Maternal Obstetric Palsy

Original Editor - Onigbinde Omotola Adam Top Contributors - Rosie Swift, Omotola Onigbinde, Kim Jackson and Sai Kripa

Introduction[edit | edit source]

Maternal obstetric palsy (also known as obstetric maternal palsy or obstetric maternal lumbosacral plexopathy) refers to an injury to the lumbosacral plexus resulting in neurological signs and symptoms that become evident during labor or after childbirth. This differs to obstetric palsy (also called Erb's Palsy) which involves brachial plexus injury of the infant during delivery.

Epidemiology[edit | edit source]

Research detailing the prevalence of maternal obstetric palsy is limited. Available evidence indicates that the condition is rare, with only a small population of women being affected[1][2]. Recent evidence suggests postpartum motor and sensory dysfunction has an incidence of 1%[3], but this figure does not distinguish the cause of dysfunction as due to labour analgesia or the intrinsics of labour. The condition is not well documented in textbooks[1].

It is worth noting that much of the research is from well-resourced settings where anaesthetics interventions to assist the labour process and medical interventions (such as caesarean section) to avoid prolonged labour are readily available. This condition appears to cross-over with obstetric fistula, where a prolonged second stage of labour (where accessing the appropriate medical intervention is difficult) results in the patient experiencing lower-limb neurological features along with vaginal fistula.

Risk factors[edit | edit source]

Risk factors vary depending on whether the cause of the dysfunction is attributed to labour analgesia or the intrinsics of labour.

  • Spinal anaesthesia over epidural anaesthesia[4]
  • Short stature[1]
  • Macrosomia (larger than usual size of foetus)[1]
  • Cephalopelvic disproportion[1]
  • Delayed/Prolonged labor[1]
  • Static position of the lower extremities during a prolonged second stage of labour[4]
  • Mid forceps rotation[1]
  • Fetal malpositioning[1]

Clinically Relevant Anatomy[edit | edit source]

Lumbar-plexus-and-its-branches.png

The lumbar plexus and sacral plexus, if taken as one entity becomes the lumbosacral plexus, the largest spinal nerve plexus. It consists of nerves originating from spinal segments L1 to S4, lumbar plexus taking its origin from L1 to L4 and sacral plexus from L5 to S4 respectively. Nerves arising from the lumbosacral plexus generally course behind the psoas major, piercing the abdominal wall antero-laterally, then course antero-medially, upon the pelvic rim or iliac crest to enter into the lower limb.

Mechanism of Injury / Pathological Process[edit | edit source]

A small number of cases of nerve damage following childbirth can be linked to the process of anaesthesia, with spinal anaesthesia having a greater incidence than epidural anaesthesia[4]. The neuraxial block can result in nerve damage by:

  • trauma - from the needle directly to the nerve fibres
  • chemical - from irritants such as contrast media, epidural steroids, detergents[4]
  • ishaemic - caused by pressure from the formation of a haematoma
  • infective - an abscess can lead to similar problems


However, the majority of maternal obstetric palsies are due to the mechanics of labour or foetal pressure on the nerves during labour.

The position of the lumbosacral plexus predisposes itself to compression during prolonged second stage of labour, especially in women who are of short stature with cephalopelvic disproportion. Neurological injury can be the result of mechanical trauma causing stretch, compression or transection of the nerve tissue. Additionally, a compromise of the blood supply may also cause injury to the nerve.

Injury to the lumbosacral plexus that is caused during labour or delivery will cause the mother to show clinical signs and symptoms that start during or after labour. The mother may experience autonomic and motor dysfunction, including impairment of the sensation of afferent pain, temperature, pressure, and proprioception.

