60 to 75mm Hg (1,14,23,46). Medical management is started by administration of intravenous short and fast acting beta-blockers (esmolol, propanolol and labetalol) and morphine for pain management (14,23,46). Sodium nitroprusside is then given to the patient to enhance vasodilation and ensure adequate visceral perfusion. Patients with contraindications to beta-clockers (2^nd or 3^rd degree heart block, decompensated heart failure, severe asthma, and sinus bradycardia) should be given non-dihydropyridine calcium channel blockers (verapamil and diltiazem) as an alternative (1,14,46).

Surgical approach to management:

• Open heart (aortic) surgery-Mainly used in the absence of aortic valve defect (12,46).
• Minimally invasive endovascular aortic repair- it can be done with endovascular composite consisting of a Dacron stent graft and a transcatheter aortic valve (if aortic valve is compromised) (2,42,45,46).
• Valve sparing aortic root replacement (David procedure) (10,12,14,46).
• Bentall procedure (10,12,41,44,46).
• Sutureless vascular-ring connector with Dacron graft aortic repair.  
• Hybrid technique- a combination of stent graft and visceral bypass grafting (10,14,46).

Aortic fenestration has been reported to be used as an interim measure to prevent organ ischemia in cases of organ involvement (22,46). Aortoiliac bypass can also be used when circulation through the iliac vessels are severely compromised to avoid limb ischemia. A case report by John S. Schor, Michael D. Horowitz, et al. (29) detailed a case about a patient with type III aortic dissection (anterograde propagation) and iliac involvement complicated by a clot at the site of aortic bifurcation; which was treated with aortic fenestration and aortoiliac bypass using a knitted Dacron graft. In this case, nonthoracic approach was employed to salvage the limbs and prevent further damage (22,46). When employing surgical management, it is important to evaluate patient’s eligibility for surgery by checking for comorbid conditions and contraindications such as renal insufficiency, advanced age, ischemic cardiomyopathy, diabetes, shock, existing cardiac tamponade and bleeding diathesis.

Prognosis: Approximately 30-40% of patients with acute aortic dissection die after reaching the emergency room. The mortality rate for type A dissections treated medically is estimated to be about 20% within the first 24 hours and 50% at 30 days after initial onset (11,14,46). If surgically managed, Type A dissections incur a mortality rate of 10% after 24 hours and close to 20% at 30 days after repair. On the other hand, for Type B dissections, the 30-day mortality can be as high as 10% for uncomplicated cases. Mortality rate is 1-2% per hour for the first day in patients who do not qualify for surgery. The presence of comorbidities and complications further increases the risk of mortality (1,10,16,18,46).

Follow-up: After the initial management, patients should undergo cardiac rehabilitation, lifestyle modification (smoking cessation, weight loss and avoidance of illicit drugs) and physical therapy if movement is limited (6,46). All patients should be educated on the need for adequate blood pressure control and medication compliance. Serial imaging is recommended with CT scan or MRI at 3-6 months interval to monitor disease progression and check for the emergence of new aneurysms or recurrent dissections (14,34,46). For patients requiring valve replacement with bioprosthetic valve, antiplatelet such as aspirin should be prescribed to prevent clot formation (7,8,46). Although, anticoagulation with warfarin should be added for patients with risk factors such as atrial fibrillation, hypercoagulable state, severe left ventricular systolic dysfunction, history of thromboembolic events; and in patients with subclinical valve thrombosis and no underlying risk factors. Patients with mechanical aortic valve require both aspirin and anticoagulation with warfarin irrespective of their risk stratification (1,22,34,46). For patients requiring anticoagulation with warfarin, early bridging with intravenous unfractionated heparin or subcutaneous heparin should be initiated and target INR should be maintained at 2.0 to 3.0 for 3-6 months or indefinitely depending on the case and type of valve used. For patients with mechanical aortic valve and underlying risks for valve thrombosis, therapeutic INR can be extended to 2.5 to 3.5 (37,38,46). If any contraindication for warfarin exist, aspirin dosage can be increased. Direct oral anticoagulants (dabigatran, rivaroxaban, apixaban, and edoxaban) should be avoided in mechanical valves (37,46).

Discussion

Exercise is known to be one of the most effective means of controlling blood pressure. Although all sports have both dynamic and static components, sports requiring a high static demand, such as weight lifting are thought to be associated with a risk of triggering acute aortic dissection (20,46). It is normal for blood pressure to rise to about 200/110 mm Hg during exercise but once it surpasses that level, there is risk of negative cardiovascular outcome (22,30,40,46). Sudden change in blood pressure during weight lifting can predispose the patient to aortic dissection. They have been several cases of aortic dissection reported in weightlifters and individuals who engaged in strenuous exercises prior to their dissection event (17,19,21,22,35,46).  It is crucial to note that all types of aortic dissection have been reported to occur in these patients; and that includes type A, and type B aortic dissections (22,46). On the contrary, blood pressure is known to reduce following a short exercise session and more so in physically active individuals that are not premeditated with antihypertensive.(34,45,46) A systematic review and meta-analysis done by Elizabeth Carpio-Rivera, José Moncada-Jiménez, et al. (3) on an heterogeneous sample population, showed that there was a significant reduction in blood pressure irrespective of the participant's initial blood pressure level, gender, physical activity level, antihypertensive drug intake, type of blood pressure measurement, time of day in which the blood pressure was measured, type of exercise performed, and exercise training program with a p value of less than 0.05 for all parameters.

