Biphasic threat to femoral head perfusion in abduction: arterial hypoperfusion and venous congestion
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- Yousefzadeh, D.K., Jaramillo, D., Johnson, N. et al. Pediatr Radiol (2010) 40: 1517. doi:10.1007/s00247-010-1602-1
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Hip abduction can cause avascular necrosis (AVN) of the femoral head in infants.
To compare the US perfusion pattern of femoral head cartilage in neutral position with that in different degrees and duration of abduction, testing the venous congestion theory of post-abduction ischemia.
Materials and methods
In 20 neonates, the Doppler flow characteristics of the posterosuperior (PS) branch of the femoral head cartilage feeding vessels were evaluated in neutral and at 30°, 45°, and 60° abduction. In three neonates the leg was held in 45-degree abduction and flow was assessed at 5, 10, and 15 min.
Male/female ratio was 11/9 with a mean age of 1.86 ± 0.7 weeks. The peak systolic velocities (PSV) declined in all three degrees of abduction. After 15 min of 45-degree abduction, the mean PSV declined and showed an absent or reversed diastolic component and undetectable venous return. No perfusion was detected at 60-degree abduction.
Abduction-induced femoral head ischemia is biphasic and degree- and duration-dependent. In phase I there is arterial hypoperfusion and in phase II there is venous congestion. A new pathogeneses for femoral head ischemia is offered.
KeywordsFemoral head ischemiaAbductionAVNDoppler USVenous hypertensionChildren
Abduction treatment in infants with developmental hip dysplasia (DDH) can cause AVN of the femoral head [1, 2]. Femoral head ischemia can also occur in a variety of childhood disorders such as Legg-Perthes, sickle cell disease, steroid therapy, synovitis, and storage diseases.
Currently, childhood and adult AVN are thought to be caused by venous hypertension of the femoral head and secondary arterial hypoperfusion [3–18]. The cause of AVN in abduction treatment for DDH, however, is presumed to be the stretching of the medial circumflex artery (MCA)  or complete obstruction of the profunda femoris artery .
In previous studies, gadolinium-enhanced MR imaging after extreme abduction has shown femoral head ischemia and enhancement defects, presumably caused by arterial compression and obstruction . To the best of our knowledge, abduction-induced femoral head ischemia has not been linked to femoral head venous congestion and intracartilaginous venous hypertension. Because the draining veins always accompany the feeding arteries with a given magnitude of external pressure during abduction, the veins should occlude much sooner than the arteries because of their lesser vessel wall resistance and intraluminal pressure.
The purpose of this report is to compare the blood flow characteristics of the posterosuperior (PS) branch of the medial circumflex artery (MCA) in neutral position with the data obtained immediately after different degrees of hip abduction, and at different times after abduction.
Material and methods
Institutional review board approval and maternal consent were obtained and Health Insurance Portability and Accountability Act (HIPAA) regulations were observed. Volunteers were recruited from well-baby clinics and the neonatal nursery. The babies were bottle fed or nursed during the procedure; no sedation was used. No US contrast agents were used to enhance the Doppler signal or achieve greater visibility of the feeding vessels.
The chondroepiphyses of the proximal left femur in 20 African-American neonates, newborn to 11 weeks old, were prospectively studied and the flow characteristics of the posterosuperior (PS) branch of the MCA were evaluated. Only the spectral Doppler flow characteristics of the PS branch of MCA were studied because: (1) the PS branch is the most instrumental feeding vessel of the femoral head [19–21], (2) the PS branch and its accompanying draining veins are anatomically situated so that they are most adversely affected during abduction, and (3) the PS branch is the most sonographically accessible vessel that can be studied both in neutral and abduction positions.
In neutral position, linear transducers of 8–13 MHz of an Acuson Sequoia 512 unit (Mountain View, CA, USA) were used by a single radiologist. During abduction, occasionally a sector transducer was used because of better fit. The PSV, the width of the systolic base, the characteristics of the diastolic flow, and the venous return were evaluated in neutral position and at three abduction angles. Power Doppler study of the femoral head, neck, and the greater trochanter was evaluated to assess the effect of abduction on overall perfusion of the entire chondroepiphysis.
