All the patients of the grade 1 and grade 2 were revived successfully, whereas none of the patients of the grade 3, could be revived. All patients in grade 1 and all patients of grade 2 except one sustained the event in intraoperative period just after the cementing and insertion of prosthesis.
In grade 3, out of the two patients, one sustained the event in intraoperative period i.e. during cementation, while the other patient sustained the BCIS episode after, 6 hours of the surgery. Thus total 11 patients had BCIS, intra-operatively during cementation and two had during the postoperative period.
Out of the 13 patients, 9 had fracture neck of femur and 4 had intertrochanteric fracture and none of the patients had a pathological fracture or bony metastasis. The mean preoperative cardiac output in these patients was 43.4 % (range 39 to 58). All patients had normal cemented bipolar prosthesis of 150 mm size length done in the previously unreamed femoral canal.
Discussion
Cemented hemi-arthroplasty is a routinely done procedure for fractures around the hip. Bone Cement Implantation syndrome (BCIS) is a rare fatal complication of cementation, which is highly underestimated and under-reported, as patients who die intra-operatively, are less likely to be reported [6]. Hence, there are not many case series or formal trials published on this topic and only few cases are only reported [1,3,6-8].
Further milder varieties of BCIS are not recognized at all or not systematically collected or published. Thus, due to this underreporting, there is lack of peer-reviewed literature available on this topic regarding incidence, accepted definition, clinical presentation and management recommendations. Hence we conducted this study to evaluate the incidence and risk factors associated with BCIS in 430 patients of cemented hemiarthroplasty done for patients of fracture around hip in a period of 5 years.
The aetio-pathophysiology of bone cement implantation syndrome (BCIS) is unknown with theories being proposed, like systemic toxic effects of methyl methacrylate, embolic episode, histamine release, complement activation, endogenous cannabinoid-mediated vasodilatation or combination of these, but none of them have been proven completely [9-12].
Patho-physiologically, the genesis of BCIS is high intramedullary pressure (often>300mmHg), generated by the expansion of exothermic sealed cement, between the prosthesis and bone, which forces “snow flurry”, which contain fat, marrow, cement particles, air, bone particles, and aggregates of platelets and fibrin into blood circulation.
The embolic snow flurry within the circulation causes mechanical and mediator release changes via histamine, complement activation, endogenous cannabinoids, vasoactive or pro-inflammatory substances, thrombin and tissue thromboplastin etc,
which manifests typical cardiovascular and hemodynamic changes of BCIS [2,9-14]. Numerous patient-related risk factors implicated in the genesis of BCIS include old age, male sex, osteoporosis, use of diuretics, poor preexisting physical reserve, impaired cardiopulmonary function, pre-existing pulmonary hypertension, patent foramen ovale, atrial-septal defect, bony metastases and concomitant hip fractures, particularly pathological or intertrochanteric fractures [2,3,6].
Patients with a previously un-instrumented femoral canal and long-stem hip arthroplasty appear to be associated with a higher incidence of BCIS [15]. We found in our series of 430 cases of cemented hemiarthroplasty, 13 sustaining BCIS, and BCIS was associated with high incidence in higher age, male gender and poor cardiac reserve patients.
Due to differences in patient’s risk factors, susceptibility and response and mediator based effect of BCIS, the degree of cardiovascular compromise is not necessarily proportional to the degree of the embolic load [16,17].
Hence there is wide spectrum of clinical presentation from milder transient hypoxia, hypotension or confusion to fulminant cardiovascular changes, which may proceed to arrhythmias, shock or cardiac arrest. Depending to SpO2 and fall in systolic pressure Donaldson proposed a severity classification, grading BCIS into three grade, grade 1 as moderate hypoxia (SpO2 <94%) or fall in Systolic blood pressure >20%, grade 2 as severe hypoxia (SpO2 <88%) or fall in Systolic blood pressure >40% and grade 3 having cardiovascular collapse which required CPR [2].
In our series, grade 1 BCIS was seen in 7 patients, grade 2 in 4 patients and grade 3 in 2 patients. First indication of clinically significant BCIS is fall in end tidal CO2 concentration with dyspnoea or altered sensorium, followed by hypoxia and hypotension [18].
Invasive hemodynamic monitoring like oesophageal doppler, intraoperative pulmonary artery catheter or transoesophageal echocardiography can detect impending BCIS at an earlier stage than standard hemodynamic monitoring, but they are not routinely used and where not used by us as well [3,6,8,17,18].
Since amount of debris present in the femoral canal is finite, BCIS is a reversible time-limited process with ceiling effect, which can recover within minutes, even from large embolic loads, if hemodynamic stability is maintained by supportive therapy [19].
The supportive management includes administration of 100% oxygen with airway control, aggressive fluid therapy resuscitation & avoid volume depletion, inotropics and vasopressors [2,6,8]. Prophylactic use of antihistaminics or steroids for treatment of cement embolism could not be found in the literature search [7].
With supportive treatment, we were able to revive all our grade 1 and grade 2 patients, but none of the grade 3 patients could be revived. Prevention of BCIS is better, and various intraoperative surgical measures can reduce the risk of BCIS.
