A fourteen-year-old boy underwent hip arthroscopy for relief of cam impingement from a slipped capital femoral epiphysis. In situ screw fixation on the right side and prophylactic screw fixation on the left side were performed one month prior to the arthroscopic procedure. The right hip showed a mild slip, with 35° of external rotation deformity at 90° of flexion with associated pain.
General anesthesia was administered, and traction was applied to the right hip with use of a commercial traction device (Smith & Nephew, Memphis, Tennessee). Hip distraction was inadequate, even with substantial traction on both legs. Traction was released, and the right hip was sterilely prepared and draped with a clear drape. The hip was then flexed to 35°, and a superior anterolateral portal was established to the peripheral compartment, as described by Dienst5. Fluid pump pressure was set at 55 mm Hg, and the irrigation fluid contained an epinephrine concentration of 1 mg/L (1:1000) in every 3000 ml bag. Substantial hip synovitis was noted. Thus, an anterior portal was established, and some of the synovium was resected with a shaver. The femoral neck prominence was delineated, and an anterior capsulotomy was performed. The arthroscope was removed from the anterolateral portal and placed in the anterior portal. We noted profuse dark red bleeding from the cannula that was left in the anterolateral portal. When the inflow port was turned on, the bleeding decreased.
The outflow port was blocked manually, and the peripheral compartment was inspected through the anterior portal. There was no bleeding in the joint, and the arthroscopic image was clear. At this point, we noted that the fluid pump was running continuously, despite all of the outflow ports being closed. The ipsilateral thigh and the abdomen did not show any swelling and remained soft. Ten minutes after the bleeding was observed, the anesthesiologist noted an increase in blood pressure from 100/60 to 200/120. Shortly thereafter, pink frothy foam came out of the endotracheal tube. Seconds later, a substantially large amount of pink fluid started to eject from the endotracheal tube. At that time, we determined that the patient had acute pulmonary edema.
The surgical procedure was abandoned, and the two portal sites were closed and covered with dressings. The patient was resuscitated with Lasix (furosemide) and fluid restriction. A Foley catheter and arterial line were inserted, and the patient was transferred to the intensive care unit. The high blood pressure slowly declined over thirty minutes. He remained stable and was extubated on postoperative day two. Postoperatively, an echocardiogram, a magnetic resonance angiogram, and an electrocardiogram showed no vascular, ischemic, or cardiac wall motion abnormalities. The patient remained stable and was discharged home on day four. He later underwent a femoral neck osteoplasty by open anterior incision through a modified Smith-Peterson approach, which he tolerated without complication.
Pulmonary edema in orthopaedic procedures is rare. Cases of pulmonary edema have been traced to use of epinephrine in the irrigation fluid, increased intramedullary pressure, negative pressure pulmonary edema, congestive heart failure, cardiomyopathy, or upper airway constriction.
Mazzocca et al. described a nineteen-year-old woman who developed pulmonary edema while undergoing arthroscopy for the reconstruction of the anterior cruciate ligament4. They referenced several cases in the otolaryngology literature that describe pulmonary edema after the administration of local epinephrine. Although they noted that there is no specific orthopaedic literature describing pulmonary edema after epinephrine induction, they suggested that the mechanism of pulmonary edema is most likely the result of increased activation of the alpha-adrenergic receptor. This activation of alpha receptors results in increased peripheral vascular resistance, which increases left-ventricular filling pressures. This results in a shift of blood volume from the peripheral circulation into the pulmonary circulation, and results in an increase in blood pressure, depressed myocardial contractility, and pulmonary edema.
Pulmonary edema and cardiorespiratory compromise can result from the intravasation of the bone marrow content into the circulation as a result of increased intramedullary pressures. In a randomized study of nineteen Norwegian pigs, Husebye et al. compared intramedually pressures between a one-step reamer irrigator and a traditional irrigator6. They found that there was a significantly higher intramedually pressure in the traditional reamer group, with an increased likelihood of pulmonary edema.