After obtaining baseline data at 0-degree angle abduction using a goniometer, the leg was flexed 90° and abducted 30°, 45°, and 60° and the flow characteristics of the same artery were recorded. In three babies, legs were held at 45-degree angle of abduction and flow pattern was evaluated at 5, 10, and 15 min.
In a single case the color Doppler scale settings were lowered to illustrate the draining veins that accompany the PS branch of the MCA. Last, the angles of the arcs at the periphery of the left femoral head cartilage, between the lower edge of the limbus and the entry point of the PS branch, were measured in two babies.
There were 11 boys and 9 girls with a mean age of 1.86 ± 0.7 weeks (range 0.1–11 weeks). Color and power Doppler imaging could illustrate the PS branch of the MCA in all 20 infants. For waveform analysis, the correction angle was <60-degrees in all cases.
Femoral head ischemia after abduction is presumed to have an arterial pathogenesis, either by stretching of the MCA during non-extreme abduction  or by complete occlusion of the profunda femoris with extreme abduction .
Similar to our US experience, MRI has shown that the severity of cartilaginous ischemia increases with both degree and duration of abduction . Using a piglet model with 70-degree abduction, segmental ischemia developed in 100% of the cartilaginous epiphyses and 85% of the physes. Marrow abnormalities were seen in 69% and the ischemia of the secondary ossification center was encountered in 56%. A smaller area of ischemia occurred in the posterior part of the femoral head and the opposing acetabular rim. Interestingly, no enhancement defects were seen if the abduction angle was less than 50º .
In the same piglet model,  angiographic studies showed that with extreme abduction, the profunda femoris artery becomes occluded completely, but not at a site where the MCA was presumed to be stretched . The site of complete obstruction appeared to be too proximal to explain a localized segmental ischemia of the femoral head. Nonetheless, the experiment supported the arterial obstruction pathogenesis for femoral head ischemia after abduction.
To the best of our knowledge, the role of venous congestion in post-abduction ischemia of the femoral head has not been explored, despite the fact that intraepiphyseal venous hypertension is believed to be the cause of femoral head AVN in disorders such as Legg-Perthes, sickle cell anemia, steroid therapy, septic arthritis, synovitis, and storage diseases [3–18].
The rationale behind the present study was that if it takes an extreme abduction of 70° or more to obstruct the main feeding artery and cause ischemia, then less extreme but prolonged abduction must have ill effects on the drainage of the veins that, as illustrated, accompany the PS branch of the MCA. After all, given an equal external compression force, the veins should collapse and obstruct much earlier than the arteries.
Although gadolinium-enhanced MR illustrates enhancement defects far better than US, our US study had unique advantages in elucidating the mechanism of ischemia.
The zone of the perfusion alterations on US was limited to the domain of the PS branch of the MCA, while the rest of the chondroepiphysis remained perfused. The segmental nature of enhancement defects on MRI and perfusion defects on US indicates that neither the theory of the obstruction of the main artery [1, 18] nor Ogden’s  theory of the stretching or compression of the MCA branch can fully explain the cause of the ischemia. If Ogden’s theory were correct, the domain of the posteroinferior (PI) branch of the MCA should not have remained normally perfused in our experiments.
In this study, Doppler US offers a biphasic pathogenesis for explaining femoral head ischemia after abduction. In phase I, immediately after abduction, decreased PSV and maintained diastolic flow indicates arterial compression. However, in phase II, 15 min after abduction, the systolic base narrows with needle-pointed PSV and abolished or reversed diastolic flow, and undetectable venous return. This indicates increased intracartilaginous impedance secondary to venous hypertension.
We believe that the greater MRI enhancement defects of the femoral head in the delayed phase, the abnormal marrow signal, and late recovery after cessation of abduction previously reported  might all be secondary to duration-dependant intracartilaginous venous hypertension, which could not have been recognized as a second phase of femoral head ischemia by MRI.