In this particular case report, the patient is an avid weightlifter who developed a type A aortic dissection while weightlifting at the gym. His initial presentation was a popping sensation in the chest, which later evolved into a neurologic sequence of transient bilateral visual loss, paresthesia and other symptoms such as headache, lightheadedness, diaphoresis, pressure-like sensation in his neck, chest and back. He reported no underlying cardiovascular risk factors, use of tobacco, recreational drugs or anabolic steroid use and denies any family history of connective tissue or genetic diseases. There was no report of any recent trauma or injury to the chest wall. Upon evaluation of his vitals, he was hypotensive with diminished pulse on his right upper and lower extremities and no marfanoid features were noted. Lab values were indicative of leukocytosis with acute renal injury secondary to inflammatory response and hypotension respectively. CT angiography of the chest and abdomen showed type A aortic dissection with anterograde propagation of the false lumen to the abdominal aorta. This finding was also supported by cardiac catheterization findings of swirling pattern and with delayed contrast washout. No radiologic chest x-ray findings were noted; head and neck CT scan result came back unremarkable with no ischemic changes seen in the brain. It is crucial to note that a negative chest x-ray does not necessarily exclude aortic dissection as shown in this case. TEE revealed rupture of the left coronary cusp with an ejection fraction of 40% to 45%. Histopathological findings showed no cystic medial necrosis but myxoid degeneration was noted on the aortic wall and cusps. Subsequently, the aortic valve was replaced with a mechanical aortic valve, with a Dacron graft used to replace the aortic root. Post-operatively, the patient was discharged on day 10 with antiplatelet and antihypertensive medications with complete recovery noted at one month follow up. This patient displayed a classic presentation of type A aortic dissection and due to prompt management complications such as aortic rupture, multiple organ failure, cardiac ischemia and renal failure were avoided. This is a clear evidence of type A aortic dissection in a young weightlifter with no underlying traditional risk factors.

Hatzaras I, Tranquilli M, et al. (18) state that “as an initial rule of thumb, it appears that lifting up to one half the individual's body weight is relatively safe, not exceeding a blood pressure of 200 mm Hg, even during the effort cycle of the lifting exercise.” This connotes that weight lifting is safe as long as the patient is educated not to cause too much cardiovascular stress. In Selena Pasadyn, et al. (45) 295 patients were given an online survey to elaborate more about their experience with type A aortic dissection. The eventual response rate on athletic component was 48% (141). Out of 132 patients, 18% stated their doctor did not talk to them about post recovery exercise regimen while 31% (40/129) stated their physicians were uncertain about the types of exercises they should or should not engage in (24). Out of 123 patients, 99 (81%) patients stated they wanted specific recommendations about what exercise regimens were safe. Due to paucity of data on specific exercise recommendations post-event (after an aortic dissection); it is clear that physicians find it difficult to educate their patients on the type and degree of exercise regimens their patients should participate in during their recovery phase. This ambiguity has caused increased isolation among patients post-event; substantial decrease in physical activity and has negatively affected the quality of life. This can also lead to recurrence of dissection if the patient exceeds the required exercise level after prior dissection event. Conversely, preceding the dissection event, out of 80 patients who exercised, 33 (41%) participated in strength work, such as weightlifting or resistance training, and 28.9% (22/76) did engage post-event. 35% (47/136) of patients also reported lifting heavy objects on a regular basis before their dissection, and 9.2% (11/119) did after their dissection. After a successful surgery, only one patient returned to competitive athletics (cycling). This shows that an association exists between strenuous activities such as weightlifting and aortic dissection. Engagement in physical exercise was reduced after dissection as noted.  For post-dissection patients, it may be beneficial to take a cautious approach and limit activities that require extreme or maximal exertion extensive sprinting or running, snow shoveling, and mowing the lawn with a non–self-propelled mower. Systolic blood pressure while running at 8 mph may increase by 108 to 162 mm Hg above resting levels but by 26 to 40 mm Hg during brisk walking at 3 mph. Squeezing a hand grip maximally for about 1 minute has shown to increase systolic blood pressure by 50mm Hg and diastolic by 30mm Hg.(6,34,46) With regards to weightlifting, it is important for the post-aortic dissection patients to use a low amount of weight and to stop several repetitions before exhaustion. They should minimize lifting heavy objects, with heavy being defined as objects that require a lot of effort and straining (such as a Valsalva maneuver) to lift (4,6,9,27-28,46). Research by De Souza Nery S, Gomides RS, et al. (46) has shown that blood pressure increased to about 230/165 mm Hg (from 130/80 mm Hg resting blood pressure) when a biceps curl was carried out with heavy weights for the maximum amount of repetitions possible.

Conclusion

Weight-lifting has been demonstrated to improve cardiorespiratory endurance and muscular strength. However, weight-lifting with more than half of the individual’s body weight may be associated with a risk of triggering aortic complications such as aortic dissection. With the growing number of individuals taking up weight training in this era, patient education to minimize cardiovascular stress should be paramount. Although, aortic dissection is less common in the younger population, Physicians need to prioritize it as one of the differentials in young weightlifters without underlying risk factors due to its high mortality. Patients with or without history of connective tissue or genetic disorders and with moderate to high risk for acute aortic dissection may need pre-assessment with an imaging modality such as echocardiography before they start weightlifting or participating in high intensity sports. And individuals with confirmed aortic root dilation should be strongly advised to refrain from strenuous exercises such as weightlifting. These patients may also benefit from blood pressure and heart rate monitoring during their exercise sessions. Exercise recommendations should be made by putting into consideration patient’s age, body mass index, underlying comorbidities and existing risk factors. The duration of exercise should also be modest to avoid unnecessary prolonged cardiovascular stress. For post-event patients (after dissection), it is important that these patients are educated on the type and level of exercise to engage in, and blood pressure should be maintained to avoid recurrence of aortic dissection or even rupture. Regardless of patient’s current health status, it is advisable not to exceed a blood pressure of 200mm/110Hg during peak exercise. Current guidelines and recommendations suggest that patients with prior history of aortic dissection should lift very low weights (less than 50 lbs.) and at submaximal levels; avoid exercise maneuvers that elicit excessive straining (Valsalva) and stop weightlifts several repetitions before fatigue. In addition, recent exercise guideline for the general population stipulates that engaging in aerobic exercise at moderate intensity (such as slow jogging, cycling at a mild pace, walking) at least 30 minutes most days of the week for about 150 minutes per week tend to yield good  cardiovascular outcomes with minimal risk for aortic dissection and other cardiovascular complications. Most maximum heart rate prediction equations have shown to overestimate the actual value and some have shown variations with respect to age, gender, physical status and body mass index of participants. Although, the recommended target heart rate regardless of age is 50% to 85% of maximum heart rate; for patients with Marfan syndrome, it is much safer to follow the Marfan foundation physical activity recommendations such as maintaining heart rate at less than 100 bpm for patients not on beta-blockers, and less than 110 bpm for patients on beta-blockers (at moderate intensity).These patients are also encouraged to avoid high intensity exercises such as weightlifting, steep climbing, and activities requiring rapid pressure changes like scuba diving.

