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A 70-Year-Old Man With Intraoperative Hypoxia and Hypotension During Total Hip ReplacementHypoxia and Hypotension During Hip Replacement FREE TO VIEW

Mariam A. Alansari, MD; Ahmed A. Abdulmomen, MD
Author and Funding Information

From the Department of Adult Critical Care Medicine, King Khalid University Hospital, College of Medicine, King Saud University, Riyadh, Saudi Arabia.

CORRESPONDENCE TO: Mariam A. Alansari, MD, Department of Adult Critical Care Medicine, King Khalid University Hospital, College of Medicine, King Saud University, PO Box 2925 (95), Riyadh 11461, Saudi Arabia; e-mail: icu_mariam@yahoo.com


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(5):e160-e162. doi:10.1378/chest.14-0411
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Published online

A 70-year-old man underwent total hip replacement surgery under general anesthesia, endotracheal intubation, and controlled ventilation, with the patient in left lateral position. Intraoperatively, the patient was hemodynamically stable, with a normal range of pulse, ECG trace, oxygen saturation as measured by pulse oximetry (Spo2), and end-tidal CO2 (etco2). Five minutes after insertion of the hip prosthesis, his heart rate dropped to 30 beats/min, BP to 40/30 mm Hg, Spo2 to 70%, and etco2 to 10 mm Hg.

Figures in this Article
Physical Examination Findings

The patient was turned to the supine position with pulse present. The airway pressure was slightly elevated. Cardiovascular examination was normal. No ST-segment changes were seen on the ECG monitor. No rash was noted in the conjunctivae or on the body. The rest of the physical examination was unremarkable. Arterial and central venous catheters were inserted. Hemodynamic stability returned with fluid boluses, use of 100% oxygen, and atropine, ephedrine, and epinephrine infusion.

Diagnostic Studies

After completion of the surgery, the patient was moved to the surgical ICU. Immediate chest radiographs were taken (Fig 1). Twelve-lead ECG findings were normal. Laboratory findings, including cardiac troponin and B-type natriuretic peptide blood test results, were within normal ranges. No other significant laboratory results were detected.

Figure Jump LinkFigure 1 –  Chest radiograph showing diffuse alveolar infiltrates involving four quadrants of the lung.Grahic Jump Location

Over the 72-h stay in the ICU, the patient was weaned from the ventilator and inotropic support. He was extubated and discharged from the ICU on day 5.

What is the diagnosis? What study should be considered that could help in the diagnosis?
Diagnosis: Bone cement implantation syndrome. Immediate echocardiography

Bone cement implantation syndrome (BCIS) is a potentially fatal intraoperative complication occurring in patients undergoing cemented orthopedic surgeries. It is commonly associated with, but not limited to, hip replacement. BCIS can occur at any stage of the surgical procedure from femoral reaming, to cement implantation, to insertion of the prosthesis or joint reduction. First reported in 1970, BCIS is now an established entity. However, BCIS is underreported because a widely accepted definition of this condition is lacking. As a result, the incidence varies widely in the literature. Patient-related risk factors implicated in the genesis of BCIS include older age, impaired cardiopulmonary function, preexisting pulmonary hypertension, poor preexisting physical reserve, osteoporosis, and pathologic or intertrochanteric fractures. Data on fatalities from BCIS are rare. The literature reports death in 0.6% to 4.3% of patients with this condition. More reporting of BCIS data will help to better our understanding.

Bone cement (an acrylic substance) is a filler as well as an adhesive. It is used to secure implants to bone or to fill joint cavities. The use of bone cement remains the standard of care for a large number of arthroplasties. The insertion of the prosthesis long stems into high-viscosity cement can result in an increase in intramedullary pressure of as high as 187% caused by mechanical compression of the medullary canal. This increase in intramedullary pressure is the most critical factor contributing to the showering of cement emboli. These emboli have a mechanical effect on the pulmonary vasculature as well as a mediator release effect within the circulation, causing complement activation, release of histamines, and stimulation of endogenous cannabinoid-mediated vasodilation and resulting in hemodynamic instability and collapse. The resulting hypotension decreases coronary perfusion pressure, creating ischemia of the right ventricle. This process produces a vicious cycle of right ventricular depression, failure, and death. These changes are known to increase significantly over the ensuing 2 days. Transesophageal echocardiography studies during arthroplasty have shown that the measured pulmonary and hemodynamic responses correlate directly with the quantity of emboli imaged in the atria (Fig 2). Most published case reports are supported by clinical findings of patient hemodynamic instability during or after the operation. However, a recent case report confirmed by autopsy and histopathologic examination a state of disseminated microembolization of medullary substances and foreign material in the heart, lungs, blood vessels, liver, and kidneys.