Katirji et al. (2002) concluded that intrapartum foot drop occurs mostly in short women and is caused by lumbosacral trunk compression by the fetal head at the pelvic brim primary pathology being predominantly demyelination and recovery is complete in up to 5 months.[2]

The peroneal nerve is frequently affected. Hunerman (1892) attributed its frequency to its position in the lumbosacral plexus, although it has also been linked to prolonged positioning which compresses the nerve at the posterior knee joint, such as prolonged squatting or prolonged use of stirrups.[4]

Femoral or obturator neuropathy may also be observed, which causes dysfunction of the knee extensors, resulting in functional limitations such as not being able to climb stairs, decreased patellar reflex and femoral sensory loss. [4]

Types[edit | edit source]

Presentation of signs and symptoms and electro diagnostic studies have helped in differentiating lumbosacral plexopathy into sub-groups, including:

  1. Intrapartum maternal lumbosacral plexopathy: it involves the lumbosacral plexopathy easily recognized while the woman is in labour[2]
  2. Postpartum maternal lumbosacral plexopathy: this manifests after childbirth[5]


Electrodiagnostic studies further describes postpartum maternal lumbosacral plexopathy into Upper and Lower Lumbosacral Plexopathy.

  • Upper lumbosacral plexopathy - involves the muscles of the lower limb and affectation to motor and sensory functions, while, lower plexopathy only involves the lower part of the plexus (s2-s4).
  • Lower postpartum lumbosacral plexopathy - is evoked when perineal sensory disturbances, whether or not associated with urinary or faecal incontinence, persist after a history of a difficult vaginal delivery with no associated lower limb sensory or motor deficits noted.[5] "The first, second and third sacral roots entering into the formation of the sacral plexus lie on the piriformis muscle and are thus unprotected against pressure on the bone"[6]

Clinical Presentation[edit | edit source]

For the upper palsy:

  • pain
  • paraesthesia, sensory loss in the L‐5 dermatome
  • weakness of ankle dorsiflexion, eversion, and inversion causing foot drop


For the lower palsy:[5]

  • Perineal sensori-neuropathy
  • Urinary incontinence
  • Faecal incontinence
  • Sexual dysfunction

Diagnostic Procedures[edit | edit source]

A detailed subjective history should be taken from the patient, to include details of the labour process and any medical interventions.

Objective diagnostic procedures will depend on the signs and symptoms displayed.

Outcome Measures[edit | edit source]

Functional Outcome Measure Scale (see Outcome Measures Database)

Physiotherapy Management / Interventions[edit | edit source]

Differential Diagnosis[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Feasby TE, Burton SR, Hahn AF. Obstetrical lumbosacral plexus injury. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine. 1992 Aug;15(8):937-40.
  2. 2.0 2.1 2.2 Katirji B, Wilbourn AJ, Scarberry SL, Preston DC. Intrapartum maternal lumbosacral plexopathy. Muscle & nerve. 2002 Sep;26(3):340-7.
  3. Wong CA. Neurologic deficits and labor analgesia. Reg Anesth Pain Med. 2004.29: 341-51. Available from https://www.semanticscholar.org/paper/Neurologic-Deficits-and-Labor-Analgesia-Wong/ce7b4843cbd097b35f17fd066dfd755ffb7f2cec. [Accessed 11 Dec 2021]
  4. 4.0 4.1 4.2 4.3 4.4 4.5 Boyce H and Plaat F. Post-natal neurological problems. Continuing Education on Anaesthesia Critical Care & Pain. 2013;13:2,63-66. Available from https://academic.oup.com/bjaed/article/13/2/63/283709 [Accessed 2 Dec 2021]
  5. 5.0 5.1 5.2 Ismael SS, Amarenco G, Bayle B, Kerdraon J. Postpartum lumbosacral plexopathy limited to autonomic and perineal manifestations: clinical and electrophysiological study of 19 patients. Journal of Neurology, Neurosurgery & Psychiatry. 2000 Jun 1;68(6):771-3.
  6. Tillman AJ. Traumatic neuritis in the puerperium. American Journal of Obstetrics and Gynecology. 1935 May 1;29(5):660-6.