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Cite as: Pak SC, Asuka E. Acute type A aortic dissection in a young weightlifter: a case study with an in-depth literature review. Southwest J Pulm Crit Care. 2020;21(2):39-53. doi: https://doi.org/10.13175/swjpcc025-20 PDF 

July 2020 Critical Care Case of the Month: Not the Pearl You Were Looking For...

Yuet-Ming Chan MD¹

David C. Miller MD²

Farshad Shirazi MD³

Janet Campion MD²

¹Department of Medicine, ²Pulmonary, Allergy, Critical Care and Sleep Medicine and ³Arizona Poison and Drug Information Center

University of Arizona School of Medicine

Tucson, AZ USA

History of Present Illness

A 75-year-old man presented with unsteady gait, difficulty concentrating and abdominal pain with loose stools. One day prior to admission, he experienced waxing and waning nausea, cramping abdominal pain, one episode of emesis and loose stools. He described acute gait disorder related to difficulty with balance. Due to concern for dehydration, he drank 10-12 cans of carbonated water without further emesis. He also experienced vague and alternating sensations of feeling “hot” in half of his body and “cold” in the other half of his body. Forty-eight hours prior to presentation, he had just returned from a five-day trip to New Orleans.

PMH, SH, and FH

The patient has hypertension and hyperlipidemia that is well-controlled. Regular medicines include losartan, diltiazem, HCTZ and simvastatin. He is a professor of medicine. He had distant tobacco use with a 10 pk-yr history. He denies recreational drug use. He endorsed drinking one glass of wine per day during his recent trip. He had eaten oysters and redfin fish during his trip.

Physical Examination

• Afebrile, HR=38, RR=12, BP=134/72, O2 sat=95% on RA
• In general, patient was slightly argumentative and in obvious distress due to abdominal pain. HEENT - nonicteric, pupils reactive, moist oral mucosa
• Neck - No elevated JVP, LAD or thyromegaly
• CV - Bradycardic, regular, no murmur
• Pulmonary - Clear to auscultation all lung fields
• Abdomen - Soft with diffuse tenderness to palpation, bowel sounds present, no HSM or mass
• Lower extremities - Cool to the touch without cyanosis, intact and symmetric distal pulses
• Neuro – Cranial nerves intact, no focal motor or sensory deficits, oriented but with difficulty concentrating on thoughts, poor short-term recall, no obvious visual or auditory hallucinations.

Laboratory

Initial laboratory testing was notable for hyponatremia of 126, otherwise a metabolic panel, complete blood count, troponin, urinalysis, urine drug screen and thyroid stimulating hormone were unremarkable. EKG showed sinus bradycardia without ischemic changes. An abdominal flat plate (KUB) showed a nonspecific bowel gas pattern without evidence of obstruction. Chest x-ray was negative for acute cardiopulmonary abnormality.

He was given 1 liter of normal saline with improvement of sodium to 131, but his pulse remained low at 36. He also developed worsening nausea and mentation, was incoherent at times, and began telling staff that “I’m going to die.”

For the initial presentation of nausea, vomiting, bradycardia, hyponatremia, mental status changes, what is your leading diagnosis?

1. Acute porphyria
2. Excessive water intake
3. Neurotoxic shellfish poisoning
4. Recreational drug use
5. Small cell lung cancer

Cite as: Chan Y-M, Miller DC, Shirazi F, Campion J. July 2020 critical care case of the month: not the pearl you were looking for. Southwest J Pulm Crit Care. 2020;21(1):1-8. doi: https://doi.org/10.13175/swjpcc002-20 PDF

Amniotic Fluid Embolism: A Case Study and Literature Review

Ryan J Elsey DO^1*, Mary K Moats-Biechler OMS-IV², Michael W Faust MD³, Jennifer A Cooley CRNA-APRN⁴, Sheela Ahari MD⁴, and Douglas T Summerfield MD¹

Departments of Internal Medicine¹,Obstetrics and Gynecology³,and Anesthesia⁴

¹Mercy Medical Center—North Iowa

Mason City, IA USA

²A.T. Still University

Kirksville, MO USA

Abstract

Amniotic fluid embolus is a rare and life threatening peripartum complication that requires quick recognition and emergent interdisciplinary management to provide the best chance of a positive outcome for the mother and infant. The following case study demonstrates the importance of quick recognition as well as an interdisciplinary approach in caring for such a condition.  A literature review regarding the current recommendations for management of this condition follows as well as a proposed treatment algorithm.

Introduction

Amniotic fluid embolus (AFE) is a rare and life-threatening complication of pregnancy; a recent population-based review found an estimated incidence ranging from 1 in 15,200 deliveries in North America and 1 in 53,800 deliveries in Europe (1). Mortality rates vary but have been reported to range from 11% to more than 60%, with the most recent population-based studies in the United States reporting a 21.6% fatality rate (1-4).  Despite best efforts, it remains one of the leading causes of maternal death (1,5,6). However, rapid diagnosis of AFE and immediate obstetric and intensive care has proven to play a decisive role in maternal prognosis and survival (7-9).

In 2016, uniform diagnostic criteria were proposed for reporting on cases of AFE. First, a report of AFE requires a sudden onset of cardiorespiratory arrest, which consists of both hypotension (systolic blood pressure < 90 mmHg) and respiratory compromise (dyspnea, cyanosis, or SpO2 < 90%). Secondly, overt disseminated intravascular coagulation (DIC) must be documented following the appearance of signs or symptoms using a standardized scoring system. Coagulopathy must be detected prior to a loss of sufficient blood to account for dilutional or shock-related consumptive coagulopathy. Third, the clinical onset must occur during labor or within 30 minutes of delivery of the placenta. Fourth, no fever ≥ 38.0° C during labor can occur (10).

The following case study qualifies as a reportable incidence of an AFE under the above criteria and further demonstrates the ability to successfully stabilize a patient with AFE due to quick recognition, interdisciplinary cooperation, and effective supportive management.

