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Post-calving paralysis

ISSN 2398-2993

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Synonym(s): dystocia calving obturator sciatic down nerve damage lower motor neurone dysfunction

Introduction

  • Post-calving paralysis describes a spectrum of neuromuscular damage of traumatic origin.
  • Cause: traumatic nerve damage during calving, usually associated with an oversized calf or prolonged second stage labor.
  • Signs: signs of lower motor neurone dysfunction which varies depending on nerves involved and severity of trauma.
  • Diagnosis: diagnosis is based on presenting signs, clinical history and careful clinical examination to rule out differential diagnoses.
  • Treatment: casualty slaughter is an option if prognosis deemed poor. Intensive nursing care is the mainstay of treatment +/- non-steroidal anti-inflammatory drugs. Unilaterally affected animals should be housed with soft bedding which provides plenty of grip. Recumbent animals require regular turning to minimize pressure myopathy.
  • Prognosis: very variable and difficult to predict. Neuropraxia generally takes around 3 weeks to resolve, but is very difficult to differentiate from permanent damage.

Age predisposition

  • All ages.
  • Heifers have been shown to be more prone to sciatic nerve damage than multiparous dams following calving.

Public health considerations

  • Animals are fit for casualty slaughter if no withdrawal periods in place and prognosis is deemed poor.

Cost considerations

  • Cost of treatment is very low as it mostly involves nursing care.

Pathogenesis

Etiology

  • Direct pressure on the obturator nerve or sixth lumbar nerve route within the maternal pelvis.
  • Caused by oversized calf or a calf that is stuck in the pelvis.

Predisposing factors

  • Oversized calf.
  • Prolonged calving.
  • Calf becoming hip-locked.
  • Small narrow maternal pelvis.

Pathophysiology

  • Within the pelvis, the obturator nerve runs along the medial shaft of the ileum, and the sixth lumbar nerve route runs ventral to the sacral ridge.
  • These nerves are vulnerable to compression during calving.
  • Compression -> ischemia -> inflammation and edema -> +/- permanent structural damage to neurons.
  • Compression can be direct and acute (the calf) or indirect and chronic (inflammation of surrounding tissues). Often a combination of both is seen.

Timecourse

  • Lower motor neurone dysfunction is seen immediately after calving.
  • If temporary neuropraxia, clinical signs gradually improve over the course of around 3 weeks.

Epidemiology

  • Occurs sporadically.
  • Selection of bull breed and individual variation can affect the likely size of the calf.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Rees G M (2015) Postpartum emergencies in the cow. In Practice 38 (1), 23-31.
  • Huxley J (2006) Assessment and management of the recumbent cow. In Practice 28, 176-184.
  • Burnett M G & Zager E L (2004) Pathophysiology of Peripheral Nerve Injury: A Brief Review. Neurosurgical Focus 16 (5), PubMed.
  • Divers T J (2004) Acquired spinal cord and peripheral nerve disease. Vet Clin North Am 20, 231-242 PubMed.
  • Cox V S & Beazile J E (1973) Experimental bovine obturator paralysis. Vet Rec 93, 109-110 PubMed.

Other sources of information

  • Noakes D (2009) Arthur’s Veterinary Reproduction and Obstetrics. 9th edn. Saunders Elsevier.