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Peripheral nerve ischaemia after internal iliac artery ligation
  1. R K SHIN,
  1. Department of Neurology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia
  2. PA 19104–4283, USA
  3. Department of Radiology
  1. Dr R K Shin shirobk{at}
  1. Department of Neurology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia
  2. PA 19104–4283, USA
  3. Department of Radiology
  1. Dr R K Shin shirobk{at}

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Ligation of the internal iliac (hypogastric) arteries has been used to control serious obstetric and pelvic bleeding. It is generally well tolerated in the young obstetric or gynaecological patient, presumably because of an extensive collateral blood supply.1-3 Acute lumbosacral plexopathies have been described, however, in older patients with vascular disease when the internal iliac arteries are interrupted.4-8 We report on a teenage patient with similar peripheral nerve ischaemia after bilateral internal iliac artery ligation for postpartum haemorrhage.

An 18 year old woman presented at 40 weeks gestation with mildly raised blood pressures, trace proteinuria, oliguria, and generalised oedema. She was diagnosed with pre-eclampsia and admitted for induction. When induction was unsuccessful, she underwent a caesarean section, which was complicated by uterine atony and a postpartum haemorrhage with an estimated blood loss of 2500 ml. After bilateral uterine artery ligation failed to control the bleeding, bilateral internal iliac artery ligation was performed with resultant haemostasis.

On the first postoperative day, she complained of left buttock pain and difficulty moving her left leg. Superficial skin breakdown over the sacrum and buttocks was noted on the second postoperative day. She developed a fever and fundal tenderness on day 4. Helical CT of the abdomen and pelvis disclosed residual gas and fluid within the endometrial canal consistent with endometritis, which was treated with intravenous antibiotics. No retroperitoneal haematoma was present. Neurological evaluation on the fifth postoperative day was limited by pain but disclosed normal strength, sensation, and reflexes in the arms and the right leg. Strength in the left leg was 2 to 3/5 on hip flexion and knee extension and 3 to 4/5 on ankle plantarflexion, ankle dorsiflexion, and toe extension. Sensation was diminished to all modalities in the entire left leg below the hip. The left patellar and ankle stretch reflexes were absent.

Magnetic resonance imaging of the thoracolumbar spinal cord was unremarkable. An initial magnetic resonance angiogram (MRA) of the pelvis showed segmental occlusions of both internal iliac arteries with distal reconstitution greater on the right than on the left. The left superior gluteal artery was not visualised. Revascularisation was considered but deferred due to the concomitant active pelvic infection. Peripheral pulses remained strong, and Doppler ultrasound of both legs showed no evidence of distal thrombus.

Nerve conduction studies 1 week after ligation were extremely limited and difficult to interpret due to generalised oedema. Sural and peroneal sensory responses were absent bilaterally. Right peroneal and left tibial motor responses were normal. A small left peroneal motor response was present in the anterior tibilais muscle. Electromyography was not performed at that time.

The fevers and endometritis gradually cleared, and over the next month left leg strength improved slowly, but incompletely, with greater proximal (4–5 in hip flexion and knee extension) than distal (2–3 in ankle plantarflexion, 0 in ankle dorsiflexion) recovery. The left leg continued to have diminished sensation to all modalities and remained areflexic. The superficial skin necrosis progressed to an open non-healing ulcer 7 cm×5 cm over the sacrum and left gluteal musculature. Magnetic resonance imaging of the region disclosed additional tissue necrosis subcutaneously along the left posterolateral buttock and inflammation in the surrounding subcutaneous tissues and underlying gluteal musculature with extension into the left sacroiliac joint. There was no evidence of rectal, uterine, or bladder ischaemia.

A follow up MRA of the pelvis 6 weeks after ligation demonstrated persistent segmental occlusion of both internal iliac arteries and less collateral flow on the left compared with the right. Again, the superior gluteal artery was not visualised on the left but appeared to fill on the right.