Case Presentation

A 34-year-old gravida 5, para 1-1-2-2, presented at 36 weeks and 1-day gestation for induction of labor. Her past medical history included esophageal atresia at birth and a past pregnancy complicated by preterm, premature rupture of the membranes. Initial labs at admission were significant for a hemoglobin of 12.2 g/dL and a platelet count of 234 x10³ u/L. The patient was subsequently started on lactated ringers at 125 ml/hr. As the patient's labor progressed, an epidural was placed 3 hours after admission. Four hours and 42 minutes after admission, an artificial rupture of the membranes was performed.

Eighteen minutes after the artificial rupture of the membranes was performed, the patient was noted to have seizure-like activity. She was given an intravenous (IV) fluid bolus and ephedrine, and the anesthesia provider was emergently contacted. When anesthesia arrived, the patient was noted to be cyanotic in bed. Patient vitals and exam were significant for emesis, a heart rate of 50 beats per minute (bpm), systolic blood pressure in the low 70s (mmHg), and a fetal heart rate in the 70s.

The differential diagnosis at this time was broad and included anesthesia drug reactions such as an intravascular epidural migration, pulmonary thromboembolism, eclampsia, or even an aortic dissection. A pulmonary embolism was felt to be unlikely due to the patient's bradycardia and sudden neurologic changes. Eclampsia was less likely at the time due to no signs of pre-eclampsia in the patient as well as the patient's current bradycardia and hypotension. Given the patient's absence of Marfan syndrome, aortic dissection was not considered to be a high probability. The patient did have signs consistent with an intravascular epidural including altered mental status, cyanosis, bradycardia, hypotension, vomiting, and a low fetal heart rate. However, at the time anesthesia felt she was more likely suffering from an acute embolic process given the timeframe between the artificial rupture of the membranes and the onset of her symptoms.

Given the patient's instability, she was emergently taken for a cesarean section and intubated to provide airway stabilization. The cesarean section began 15 minutes after seizure like symptoms started and upon delivery, the infant was subsequently transferred to a tertiary center for therapeutic hypothermia.

Intraoperatively, the patient was noted to maintain a peripheral capillary oxygen saturation (SpO2) of >90%. However, end tidal C02 was elevated to 54 mmHg despite hyperventilation and peak airway pressures were elevated to 38 cmH₂O. Albuterol and sevoflurane were subsequently utilized in an attempt to increase bronchodilation. Following completion of the caesarian section, peak airway pressures normalized to less than 30 cmH₂O but end tidal CO2 levels remained as high as 52 mmHg despite hyperventilation. Blood pressure was significant for systolic pressure of 80 mmHg.  IV phenylephrine was administered. Additionally, uterine massage was performed to aid in hemorrhage control and the patient was administered IV oxytocin, methylergonovine maleate, carboprost, and vaginal misoprostol.  A repeat complete blood count was performed one hour after symptom onset which showed a hemoglobin of 10.3 g/dL and a platelet count of 103 x10³ u/L.

In this case, the patient’s care team had a high suspicion of an AFE with symptoms that followed the uniform diagnostic criteria for an AFE. The patient had hemodynamic instability, coinciding with the recent rupture of membranes. Her systolic blood pressure was < 90 mmHg and her end tidal C02 levels (in mmHg) were elevated to the high 40s and low 50s. The critical care team was notified of her condition and the patient was subsequently transferred to the Intensive Care Unit (ICU) on mechanical ventilation and sedated with fentanyl and versed.

Upon arrival to the ICU, a DIC panel was performed revealing DIC. Labs showed a fibrinogen level of 52 mg/dL, A D-dimer greater than 128,000 ng/mL, and a platelet count of 80,000 u/L despite the administration of one pooled unit of platelets. The patient's international normalized ratio (INR) was 1.3 with a baseline INR of 0.9. Due to multiple laboratory abnormalities and a clinical condition consistent with DIC, aggressive transfusions were performed per the standard of care for patients suffering with DIC. A peripheral smear was obtained revealing schistocytes (Figure 1) which verified the DIC diagnosis.

Figure 1. The patient's peripheral blood smear four hours after onset of symptoms which demonstrates schistocytes indicative of DIC.

Hematology was emergently consulted and it was recommended to avoid additional platelet transfusions unless platelet counts dropped below 10,000 to 20,000 u/L. One milligram (mg) of subcutaneous phytonadione was also given five hours after symptom onset in an effort to decrease bleeding.

Cardiology was consulted and performed an emergent echocardiogram to assess the patient’s heart function and rule out any cardiac abnormalities. Given her past history of esophageal atresia, there was particular concern about an underlying ventricular septal defect, patent ductus arteriosus, or tetralogy of Fallot (11). The echocardiogram revealed a dilated, yet functional right ventricle, which was expected in the setting of an AFE. ICU physicians at a tertiary care center were provisionally consulted to confirm that the patient was a candidate for arteriovenous extracorporeal membrane oxygenation (AV-ECMO) should she suffer further cardiopulmonary collapse. Labs, including hemoglobin, platelets, fibrinogen activity, and ionized calcium were drawn every two hours during the acute phase of the patient's management and abnormalities were addressed as required over the subsequent two hours. The patient's hemoglobin was noted to decline to as low as 6.7 g/dL. Of note, lab draws did suffer some sample lysis due to the patient's coagulation abnormalities. The patient did initially require phenylephrine for blood pressure support. Additionally, she was placed on an experimental septic shock protocol which involved the administration of 1500 mg of ascorbic acid every six hours, 60 mg of methylprednisolone every six hours, and 200 mg of thiamine every 12 hours. The patient began to stabilize around 10 to 12 hours after her AFE symptoms began and pressor support was titrated off, at which point blood draws were liberalized to every four hours. The patient continued to improve and remained stable overnight. 

On hospital day two, the patient was noted to be alert and was successfully extubated. Following extubation, the physical exam found her to be neurologically and hemodynamically intact. During her stay in the ICU, the patient received a total of eight units of packed red blood cells, five units of fresh frozen plasma, one pooled unit of platelets, and one unit of cryoprecipitate. The patient was ultimately discharged from the hospital on day four with no long-term sequelae noted.

The patient was informed that data from the case would be submitted for publication and gave her consent.