Figure Jump LinkFigure 2 –  Transesophageal echocardiogram in a patient with bone cement implantation syndrome, showing echogenic material (fat and marrow) in the RA and RV. None is seen in the LA or LV, indicating a filtering of debris by the pulmonary vasculature. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.Grahic Jump Location

BCIS is characterized by hypoxia, hypotension, or both; arrhythmias with or without loss of consciousness; and cardiac arrest. The range of BCIS case severity is as follows:

  • • Grade 1: moderate hypoxia (oxygen saturation as measured by pulse oximetry < 94%) or fall in systolic BP > 20%

  • • Grade 2: severe hypoxia (oxygen saturation as measured by pulse oximetry < 88%) or fall in systolic BP > 40% or unexpected loss of consciousness

  • • Grade 3: cardiovascular collapse requiring CPR

The first indication of BCIS in the anesthetized patient is a fall in end-tidal CO2 concentration. It helps to detect BCIS earlier than allowed by standard monitoring; thus, dyspnea and altered sensorium could be early signs of BCIS in a patient undergoing local anesthesia. Cardiac arrest and death are the most catastrophic symptoms associated with BCIS. Chances of survival is increased if the situation is immediately recognized and supportive measures are initiated promptly.

Adverse reactions during and after cemented major joint replacement that may necessitate ICU admission include persistent hypotension, acute lung injury/ARDS resulting in persistent hypoxemia (Fig 1), pulmonary embolism, acute pulmonary hypertension, and right-sided heart strain. Other complications include pulmonary edema, bronchoconstriction, hypothermia, and thrombocytopenia.

Differential diagnosis of BCIS includes fat embolism syndrome (FES), which is a well-recognized complication of orthopedic surgery. The classic clinical triad for the diagnosis of FES is pulmonary insufficiency, neurologic derangement (in 86% of patients), and petechial rash (in 50% of patients). The diagnosis of FES requires two of the clinical triad as major criteria and four minor criteria, which are tachycardia, pyrexia, jaundice, retinal involvement, renal involvement, and fat macroglobulinemia. Signs and symptoms of FES usually become apparent within 24 to 48 h after insult compared with BCIS where hypoxia and hypotension usually occur within 30 min from cementing during the orthopedic procedure.

Clinical Course

Strategies to reduce surgical risk of BCIS include venting the medulla, medullary lavage, minimizing the length of the prosthesis, and using a noncemented prosthesis. Venting the medulla permits air to escape from the end of the cement plug and reduces embolization. These strategies are very helpful in preventing BCIS to a large extent and are highly recommended by patient safety advisories.

Guideline recommendations for BCIS management approaches are lacking. Thus, management is guided by basic physiologic principles. In the operating theater, oxygen concentration should be increased to 100%; aggressive fluid resuscitation initiated; and a central venous catheter inserted for the administration of inotropic drugs, if needed. The choice of vasopressor is generally sympathetic α1-agonist in view of the right-side heart failure and vasodilation. These should be continued into the postoperative period and the patient moved to the ICU.

In the ICU, supportive care remains the mainstay of therapy. As clinically indicated, hemodynamics should be maintained with fluids and vasopressors. In patients meeting diagnostic criteria for acute lung injury/ARDS, mechanical ventilation with lung protective ventilation strategies should be followed.

  • 1. BCIS is a potentially fatal intraoperative complication that can occur in any patient undergoing cemented orthopedic surgeries.

  • 2. The first indication of BCIS in the anesthetized patient is a fall in end-tidal CO2 concentration. Other characteristics may include hypoxia, hypotension, or both; arrhythmias with or without loss of consciousness; and cardiac arrest.

  • 3. Strategies to reduce surgical risk of BCIS include venting the medulla, medullary lavage, minimizing the length of the prosthesis, and using a noncemented prosthesis.

