Several studies have evaluated the fracture rate in those with epilepsy. According to the study by Finelli and Cardi, fracture incidence was 1.1% in 2800 cases of seizures[2]. Among these, 0.3% of the fractures were directly associated with convulsive seizures and without additional trauma. Frey et al. analyzed 411 patients between 2007 and 2019 at epilepsy centers in Frankfurt and Marburg, where 6 patients sustained fractures with no obvious injuries[3]. Salas-Puig et al. observed 406 patients with generalized seizures; the rate of accidental fracture associated with generalized seizures was 3.9%[4]. A meta-analysis of 3145 articles on generalized convulsive seizures conducted by Grzonka P et al. screened 39 publications reporting on fractures in patients with convulsive seizures[5]. Their findings indicated that fracture is an uncommon complication of seizures, which was also the same stance of Michael Tan, who further stated that fractures are extremely rare in the absence of trauma[6].
Grzonka P et al. determined that bilateral posterior fracture-dislocations of the shoulder were the most common injuries and the incidence of bilateral femoral fractures was the lowest among all fractures following convulsive seizures. There is no mention about the incidence of pelvic fractures combined with femoral fractures[5]. Our case is an example of a rare Garden type III femoral neck fracture with Tile type B3 pelvic fracture caused by seizure activity. To the best of our knowledge, this is the first case of a non-traumatic, convulsive seizures -induced Garden type III femoral neck fracture and Tile type B3 pelvic fracture with dissociation of the symphysis pubis.
Most general epileptic seizures are electrically induced, although some metabolic diseases such as hypoglycemia or uremia may also be responsible[7]. Hypocalcemia caused by stage 5 CKD was thought to be the cause of this patient’s seizure. CKD is complicated by abnormalities in calcium and phosphorus metabolism, which worsens as the disease progresses. With worsening CKD, electrolyte disturbances in the body lead to a series of serious complications. Among them, disorders of calcium ion metabolism are closely related to bone mineral metabolism and abnormal muscle activity[8]. Hypocalcemia-induced neurological manifestations include tetany, seizures, and delirium, which indicate the important role of calcium in reducing the threshold for excitability in the central nervous system[9]. Our patient had stage 5 CKD with renal insufficiency that resulted in poor calcium homeostasis, thus increasing the chances of convulsive seizures compared to that in normal people[10]. The parathyroid hormone receptor (PTHR) exists in the renal tubule but the parathyroid hormone (PTH) is unable to bind to the receptor when the renal tubules are atrophied and non-functional. Calcium absorption is markedly reduced in the renal tubules. Hence, the calcium-conserving effects of PTH are not achieved and more calcium is excreted. The homeostasis of calcium and phosphate reabsorption is disrupted, resulting in hypocalcemia and hyperphosphatemia. In addition, another common biochemical manifestation is low 1,25-dihydroxyvitamin D levels[11].
O’Neill hypothesized that hypocalcemia occurs in the late stages of CKD[12], but altered mineral metabolism occurs much earlier, mainly as secondary hyperparathyroidism according the study of Levin[13]. The main reasons for this are decreased synthesis of osteotriol in the kidney, decreased serum calcium concentration, increased phosphate concentration, decreased bone sensitivity to PTH[14], and reduced calcium-sensitive receptors leading to hyperparathyroidism. Our patient was diagnosed with hyperparathyroidism, which in turn adversely affected bone remodeling, enhanced bone resorption but hindered bone mineralization, and ultimately decreased bone density that led to the occurrence of renal bone disease with weaker and more brittle bone. The potential risk for fractures is, thus, greatly increased. Furthermore, hyperphosphatemia inhibits 25-hydroxyvitamin D 1α-hydroxylase in the kidney, further reducing the synthesis of 1,25-dihydroxyvitamin D. Low levels of 1,25-dihydroxyvitamin D eventually exacerbate hyperparathyroidism indirectly through decreased intestinal absorption of calcium, leading to the formation of a vicious cycle.
Multifactorial etiologies induce fractures in patients with CKD[15]. If we evaluate the patient’s bone quality indirectly using peripheral quantitative CT or directly using bone biopsy, the histological features of renal osteopathy, comprising bone mass reduction, osteoporosis, or an increase in fibrous bone, may be found. Our patient's poor bone quality was noted during the operation. She neglected performing exercise and spent much time indoors with no exposure to sunlight, leading to loss of appetite; this could have led to the metabolic disorders. Ultimately, all of these accelerated the process of renal bone disease. Muscle groups such as the flexion muscles, the adductor muscles and the abductor muscles, their strong contraction resulted in simultaneous fractures of the right femoral neck, bilateral upper and lower pubic branches, and sacrum although she wasn’t strong (Fig. 3).
It should be noted, however, that the location, type, and cause of fractures like this are rare. The flexor, adductor, and abductor muscle groups and their strong contraction resulted in simultaneous fractures of the right femoral neck, bilateral upper and lower pubic rami, and right side of the sacrum despite our patient not being muscular.