A Review of the Literature

AFE remains one of the leading causes of direct, maternal mortality among developed countries (1,12,13). Multiple reviews have studied the incidence of AFE, which varies widely, from 1.9 per 100,000 to 7.7 per 100,000 pregnancies, with the reported fatality rate due to AFE ranging from 11% to more than 60%, depending on the study (1,2,4,14). The difficulty in reporting an accurate incidence and fatality rate is likely secondary to the fact that AFE remains a diagnosis of exclusion. AFE is traditionally diagnosed clinically during labor in a woman with ruptured membranes and a triad of symptoms, including unexplained cardiovascular collapse, respiratory distress, and DIC. (1,2,15-18). Additional symptoms may include hypotension, frothing from the mouth, fetal heart rate abnormalities, loss of consciousness, bleeding, uterine atony, and seizure-like activity (15,16,19).

The majority of women who fail to survive an AFE die during the acute phase (median of one hour and 42 minutes after presentation) (2,6). Surviving beyond the acute phase dramatically improves their overall chance of survival; however, survival is not without long term morbidities. Analysis performed in the United Kingdom in 2005 and again in 2015 showed that 7% of woman surviving AFE have permanent neurological injury, including persistent vegetative state/anoxic/hypoxic brain injury or cerebrovascular accident (2,7). Among survivors,17% were shown to have other comorbidities, including sepsis, renal failure, thrombosis or pulmonary edema and 21% required a hysterectomy (2,6).

Despite several decades of research, the pathogenesis of an AFE continues to remain somewhat clouded. Multiple theories have been postulated concerning the clinical manifestations occurring with an AFE and their relationship with the passage of amniotic fluid into the systemic maternal circulation. The first theory proposed described amniotic debris passing through the veins of the endocervix and into maternal circulation, resulting in an obstruction (1,6). This theory has fallen out of favor as there is no physical evidence of obstruction noted on radiologic studies, autopsies, or experimentally in animal models (1,20,21).  Additionally, multiple studies have found that that the passage of amniotic and fetal cells into maternal circulation are very common during pregnancy and delivery (6). Thus, most theories today focus on humoral and immunological factors and how they affect the body (5,22,23).  Current research focuses on the effect of amniotic fluid on the body after it has already entered into maternal circulation. It is theorized that the amniotic fluid results in the release of various endogenous mediators, resulting in the physiologic changes that are seen with an AFE. Proposed mediators include histamine (22), bradykinin (24), endothelin (25,26), leukotrienes (27), and arachidonic acid metabolites (28).

The hemodynamic response to AFE is biphasic in nature. It consists of vasospasm, resulting in severe pulmonary hypertension, and intense vasoconstriction of the pulmonary vasculature secondary to the amniotic fluid itself, which can lead to ventilation-perfusion mismatch and resultant hypoxia (5,6,29). On an echocardiogram, the initial phase of an AFE consists of right ventricular failure demonstrated by a severely dilated, hypokinetic right ventricle with deviation of the interventricular septum into the left ventricle (18). Following the initial phase of right ventricular failure, which can lasts minutes to hours, left ventricular failure along with cardiogenic, pulmonary edema becomes the prominent finding (1,5). This occurs due to a reduction in preload as well as systemic hypotension. These changes may decrease coronary artery perfusion, which can result in myocardial injury, precipitation of cardiogenic shock, and worsening of distributive shock (1,6,30).

DIC is present in up to 83% of patients experiencing an AFE; however, its onset during presentation can be variable (31). It may present within the first ten minutes following cardiovascular collapse, or it may precipitate up to nine hours following the initial clinical manifestation (5,31,32). The precipitating pathophysiology behind DIC in AFE is poorly understood, but is likely to be consumptive, rather than fibrinolytic, in nature. In an AFE it is currently theorized that tissue factor, which is present in amniotic fluid, activates the extrinsic pathway by binding with factor VII, triggering clotting to occur by activating factor X, resulting in the consumptive coagulopathy (1,33-35). Ultimately, it is felt that this coagulation leads to vasoconstriction of the microvasculature and thrombosis by producing thrombin that is secreted into the endothelin, leading to the changes seen in DIC (1,5,6,14,18).

Recommended Management for AFE Based on Current Literature

Early recognition of AFE and immediate obstetric and intensive care has proven to play a decisive role in maternal prognosis and survival (7,8).  In order to survive an an AFE, patients require immediate multidisciplinary management with a focus on maintaining oxygenation, circulatory support, and correcting coagulopathy (1,6).  

A literature review of the current management for patients presenting with AFE recommends standard initial lifesaving supportive care. This should begin with immediate protection of the patient's airway via endotracheal intubation and early, sufficient oxygenation using an optimized positive end-expiratory pressure (FiO2:PEEP) ratio, which also decreases the risk of aspiration (1,5,29). Two large bore IV lines should be placed for crystalloid fluid resuscitation. In the setting of a cardiopulmonary arrest, cardiopulmonary resuscitation should be initiated and an immediate caesarian section within three to five minutes should be performed in the presence of a fetus ≥ 23 weeks gestation (5,18,36-38). This serves several purposes, including decreasing the risk of the infant suffering from long term neurologic injury secondary to hypoxia, improving venous flow to the right heart by emptying the uterus, and reducing pressure on the inferior vena cava to decrease impedance to blood flow, which decreases systemic blood pressure (1,5,31,39,40).

During the initial phase, attention should be paid to avoid hypoxia, acidosis, and hypercapnia due to their ability to increase pulmonary vascular resistance and lead to worsening of right heart failure and recommendations include sildenafil, inhaled or injected prostacyclin, and inhaled nitric oxide (6). Recommendations to treat for hypotension during this phase include the utilization of vasopressors, such as norepinephrine or vasopressin (1,6,18,37,41). Hemodynamic management during the second phase should focus on the patient's left-sided heart failure by optimizing cardiac preload via vasopressors to maintain perfusion and utilizing inotropes such as dobutamine or milrinone to increase left ventricular contractility (1,6,18).

