Anaphylactic shock during cement implantation of a total hip arthroplasty in a patient with underlying mastocytosis: case report of a rare intraoperative complication

BCIS has been observed in prosthetic hip surgery for many years, and is still not fully understood. A severity classification has been proposed; grade 1: moderate hypoxia (SpO2,94 %) or hypotension [fall in systolic blood pressure (SBP) .20 %], grade 2: severe hypoxia (SpO2 ,88 %) or hypotension (fall in SBP .40 %) or unexpected loss of consciousness, and grade 3: cardiovascular collapse requiring cardiopulmonary resuscitation [1]. In our case a grade 2 BCIS occurred after cementing the acetabular component; systemic blood pressure drop more than 30 % and severe hypoxia (saturation 80 %). The patient recovered in 15 min after rapid fluid induction, 100 % oxygen administration, and vasoconstrictive drug therapy. He did not lose consciousness, did not develop angioedema or an urticarial rash, and remained hemodynamic stable with blood loss not more than expected after elective hip surgery. All our eligible patients receive cemented acetabular components during total hip surgery. Nationwide registry shows better performance of cemented cups over uncemented cups [7]. Also less damage to the acetabular host bone with a cemented component during future revision surgery is to be expected [8]. Acetabular pressure rises after cup placement, especially during cementation, and an average of 375 mmHg has been reported [9]. As a consequence extrusion of bone marrow content with diffuse microembolism of the lungs may occur. In our case pulmonary fat embolism was excluded; there were no signs of breathing abnormalities during physical examination, only a short period of hypoxia occurred, and no electrocardiography or cardiac ultrasound abnormalities were encountered. Normovolemic hypotension without angioedema or rash may also be caused by an anaphylactoid mechanism observed in mastocytosis [6]. Recently our patient was diagnosed with systemic indolent mastocytosis through an iliac crest biopsy. Anaphylaxis in mastocytosis can be either IgE-mediated or non IgE-mediated, such as those experienced with nonsteroidal anti-inflammatory drugs or muscle relaxants. In our hospital all primary THA patients undergo a standardized anesthesia, analgesia and perioperative program to enhance recovery. Low dose bupivacaine and a multimodal opioid-sparing regimen facilitate early mobilization and allow rehabilitation to be initiated a few hours postoperatively. Our patient received intravenous nonsteroidal anti-inflammatory drugs at least one hour preoperatively, and no muscle relaxants were given. The acute response after cement application suggests a reaction on polymethylmethacrylate (PMMA) bone cement. Earlier, PMMA mediated histamine release with increased plasma histamine concentrations after bone cement implantation in the femoral shaft has been described [4]. More recent hypersensitivity to PMAA following joint replacement has also been reported [10, 11]. Krüger et al. described a patient with mastocytosis who underwent kyphoplasty for multiple osteoporotic vertebral fractures using radiopaque calcium phosphate bone cement under antihistamine and prednisolone coverage [12]. Arterial hypotension was encountered that transiently required vasopressor support. The critical threshold of intramedullary pressure that causes fat embolism is unclear, but pressure peaks as great as 300 mmHg were found to produce significant bone marrow release [13]. Intravertebral pressure during kyphoplasty, however, is substantially lower, and remains well below 300 mmHg [14]. A pressure-induced mast cell degranulation mechanism seems more suitable. Although rare an allergic reaction to calcium phosphate cement has been noted in skull reconstruction [15]. Even severe hypoxia with ventricular failure as a sign of possible aggregate anaphylaxis has been seen after formation of intravenous calcium phosphate precipitant [16]. Therefore, it seems more likely that Krügers’ observation and our case highlight the capacity of bone cement to trigger a disproportionate display of mast cell activity in mastocytosis patients with a BCIS response as a result. The use of corticosteroids has been advised to prevent anaphylaxis in patient with mastocytosis. In both patients corticosteroids were administered before intervention, which did not prevent BCIS unfortunately.