Messerschmitt and Stambough described the case of a forty-nine-year-old man who developed negative pressure pulmonary edema while undergoing elective knee arthroscopy7. Negative pressure pulmonary edema is the result of attempted ventilations against an acutely obstructed upper airway, resulting in the generation of negative pressure, which increases hydrostatic pulmonary capillary pressure and results in a fluid shift across the alveolar capillary endothelium. Negative pressure pulmonary edema is often seen in young athletic patients since they have well-developed thoracic muscles that enable them to generate increased negative pressure8.
We found no reports of pulmonary edema caused by fluid irrigation in the orthopaedic literature. However, pulmonary edema as a result of fluid irrigation has been noted in hysteroscopic procedures, due to high-pressure irrigation9,10.
Other major causes of pulmonary edema appeared less likely in our patient. Iatrogenic fluid overload was unlikely since intravenous fluid levels were carefully calculated for weight and, at that point in the surgery, only a minimal amount of intravenous fluid had been infused. Negative pressure pulmonary edema can present rapidly after acute upper airway obstruction; it also often presents after upper airway pathology in the presurgical period as well as with laryngospasm in the postoperative period. With the establishment of a patent airway, positive pressure, and oxygenation, pulmonary edema usually resolves. Anaphylaxis is also a cause of pulmonary edema. This was less likely the cause in our case since there was no angioedema, petechiae, bronchospasm, or other anaphylactic-type reactions. Epinephrine-induced pulmonary edema is preceded by cardiac manifestations11 (usually ventricular tachycardia)12,13. Both Mazzocca et al. and Cho et al. reported that their patients had a decreased cardiac ejection fraction postprocedure4,11.
In our patient, the most likely mechanism of pulmonary edema was related to the circulatory stress imposed by high-pressure irrigation with normal saline solution in a short period of time. It is possible that the copious bleeding (a result of vessel compromise) provided an access route for the irrigation fluid, which quickly overwhelmed the circulatory capacity. Unlike the case reported by Mazzocca et al.4, our patient had neither preceding antecedent tachycardia nor postprocedure changes to cardiac function, which made us less likely to conclude that epinephrine was involved.
The excessive fluid inflow in such a short period supported rapid intravasation of fluid, which can cause pulmonary edema, independent of pump pressure or epinephrine. Vascular abnormalities could have contributed to rapid vascular fluid uptake. However, the magnetic resonance angiogram did not show any vascular abnormalities in the hip region.
Pulmonary edema resulting from orthopaedic arthroscopic procedures remains rare. The combination of epinephrine-infused irrigation fluid and pump-driven irrigation is essential in ensuring a bloodless field and clear visualization. In vitro studies have suggested that arthroscopic fluid containing a 1:3,000,000 concentration of epinephrine is less chondrotoxic than fluid containing a 1:300,000 concentration of epinephrine14. The use of higher concentrated epinephrine irrigation fluid is contraindicated in patients with preexisting heart conditions. Similarly, studies have shown a correlation between a patient’s diastolic pressure and the intra-articular fluid pressure required for joint distention15. The use of a gravity inflow system, or the use of a pump-driven arthroscopic irrigation system without a dedicated outflow tract, place the patient at increased risk of iatrogenic joint capsule damage and fluid extravasation. Combined with an excessive epinephrine concentration, excessive intra-articular pressures can result in fluid extravasation, circulatory compromise, or neurovascular damage.
In this case report, we describe a rare and potentially dangerous complication of high-pressure fluid irrigation in hip arthroscopy. It is important for orthopaedic surgeons and anesthesiologists to be aware of the causes, presentation, and complications of acute pulmonary edema in the operative and postoperative setting. Once pulmonary edema has been identified, it is important for the surgical team to maintain airway patency and start symptomatic treatment of the edema. Clear communication between members of the surgical team will prevent the patient’s condition from worsening acutely.
Disclosure: None of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of any aspect of this work. One or more of the authors, or his or her institution, has had a financial relationship, in the thirty-six months prior to submission of this work, with an entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. No author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the article.