Due to the relationship between AFE and DIC, current recommendations suggest early assessment of the patient's coagulation status. Additionally, in the setting of a massive hemorrhage, blood product administration should not be delayed while awaiting laboratory results (18). Early corrective management of the patient's coagulopathy should be aggressive in nature, especially in the setting of a massive hemorrhage. Tranexamic acid and fibrinogen concentrate (for fibrinogen levels below 2 g/L) are essential in the treatment of hyper-fibrinolysis. Additionally, multiple obstetric case studies have shown fibrinogen replacement to benefit from bedside rotational thromboelastometry if available due to its ability to rapidly diagnosis consumptive versus fibrinolytic coagulopathy at the bedside (5,42,43). Hemostatic resuscitation with packed red blood cells, fresh-frozen plasma, and platelets at a ratio of 1:1:1 should be administered (6,18). Cryoprecipitate replacement is recommended as well due to the consumptive nature of DIC in AFE, and its importance should not be understated. A 2015 population-based cohort study showed that women with AFE who died or had permanent neurologic injury were less likely to have received cryoprecipitate than those who survived and were without permanent neurologic injury (1,2).  Furthermore, due to the dynamic processes of chemodynamical labs, including hemoglobin, platelet count, and fibrinogen must be monitored closely to prevent complications or over transfusion (14).

Uterine atony is a common feature with AFE and it is recommended to immediately administer uterotonics during the postpartum period to prevent its occurrence (5,44). Should it occur, uterine atony should be managed aggressively via uterotonics such as oxytocin, ergot derivatives, and prostaglandins; refractory cases may require packing material for uterine tamponade, uterine artery ligation, or even a hysterectomy for the most severe (5,8,18).

In addition to the treatments listed above, multiple case reports support the use of aggressive or novel therapeutic modalities to aid in the treatment of AFE; however, for many of the treatments, evidence supporting increased survival of an AFE is merely anecdotal (18). Among the best supported ancillary treatments is nonarterial extracorporeal membrane oxygenation as a possible therapeutic treatment for patients with refractory acute respiratory distress syndrome. However, due to the profoundly coagulopathic state of AFE and the active hemorrhage occurring with AFE, the use of anticoagulation may profoundly worsen bleeding. Consequently, extracorporeal membrane oxygenation is controversial and not routinely recommended in the management of AFE (6,18). Similarly, post-cardiac arrest therapeutic hypothermia with a range of 32°C to 34°C is often avoided in patients with AFE due to the increased risk of hemorrhage given their predisposition for DIC (18). However, in patients not demonstrating DIC and overt bleeding, targeted temperature management to 36°C and preventing hyperthermia is an option that should be considered (17,45,46). Factor VIIa procoagulant, which increases thrombin formation, has been utilized anecdotally, but strong supporting data is lacking; it should only be considered if following the replacement with massive coagulation factors, hemostasis and bleeding fail to improve (5,47).  Additionally, it is important to note that factor VIIa replacement is only effective if other clotting factors have been replaced (1,6,48,49). Novel therapeutic modalities mentioned in the literature also include continuous hemofiltration, cardiopulmonary bypass, nitric oxide, steroids, C1 esterase inhibitor concentrate, and plasma exchange transfusion. While there are case reports published to suggest that all of the aforementioned therapies may provide some level of improvement in patients with AFE, the positive results from these cases may be due to their administration during the intermediate phase of AFE as opposed to the acute phase of AFE, where the majority of mortality occurs—once patients have surpassed the early, acute phase, survival chances greatly improve with continued supportive care (1,6).

AFE has traditionally been viewed as a condition associated with poor outcomes and a high mortality rate for both the mother and the infant. However, with quick AFE recognition, high quality supportive care, and interdisciplinary cooperation, patients can have positive outcomes. Based on the success with the patient presented in this case and the review of the current literature as seen above, the authors have proposed an algorithm (Figure 2) for the treatment of future patients experiencing AFE.

Figure 2. Proposed interdisciplinary treatment algorithm for acute management of an AFE.

By following the algorithm, the authors believe that the outcomes for AFE patients can be improved.

Abbreviations

PEEP: positive end-expiratory pressure; BP: blood pressure; TV: tidal volume; ACLS: Advanced cardiac life support; ABG: Arterial blood gas; CBC: Complete blood count; CMP: Complete metabolic profile; INR: International normalized ratio; PTT: Partial prothrombin time; ART line: Arterial line; NO: Nitric oxide; ARDS: Acute respiratory distress syndrome; ECMO: Extracorporeal membrane oxygenation; FFP: Fresh frozen plasma; Plt: Platelet; pRBCs: Packed red blood cells; NE: Norepinephrine.

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Cite as: Elsey RJ, Moats-Biechler MK, Faust MW, Cooley JA, Ahari S, Summerfield DT. Amniotic fluid embolism: A case study and literature review. Southwest J Pulm Crit Care. 2019;18(4):94-105. doi: https://doi.org/10.13175/swjpcc105-18 PDF 

April 2019 Critical Care Case of the Month: A Severe Drinking Problem

Francisco J. Marquez II MD

Department of Pulmonary and Critical Care Medicine

Banner University Medical Center/University of Arizona – Phoenix

Phoenix, AZ USA

History of Present Illness

A 55-year-old Caucasian man, presented to an outside hospital with altered mental status.

Past Medical/Social History

• Severe alcohol and intermittent fentanyl abuse
• Homelessness

Physical Exam

• Hypothermic and hypertensive.
• Patient encephalopathic without any acute deficits
• Pupils are normal sized and react to light

Which of the following should be obtained or done in his initial evaluation? (Click on the correct answer to proceed to the second of six pages)

1. CBC
2. Electrolytes
3. Give naloxone (Narcan®) and glucose
4. 1 and 3
5. All of the above

Cite as: Marquez FJ II. April 2019 critical care case of the month: A severe drinking problem. Southwest J Pulm Crit Care. 2019;18(4):67-73. doi: https://doi.org/10.13175/swjpcc003-19 PDF 

Ultrasound for Critical Care Physicians: An Unexpected Target Lesion

Jantsen Smith, MD

Department of Internal Medicine

University of New Mexico Hospital

Albuquerque, NM USA

A 39-year-old woman was admitted to the hospital for shortness of breath. Her medical history was significant for human immunodeficiency virus infection (not on anti-retroviral therapy), superior vena cava (SVC) syndrome with history of SVC stenting, cerebrovascular accident complicated by seizure disorder and swallowing difficulties, moderate pulmonary hypertension, end-stage renal disease on hemodialysis with past episodes of acute hypoxic respiratory failure related to fluid overload. Shortly after admission, the patient experienced a cardiac arrest due to hypoxia and necessitated emergent intubation. This was presumed to be due to fluid overload. Nephrology was consulted for emergent dialysis (the patient had a right upper extremity fistula for dialysis access). Dialysis was initiated through a right arm fistula. On day three of admission, the patient was noted to have worsening right upper extremity and breast swelling and pain. Physical exam revealed indurated edema of the skin of the breast. Point of care ultrasound was performed of the patient’s right neck, and the following ultrasound was obtained approximately 4cm above the clavicle in the right lateral neck.

