Subacute proximal leg weakness after a minor traffic accident in a patient treated with anticoagulants

Abstract

One day after a minor accident, an 85-year-old man developed headache and proximal left leg weakness. He was on warfarin due to atrial fibrillation. On hospital admission, a right posterior parasagittal subdural haematoma that was visualised on CT was considered as cause of all symptoms. Although no surgical intervention was performed he stayed for 2 weeks in a neurosurgical ward. Clinical deterioration occurred within the first days as he was not able to stand on his left leg or rise up from the sitting position. Headache had ceased, but the patient reported low abdominal pain. This condition remained stable for over 2 months although haematoma size decreased significantly. He was then examined for the first time by a neurologist who documented typical clinical features of femoral nerve palsy. Pelvic CT established the diagnosis of traumatic iliacus- and iliopsoas-muscle haematoma under anticoagulants as cause of subacute femoral mononeuropathy.

Background

This report underlines the importance of detailed clinical examination of patients with acute neurological deficits and shows that relying solidly on imaging findings may lead to wrong diagnostic conclusions and therapeutic decisions.

A proximal leg weakness due to an easy to diagnose peripheral nerve lesion, namely femoral mononeuropathy, was erroneously attributed to a traumatic subdural haematoma in a patient who was already treated with anticoagulants. The only plausible explanation is that the colleagues in the emergency room focused on the reported minor head trauma and the presence of a subdural haematoma on CT. They obviously failed to determine the discrepancy between the haematoma localisation and the clinical features. They probably did not examine the patient thoroughly and this might explain how the typical motor and sensory deficit of peripheral nerve palsy was overseen, leading to the assumption of a subacute cerebral lesion on the grounds of a traumatic subdural haematoma as cause of headache and leg paresis. Moreover, no attention was given as further neurological deterioration and low abdominal pain occurred after the initial headache had already ceased. This symptom constellation clearly questions the initial diagnosis of subdural haematoma and should have led to diagnostic re-evaluation.

We strongly believe that this case report gives an important clinical lesson that helps learning from mistakes.

Case presentation

An 85-year-old man, with atrial fibrillation treated with warfarin, was hit by a bicycle and fell on the ground. Since no serious injuries were noted, he just walked home. However, 1 day later he reported slight headache and had difficulties when walking and climbing stairs because of proximal left leg weakness. On hospital admission, a few hours later a brain CT-scan revealed a posterior parasagittal subdural haematoma on the right side (figure 1A), which was at this point considered by the neurosurgeons as cause of his symptoms. The INR-value at this point was 2.4. Although the patient was transferred to the neurosurgical ward no surgical intervention was performed. Oral anticoagulation was stopped and thrombosis prevention with low-molecular-weight heparin was started. Within the following 2 days his condition worsened significantly as he was no longer able to rise up from the sitting position or stand on his left leg. He also reported low abdominal pain while the initial headache had already ceased. As expected the subdural haematoma was practically resolved within the next 2 months (figure 1B). However, his condition remained the same without any clinical improvement. At this point the patient was examined for the first time by a neurologist. On detailed examination, typical motor and sensory deficits indicative of proximal femoral nerve palsy were documented. Severe weakness of the left quadriceps and iliopsoas muscles (MRC 2/5) and hypoesthesia of the lateral and anterior thigh were documented. The history of a fall on the ground under effective anticoagulation allowed the assumption of a retroperitoneal hematoma affecting the proximal portion of the femoral nerve. An abdominal and pelvic CT-scan verified the clinical diagnosis by demonstrating a large haematoma of the left iliacus and iliopsoas muscles, which obviously compressed the left femoral nerve (figure 2).

Figure 1.

(A) Brain CT-scan performed during hospitalisation (A) showing a right parasagittal subdural haematoma. (B) Follow-up examination 8 weeks later showing a residual hygroma while no clinical improvement was documented.

Figure 2.