Therefore, the cartilage ischemia after abduction is caused first by arterial obstruction, followed by further reduction of arterial perfusion, this time because of intracanalicular epiphyseal venous hypertension. Doppler flow pattern in the immediate post-abduction period was identical to that described following compression of the feeding artery, i.e. dampening of the PSV with sustained diastolic flow . By 15 min and beyond, however, the Doppler pattern changed and signified increased tissue impedance and vascular bed resistance seen in venous hypertension.
On MRI experiments, enhancement defects were not seen in abductions <50° . However, the PSV declined from baseline values in our Doppler US experiments with abduction angles of 30° (P = 0.15) and 45° (P = 0.003). Furthermore, at 45-degree abduction, power Doppler demonstrated a perfusion defect in the domain of the PS branch of the MCA and at 60-degee abduction spectral Doppler did not detect any measurable flow.
Last, unlike our US observation, the MRI literature does not show the dominant perfusion role of the PS branch of the MCA and does not single out this artery as the main target of abduction’s ill effects.
Exactly what compresses the PS branch of the MCA and the accompanying draining veins has not been satisfactorily explained. Neither the theory of stretching or compression of the MCA in abduction  nor the complete obstruction of the profunda femoris [1, 18] explains the selective perfusion defects seen only at the domain of the PS branch of the MCA.
We believe that the compressing structure is the lower edge of the labrum ring. As demonstrated in neutral position, there is a safe but short distance between the lower edge of the labrum ring and the entry point of the PS branch. As the abduction rotates the femoral head counterclockwise, the entry point of the PS branch and the exit point of the accompanying veins will come in contact with and be compressed by the labrum edge. This fully explains both phases of arterial hypoperfusion and venous hypertension of the femoral head, selectively in the domain of the PS branch of the MCA in both our clinical Doppler US observations and prior MRI experiments.
In infants, avascular necrosis only develops with abduction greater than 55° . This is more compatible with prior MRI experiments than our current US observations. This might be because decreased perfusion by Doppler US precedes actual clinical tissue ischemia and enhancement defects by MRI. The perfusion void on power Doppler might represent current equipment limitations in detecting very low-velocity flow. It is true that by spectral Doppler, the blood flow markedly decreased at 45-degree abduction but never ceased to exist. Therefore, perfusion defects by power Doppler forecast impending tissue ischemia before it is well established.
In treating hip dysplasia, the practical challenge is to anticipate and choose an ideal angle of abduction that minimizes the risk of redislocation yet carries the lowest risk of developing avascular necrosis of the dysplastic and the normal hip . US-assisted measurement of the distance between the edge of the labrum and the point of entry of the PS branch might finally enable us to predict the safe angle of abduction before these two reference points come into contact with each other and compromise femoral head perfusion. According to our study, the least-threatening angle of abduction is 30°, followed by 45°. Sixty degrees of abduction inflicted the worst ischemia and should be abandoned.
One of the limitations of our study is that all US studies were performed by a single radiologist. This study constitutes preliminary research in a small number of newborns and a smaller number of those who could tolerate 15 min of abduction. The limiting factors were the IRB-imposed conditions, lack of the use of sedation, and no use of a contrast agent, as well as the inherent limitations of clinical investigations. Further studies in infants with hip dysplasia before and after abduction, perhaps assisted by the use of US contrast agents, are needed.
Doppler studies can successfully evaluate the blood supply to the femoral head cartilage in newborns and young infants without the use of US contrast agents or sedation. The perfusion defects of the femoral head cartilage can be demonstrated convincingly in varying degrees of abduction. The abduction-induced ischemia is in the domain of the PS branch of the MCA, with the rest of the femoral chondroepiphysis least affected. Decreased femoral head perfusion after abduction is biphasic, not monophasic as it was presumed to be. The structure that compresses the feeding artery and the draining veins might be the rim of the labrum. Doppler illustration of the cessation of blood flow during hip dysplasia treatment justifies cast adjustment with lesser degree of abduction; 30-degree abduction carries the lowest and 60-degree the highest regarding the threat of ischemia. Using US might enable us to predict how much abduction is safe before the two reference points come in contact with each other. Femoral head cartilage venous hypertension in abduction should be added to the list of childhood disorders in which AVN is believed to be caused by venous hypertension of the femoral head epiphysis.