Video 1. Ultrasound image of the right neck in the transverse plane.

What is the most likely cause of this patient’s right upper extremity and breast swelling? (Click on the correct answer for an explanation).

1. Right breast cellulitis
2. Ascending SVC thrombus
3. Lymphatic blockage of right axillary nodes
4. Fluid overload complicated by third spacing in the R upper extremity

Cite as: Smith J. Ultrasound for critical care physicians: An unexpected target lesion. Southwest J Pulm Crit Care. 2019;18(3):63-4. doi: https://doi.org/10.13175/swjpcc011-19 PDF

October 2018 Critical Care Case of the Month: A Pain in the Neck

Robert A. Raschke, MD

Critical Care Medicine

HonorHealth Scottsdale Osborn Medical Center

Scottsdale, AZ USA

History of Present Illness

A 54-year-old man was admitted after he had a decline in mental status. He complained of neck and back pain for one week prior to admission for which he took acetaminophen. He was seen in the emergency department two days prior to admission and diagnosed with “arthritis” and prescribed oxycodone/acetaminophen and cyclobenzaprine. On the day of admission be became unresponsive and was transported by ambulance to the emergency department where he was intubated for airway protection.

Past Medical History, Social History, Family History

• Alcoholism
• Hepatitis C
• Esophageal varices
• Family history is noncontributory

Physical Examination

• Vitals: T 102° F, BP 150/60 mm Hg, P 114 beats/min, 20 breaths/min
• Unresponsive
• Dupuytren’s contractures, spider angiomata
• 3/6 systolic murmur
• Deep tendon reflexes 3+  
• Bilateral Babinski’s sign (toes upgoing)

Which of the following are diagnostic considerations at this time? (Click on the correct answer to be directed to the second of six pages)

1. Bacterial endocarditis
2. Hypoglycemia
3. Liver failure
4. 1 and 3
5. All of the above

Cite as: Raschke RA. October 2018 critical care case of the month: a pain in the neck. Southwest J Pulm Crit Care. 2018;17(4):108-13. doi: https://doi.org/10.13175/swjpcc098-18 PDF

August 2018 Critical Care Case of the Month

Emma Simpson, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA

History of Present Illness

A 19-year-old gravida 1, para 0 woman in her early second trimester presented to the Emergency Department with intractable vomiting, green sputum icteric sclerae, chest pain, palpitations and weakness for one week prior to presentation. She was visiting the US from an island in Micronesia. The patient has been experiencing feelings of general malaise since the beginning of her pregnancy: she experienced severe nausea and vomiting throughout her first trimester, and a 4.5 kg weight loss in the 2 months prior to presentation.

PMH, SH, FH

Before becoming pregnant, the patient was active and healthy. She does not smoke and her family history is unremarkable.

Physical Examination

Physical exam showed a thin, small young woman. Her physical examination showed a tachycardia of 114 and icteric sclera but was otherwise unremarkable.

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

1. Admit to the hospital with measurement of electrolytes, transaminases and bilirubin
2. Discharge to home with a prescription for pyridoxine/doxylamine
3. Ultrasound
4. 1 and 3
5. All of the above

Cite as: Simpson E. August 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;17(2):53-8. doi: https://doi.org/10.13175/swjpcc092-18 PDF 

July 2018 Critical Care Case of the Month

Stephanie Fountain, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA 

History of Present Illness

A 45-year-old man was brought to the Emergency Room by his mother complaining of weakness, dizziness, and trouble swallowing. He was also incontinent of stool and looked “sunburned”.

Past Medical History

He has a past medical history of:

• Schizophrenia
• Depression
• Polysubstance abuse
• Crohn’s disease
• Type 2 diabetes
• Hyperlipidemia

Medications

• Prazosin
• Venlafaxine
• Risperidone
• Buspirone
• Oxcarbazepine
• Gabapentin
• Hydroxyzine
• Lithium
• KCL
• Metformin
• Atorvastatin
• Adalimumab
• Mesalamine
• Prednisone
• Ferrous sulfate

Physical Examination

• Vitals: 80 kg / 97.3 degrees / 101 bpm / 100% 28RR  / BP 111/72 
• The patient was toxic appearing and flushed.
• Oriented to self only, very lethargic
• Dry mucous membranes
• Lungs clear to auscultation and percussion
• Heart tachycardic but no murmurs
• Abdomen without organomegaly, masses or tenderness
• Extremities without edema

Which of the following should be done at this time? (Click on the correct answer to be directed to the second of six pages)

1. Electrolytes
2. Lumbar puncture
3. Urine drug screen
4. 1 and 3
5. All of the above

Cite as: Fountain S. July 2018 critical care case of the month. Southwest J Pulm Crit Care. 2018;17(1):7-14. doi: https://doi.org/10.13175/swjpcc085-18 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 

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 

Ultrasound for Critical Care Physicians: A Pericardial Effusion of Uncertain Significance

Brandon Murguia  M.D.

Department of Medicine

University of New Mexico School of Medicine

Albuquerque, NM USA

A 75-year-old woman with known systolic congestive heart failure (ejection fraction of 40%), chronic atrial fibrillation on rivaroxaban oral anticoagulation, morbid obesity, and chronic kidney disease stage 3, was transferred to the Medical Intensive Care Unit for acute hypoxic respiratory failure thought to be secondary to worsening pneumonia.

She had presented to the emergency department 3 days prior with shortness of breath, malaise, left-sided chest pain, and mildly-productive cough over a period of 4 days. She had mild tachycardia on presentation, but was normotensive without tachypnea, hypoxia, or fever. Routine labs were remarkable for a leukocytosis of 15,000 cells/μL. Cardiac biomarkers were normal, and electrocardiogram demonstrated atrial fibrillation with rapid ventricular rate of 114 bpm. Chest x-ray revealed cardiomegaly and left lower lobe consolidation consistent with bacterial pneumonia. Patient was admitted to the floor for intravenous antibiotics, cardiac monitoring, and judicious isotonic fluids if needed.