Pelvic CT image showing left iliacus and iliopsoas muscle haematoma.

Investigations

In the acute setting, a CT scan of the brain was performed. Based on the history of trauma, oral anticoagulant intake and subacute neurological symptoms this radiological examination was fully justified. However, the above mentioned imaging findings were erroneously considered as cause of symptoms. A detailed neurological examination at the time of hospital admission would have been sufficient to distinguish between a central and a peripheral nervous system lesion. This way the diagnosis of femoral mononeuropathy would be clinically established, a cerebral lesion could safely be excluded as cause of symptoms. However, this obviously failed because no trained neurologist examined the patient in the emergency room.

Further neurological diagnostics with conduction studies and electromyography would have only been useful for excluding the differential diagnostic alternatives of L3 and L4 radicular lesions. In the present case and based on the typical clinical findings that strongly suggest proximal femoral nerve palsy we strongly believe that both these investigations are not necessary. The patient’s history that includes oral anticoagulation and a recent accident with a fall on the ground allows the assumption of a retroperitoneal haematoma. Therefore, a pelvic CT or MRI scan was urgently warranted in order exclude such a space occupying lesion and assist therapeutic decisions. Unfortunately, such an imaging investigation was performed with a delay of 2 months when was simply too late for any discussion about possible therapeutic alternatives.

Differential diagnosis

An L3 or L4 radiculopathy should be considered as the most important differential diagnosis, where slight differences regarding motor findings, sensory distributions and pain location play a key role in distinguishing between such root lesions and an isolated femoral nerve palsy. However, when considering the details of the patient’s history, namely warfarin intake, fall on the ground, subacute onset of symptoms, gradual worsening and low abdominal pain, we believe that the above mentioned clinical features strongly support the diagnosis of a proximal femoral nerve entrapment and practically provide no arguments to further search for signs of L3 or L4 radiculopathy by means of electromyography, conduction studies or imaging of the lumbar spine.

Treatment

Current evidence regarding femoral neuropathy due to iliacus haematomas and its treatment relies on a limited number of case reports.^1–8 Complete or partial recovery after surgery has been reported.^1–6 However, there are other reports describing good recovery with non-operative management.^{7 8} The limited available data do not allow safe conclusions and guidelines regarding optimal treatment of femoral neuropathies caused by traumatic iliacus hematoma. Factors such as progression of the neurological deficit and haemodynamic stability might be considered when deciding for or against surgery in the acute setting of such uncommon cases.

Outcome and follow-up

Under physical therapy the patient’s condition improved slightly within the next 4 months. He is now able to stand alone without support. However, walking is still substantially handicapped.

Discussion

Femoral neuropathy is uncommon and mostly related to compression or trauma that leads to local nerve ischaemia as result of iliacus compartment syndrome.^1–8 Haematoma is the most frequent iliacus muscle lesion and is considered as major complication of anticoagulant treatment and haemophilia.² In such expansive compressing lesions femoral nerve deficits may develop quit fast imitating acute cerebral syndromes.³ In the present case, the patient was initially not thoroughly examined. This way the prominent imaging findings were overrated leading erroneously to the diagnosis of subdural haematoma as cause of proximal leg weakness. This could have been avoided if a trained neurologist had examined the patient in the emergency room. That way the discrepancy between cerebral lesion location and clinical features would have been noted early. The exact description of all clinical findings would have been sufficient to set the correct topographic diagnosis in time allowing further focused diagnostics and eventually therapeutic interventions.

Learning points.

• Detailed clinical neurological examination is warranted in all patients presenting with acute or subacute neurological symptoms.

• Diagnostic conclusions cannot rely solidly on imaging findings.

• Further evaluation and reconsideration is needed when discrepancies between imaging and clinical findings arise.

• Intracranial haematoma and pelvic haematoma affecting the femoral nerve can cause subacute proximal leg weakness in patients with trauma who are treated with anticoagulants.