  • 4. Supportive care remains the mainstay of therapy for BCIS, with the choice of vasopressor generally being sympathetic α1-agonist.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Byrick RJ, Forbes D, Waddell JP. A monitored cardiovascular collapse during cemented total knee replacement. Anesthesiology. 1986;65(2):213-216. [CrossRef] [PubMed]
 
Byrick RJ, Bell RS, Kay JC, Waddell JP, Mullen JB. High-volume, high-pressure pulsatile lavage during cemented arthroplasty. J Bone Joint Surg Am. 1989;71(9):1331-1336. [PubMed]
 
Nazon D, Abergel G, Hatem CM. Critical care in orthopedic and spine surgery. Crit Care Clin. 2003;19(1):33-53. [CrossRef] [PubMed]
 
Motobe T, Hashiguchi T, Uchimura T, et al. Endogenous cannabinoids are candidates for lipid mediators of bone cement implantation syndrome. Shock. 2004;21(1):8-12. [CrossRef] [PubMed]
 
Pennsylvania Patient Safety Reporting System. Bone cement implantation syndrome. PA-PSRS Patient Safety Advisory. 2006;3(4):1-8.
 
Memtsoudis SG, Rosenberger P, Walz JM. Critical care issues in the patient after major joint replacement. J Intensive Care Med. 2007;22(2):92-104. [CrossRef] [PubMed]
 
Donaldson AJ, Thomson HE, Harper NJ, Kenny NW. Bone cement implantation syndrome. Br J Anaesth. 2009;102(1):12-22. [CrossRef] [PubMed]
 
Govil P, Kakar PN, Arora D, Das S, Gupta N, Govil D, et al. Bone cement implantation syndrome: a report of four cases. Indian J Anaesth. 2009;53(2):214-218. [PubMed]
 
Issack PS, Lauerman MH, Helfet DL, Sculco TP, Lane JM. Fat embolism and respiratory distress associated with cemented femoral arthroplasty. Am J Orthop (Belle Mead NJ). 2009;38(2):72-76. [PubMed]
 
Razuin R, Effat O, Shahidan MN, Shama DV, Miswan MFM. Bone cement implantation syndrome. Malays J Pathol. 2013;35(1):87-90. [PubMed]
 

Figures

Figure Jump LinkFigure 1 –  Chest radiograph showing diffuse alveolar infiltrates involving four quadrants of the lung.Grahic Jump Location
Figure Jump LinkFigure 2 –  Transesophageal echocardiogram in a patient with bone cement implantation syndrome, showing echogenic material (fat and marrow) in the RA and RV. None is seen in the LA or LV, indicating a filtering of debris by the pulmonary vasculature. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.Grahic Jump Location

Tables

Suggested Readings

Byrick RJ, Forbes D, Waddell JP. A monitored cardiovascular collapse during cemented total knee replacement. Anesthesiology. 1986;65(2):213-216. [CrossRef] [PubMed]
 
Byrick RJ, Bell RS, Kay JC, Waddell JP, Mullen JB. High-volume, high-pressure pulsatile lavage during cemented arthroplasty. J Bone Joint Surg Am. 1989;71(9):1331-1336. [PubMed]
 
Nazon D, Abergel G, Hatem CM. Critical care in orthopedic and spine surgery. Crit Care Clin. 2003;19(1):33-53. [CrossRef] [PubMed]
 
Motobe T, Hashiguchi T, Uchimura T, et al. Endogenous cannabinoids are candidates for lipid mediators of bone cement implantation syndrome. Shock. 2004;21(1):8-12. [CrossRef] [PubMed]
 
Pennsylvania Patient Safety Reporting System. Bone cement implantation syndrome. PA-PSRS Patient Safety Advisory. 2006;3(4):1-8.
 
Memtsoudis SG, Rosenberger P, Walz JM. Critical care issues in the patient after major joint replacement. J Intensive Care Med. 2007;22(2):92-104. [CrossRef] [PubMed]
 
Donaldson AJ, Thomson HE, Harper NJ, Kenny NW. Bone cement implantation syndrome. Br J Anaesth. 2009;102(1):12-22. [CrossRef] [PubMed]
 
Govil P, Kakar PN, Arora D, Das S, Gupta N, Govil D, et al. Bone cement implantation syndrome: a report of four cases. Indian J Anaesth. 2009;53(2):214-218. [PubMed]
 
Issack PS, Lauerman MH, Helfet DL, Sculco TP, Lane JM. Fat embolism and respiratory distress associated with cemented femoral arthroplasty. Am J Orthop (Belle Mead NJ). 2009;38(2):72-76. [PubMed]
 
Razuin R, Effat O, Shahidan MN, Shama DV, Miswan MFM. Bone cement implantation syndrome. Malays J Pathol. 2013;35(1):87-90. [PubMed]
 
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