On night 2 of hospitalization, the patient developed respiratory distress with tachypnea, pulse oximetry of 80-85%, and increased ventricular response into the 140 bpm range. The patient remained normotensive. A portable anterior-posterior chest x-ray showed cardiomegaly and now complete opacification of the left lower lobe. She was transferred to the MICU for suspected worsening pneumonia and congestive heart failure.

Upon arrival to the intensive care unit, vital signs were unchanged and high-flow nasal cannula was started at 6 liters per minute. A focused point-of-care cardiac ultrasound (PCU) was done, limited in quality by patient body habitus, but nonetheless demonstrating the clear presence of a moderate pericardial effusion on subcostal long axis view.

Figure 1: Subcostal long axis view of the heart.

What should be done next regarding this pericardial effusion? (Click on the correct answer for the answer and explanation)

1. Observe, this is not significant.
2. Additional echocardiographic imaging /evaluation.
3. Immediate pericardiocentesis.
4. Fluid challenge.

Cite as: Murguia B. Ultrasound for critical care physicians: a pericardial effusion of uncertain significance. Southwest J Pulm Crit Care. 2016;13(5):261-5. doi: https://doi.org/10.13175/swjpcc127-16 PDF

October 2016 Critical Care Case of the Month

Stephanie Fountain, MD

Banner University Medical Center Phoenix

Phoenix, AZ USA

Critical Care Case of the Month CME Information

Members of the Arizona, New Mexico, Colorado and California Thoracic Societies and the Mayo Clinic are able to receive 0.25 AMA PRA Category 1 Credits™ for each case they complete. Completion of an evaluation form is required to receive credit and a link is provided on the last panel of the activity. 

0.25 AMA PRA Category 1 Credit(s)™

Estimated time to complete this activity: 0.25 hours 

Lead Author(s): Stephanie Fountain, MD.  All Faculty, CME Planning Committee Members, and the CME Office Reviewers have disclosed that they do not have any relevant financial relationships with commercial interests that would constitute a conflict of interest concerning this CME activity.

Learning Objectives:
As a result of this activity I will be better able to:

1. Correctly interpret and identify clinical practices supported by the highest quality available evidence.
2. Will be better able to establsh the optimal evaluation leading to a correct diagnosis for patients with pulmonary, critical care and sleep disorders.
3. Will improve the translation of the most current clinical information into the delivery of high quality care for patients.
4. Will integrate new treatment options in discussing available treatment alternatives for patients with pulmonary, critical care and sleep related disorders.

Learning Format: Case-based, interactive online course, including mandatory assessment questions (number of questions varies by case). Please also read the Technical Requirements.

CME Sponsor: University of Arizona College of Medicine

Current Approval Period: January 1, 2015-December 31, 2016

Financial Support Received: None

A 27-year-old Caucasian man with past medical history of opioid abuse (reportedly sober for 10 years on buprenorphine), post traumatic stress disorder, depression and anxiety presented to the emergency department complaining of dysarthria after taking diphenhydramine and meclizine in addition to his prescribed trazodone and buprenorphine to try to sleep. He was discharged to home after his symptoms appeared to improve with intravenous fluid.

He returned to the emergency department the following afternoon with worsening dysarthria, dysphagia, and subjective weakness. The patient was non toxic appearing, afebrile, vital signs were stable and his strength was reported as 5/5. Computed tomography  of his head did not show any evidence of acute intracranial abnormality. Given his ongoing complaints, he was admitted for observation to the general medicine wards.

That night a rapid response was initiated when the nurse found the patient to be unresponsive, but spontaneously breathing. The patient’s clinical status did not change with naloxone administration. An arterial blood gas obtained demonstrated a profound respiratory acidosis with a pH of 7.02 and a pCO2 of 92. He was emergently intubated. A chest x-ray was performed (Figure 1).

Figure 1. Panel A: admission portable chest x-ray. Panel B: chest -ray immediately after intubation. 

Which of the following are present on his chest X-ray? (Click on the correct answer to proceed to the second or four panels)

1. Left lung atelectasis
2. Left pleural effusion
3. Right mainstem intubation
4. 1 and 3
5. All of the above

Cite as: Fountain S. October 2016 critical care case of the month. Soutwest J Pulm Crit Care. 2016:13(4):159-64. doi: http://dx.doi.org/10.13175/swjpcc095-16 PDF

Ultrasound for Critical Care Physicians: Unraveling a Rapid Drop of Hematocrit

Deepti Baheti, MBBS

Pablo Garcia, MD

Department of Internal Medicine and LifeBridge Critical Care

Sinai Hospital of Baltimore.

Baltimore, MD USA

An 85-year-old woman was admitted to our hospital with complaints of shortness of breath on exertion. Her medical history was significant for hypertension, pulmonary embolism and stage III chronic kidney disease. She was diagnosed with severe decompensated pulmonary hypertension and started to improve with diuretics. While hospitalized, she suffered an asystolic arrest and was successfully resuscitated. As a result of chest compressions, the patient developed multiple anterior rib fractures. Within a few days of recovering from her cardiac arrest, she was anticoagulated with enoxaparin as a bridge to warfarin for her prior history of pulmonary embolism. Five days after initiation of enoxaparin and warfarin, she was noted to have an acute drop in her hemoglobin from 8 g/dl to 5 g/dl. A thorough physical examination revealed a large area of swelling in her left anterior chest wall. Point-of- care ultrasound was utilized to image this area of swelling centered at the 3rd intercostal space between the mid-clavicular and anterior axillary line (Figures 1 and 2).

Figure 1. Ultrasound image of the chest wall in the sagittal plane.

Figure 2. Ultrasound image of the chest wall in the transverse plane.

What is the cause of this patient’s acute anemia? (Click on the correct answer for an explanation)

1. Chest wall hematoma
2. Hemolysis
3. Hemoperitoneum
4. Hemothorax

Cite as: Baheti D, Garcia P. Ultrasound for critical care physicians: unraveling a rapid drop of hematocrit. Southwest J Pulm Crit Care. 2016;13(2):84-7. doi: http://dx.doi.org/10.13175/swjpcc078-16 PDF