Femoral vein catheterization is often used in resuscitation and in critical care units. Although long-term complications, such as deep vein thrombosis or catheter-related sepsis, may be major concerns, serious acute complications are uncommon after this procedure. We report an uncommon complication, femoral nerve palsy, after a commonly used procedure in the critical care unit.
A 51-yr-old man was admitted to the intensive care unit (ICU) because of severe heat stroke. He was hypotensive, unconscious, and had a core temperature of 42°C when he was admitted. He quickly developed rhabdomyolysis, coagulopathy (platelet count 30 × 109/L, international normalized ratio 3.5, activated partial thrombin time 80 s), acute renal failure, and circulatory failure. Mechanical ventilation, sedation, and the administration of inotropic drugs were commenced. Blood components, including platelet concentrate, cryoprecipitate, and fresh-frozen plasma, were administered to prevent bleeding. Continuous venovenous hemodiafiltration (CVVHD), without the use of an anticoagulant, was used as renal replacement therapy. Before attempting to cannulate the femoral vein, 6 U of fresh-frozen plasma and platelet concentrate was administered, and the coagulopathy was partially corrected after the blood component transfusion (platelet count 75 × 109/L, international normalized ratio 1.8, activated partial thrombin time 54 s). Using the Seldinger technique (1), the right femoral vein was identified just medial to the femoral artery with a 16-gauge needle. Resistance was felt when a guidewire was passed through the needle. The femoral vein was not reentered during a second attempt, and the procedure was abandoned. The right groin was compressed for 20 min to prevent hematoma formation. The femoral artery was not punctured during the procedure, and no external hematoma was visible over the right groin after the procedure. The left femoral vein was cannulated instead for the CVVHD.
Seven days after the procedure, the patient regained consciousness, was able to communicate with the medical staff, and complained of right thigh numbness and weakness. A neurological examination revealed inability to flex the right hip and extend the right knee, absence of knee jerk reflex, and sensory deficit over the anteromedial thigh. A nerve conduction study confirmed the presence of right femoral nerve palsy. A contrast-enhanced abdominopelvic computed tomography (CT) scan was performed 10 days after the femoral vein puncture and showed that the right iliopsoas muscles were markedly swollen from the level of L3 to the level at the caudal aspect of the sacroiliac joints (Figure 1). The anteroposterior and transverse diameters of the right iliacus muscle were 4.2 and 8.4 cm, respectively. The common femoral and iliac arteries were well opacified, without intraluminal filling defects or external compression. The findings were compatible with a partially resolved right iliopsoas hematoma. The patient slowly recovered and could walk unaided after another 4 wk. A repeated abdominopelvic CT scan was performed 4 wk after the femoral vein puncture and showed that the right iliopsoas hematoma had resolved further and that the maximal diameter of the right iliacus muscle was 2.8 cm.
Although long-term complications such as deep vein thrombosis or catheter-related sepsis may be major concerns, serious acute complication are uncommon after femoral vein catheterization (2), and femoral nerve palsy after this procedure has not been previously reported.
The femoral nerve is supplied by the second to fourth lumbar nerve roots and provides motor innervation to the quadriceps, sartorius, pectineus, and iliopsoas. It supplies sensory innervation to the anteromedial thigh and medial leg. The nerve lies in the groove between the iliacus and psoas muscles, which form a common tendon inserting into the lesser trochanter of the femur (3). Femoral nerve palsy has been reported after acetabular fracture, cardiac catheterization, or anterior lumbar spinal fusion, and spontaneously in hemophilia (3–6). The entrapment of the femoral nerve by an iliopsoas hematoma is the most likely cause of the femoral nerve palsy (3,7).
Although an external hematoma may not be apparent, retroperitoneal hematoma can occur in 0.15% of patients after femoral artery cannulation and can result in ipsilateral femoral nerve palsy (7). The presence of severe coagulopathy or systemic anticoagulation and a high femoral arterial puncture increases the risk of hematoma formation (7,8). In our patient, the iliopsoas hematoma could have occurred spontaneously from the severe coagulopathy, as the iliacus swelling was limited distally to the caudal aspect of the sacroiliac joint. However, the difficult catheterization of the right femoral vein was also a probable precipitating cause. The failure to pass a guidewire through the needle suggested that the needle might have transfixed the vein. Anatomically, the femoral artery lies anterior to the iliopsoas muscle and the femoral vein lies anterior to the pectineus muscle. This may explain why iliopsoas hematoma is uncommon after femoral vein puncture, compared with femoral artery catheterization. However, an overpenetrating needle, especially if directed more laterally, can still damage the iliopsoas muscle during femoral vein catheterization. An insidious IM bleed caused by the needle injury, compounded by the coagulopathy, can result in an iliopsoas hematoma without causing any external swelling. The hemorrhage might also have occurred within the pectineus muscle, when it was damaged by an overpenetrating needle. It is unknown whether hemorrhage within the pectineus muscle could have spread to the iliopsoas muscle.
Conscious patients may complain of lower abdominal pain and neurological symptoms in the lower extremity when the femoral nerve is compressed. The iliopsoas hematoma, being invisible externally, delayed the presentation of this complication in our patient until he regained consciousness and started to mobilize. An earlier diagnosis is possible with a high index of suspicion and a low threshold for performing an abdominopelvic CT scan in such a patient. Although surgical decompression has been suggested in this situation to reduce the neurological damage (7), this may not be advisable or feasible in a critically ill patient. Conservative management, including correction of coagulopathy, active knee and hip movement, and maintaining the hip in the flexed position, has been reported to produce satisfactory results (3). Our patient also had complete neurological recovery with conservative management. The lack of contrast enhancement of the swollen iliopsoas muscle and its spontaneous resolution without specific therapy make the diagnosis of iliopsoas abscess unlikely in our patient.
In conclusion, in the presence of severe coagulopathy, iliopsoas hematoma may occur after femoral vein catheterization when the iliacus muscle is punctured, resulting in femoral nerve palsy. An early diagnosis of this complication can be difficult in critically ill and unconscious patients. A high index of suspicion of this complication is recommended when femoral venous catheterization is performed in a patient with severe coagulopathy. Complete correction of the preexisting coagulopathy before the procedure, avoiding multiple attempts, and transfixing the femoral vein during the procedure may help to reduce the risk of this uncommon complication.
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