Electromyography of selected muscles of the left leg at that time (6 weeks after ligation) showed 2+ to 4+ fibrillations and positive sharp waves in the vastus lateralis, tibialis anterior, and lateral gastrocnemius muscles, consistent with acute denervation. There were no voluntary units in the tibialis anterior and low firing rates in the gastrocnemius. Low amplitude polyphasic motor units in vastus lateralis suggested early proximal recovery. Nerve conduction studies showed diminished left sural sensory amplitudes and slowed velocities (2.8 μV, 36.0 m/s). The left peroneal motor responses were markedly attenuated, and the left posterior tibial motor velocities were slowed (32.0 m/s). The right sural sensory (13.2 μV, 42.0 m/s) and peroneal motor (2.3 mV, 46.0 m/s) responses were normal.

In general, the internal iliac artery divides into an anterior and a posterior division. The anterior division is formed by the inferior gluteal artery and its branches, which supply the pelvic viscera, the lower buttocks, and the back of the thigh. The posterior division is formed by the superior gluteal artery and its branches, which supply the gluteal musculature, the femoral nerve, and the sciatic nerve roots.9

Ligation of the internal iliac arteries has been accepted as a safe and effective means of controlling serious haemorrhaging from the uterus or lower pelvis after delivery or after gynaecological surgery.1-3 The lack of ischaemic complications from ligation of the internal iliac artery is thought to be due to the multiple sources of collateral blood flow present in the pelvis.

There are, however, reports of buttock ischaemia or lumbosacral plexopathies as a complication of interruption of the internal iliac arteries during aortic bypass procedures or aortoiliac aneurysm resection.4-5 In a study of 11 patients (mean age 67, range 53 to 87) with aortoiliac occlusive disease or aortoiliac aneurysmal disease, seven developed ischaemic injury to the lumbosacral plexus after bilateral internal iliac artery ligation.6 In four of those patients, buttock necrosis with extension to the bony pelvis was also seen. In another report, four women (mean age 37, range 33 to 47) with insulin dependent diabetes and end stage renal disease developed ipsilateral lumbosacral plexopathies when the internal iliac artery was ligated during kidney transplantation.7Electromyography showed denervation of the tibialis anterior, gastrocnemius, and vastus medialis in one patient and of the tibialis anterior and gastrocnemius in another. Ischaemia of the sciatic and femoral nerves and buttocks also occurred after internal iliac artery embolisation in patients with terminal pelvic malignancies who received radiotherapy.8

Our 18 year old patient developed a combination of leg weakness, leg numbness, and buttock necrosis after internal iliac artery ligation, as described in older vasculopathic patients. In the patients described in the literature, as in our patient, the clinical and electromyographic findings do not distinguish between combined femoral and sciatic nerve lesions, a lumbosacral plexopathy, or a combination of the two. Our patient's presentation, however, can be most succinctly explained by an infarction in the territory of the left superior gluteal artery and its branches, resulting in ischaemia to the gluteal musculature, the femoral nerve proper, and the sciatic nerve roots. This localisation is supported by serial MR angiograms of the pelvis in which the left superior gluteal artery and its branches were not visualised.

It has been shown that, in experimental ligation of the internal iliac artery of rats, moderate ischaemia is associated with demyelination, whereas severe ischaemia produces wallerian degeneration.10 In our patient, the reduction in the left sural sensory amplitude and slowing of the left sural sensory and posterior tibial motor conduction velocities were more consistent with axonal degeneration than demyelination, implying a significant degree of injury.

Our patient had no pre-existing vascular risk factors that would have predisposed her to ischaemic complications, but possible contributing factors in her case include pre-eclampsia, prior bilateral uterine artery ligation, and postpartum endometritis. Pre-eclampsia is associated with changes in the renin-angiotensin-aldosterone axis, an increased thromboxane to prostacyclin ratio, and an increase in plasma endothelin.11 These factors result in vasoconstriction and platelet aggregation, which could interfere with pelvic collateralisation. The ligation of both uterine arteries before the internal iliac artery ligations may have reduced pelvic collateral flow. Postpartum pelvic infections can also alter vascular tone or extend to involve ovarian and pelvic vessels, potentially interfering with collateralisation.12

In summary, although internal iliac artery ligation is generally well tolerated because of multiple collateral sources of blood supply, complications such as peripheral nerve injury and necrosis of the gluteal musculature can occur. Although this occurs most commonly in patients with severe aortoiliac vascular disease or vascular risk factors such as insulin-dependent diabetes mellitus or radiotherapy treatment, it can occur even in their absence.


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