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LETTER TO EDITOR
Year : 2019  |  Volume : 63  |  Issue : 1  |  Page : 75-76  

Transient isolated unilateral oculomotor nerve palsy following accidental dural puncture after bilateral total knee replacement


1 Department of Anaesthesiology, Sakra World Hospital, Bengaluru, Karnataka, India
2 Department of Orthopaedics, Sakra World Hospital, Bengaluru, Karnataka, India

Date of Web Publication10-Jan-2019

Correspondence Address:
Dr. B G Arun
Department of Anaesthesiology, Sakra World Hospital, Bengaluru - 560 103, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ija.IJA_604_18

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How to cite this article:
Arun B G, Puttaswamygowda C, Kulkarni A. Transient isolated unilateral oculomotor nerve palsy following accidental dural puncture after bilateral total knee replacement. Indian J Anaesth 2019;63:75-6

How to cite this URL:
Arun B G, Puttaswamygowda C, Kulkarni A. Transient isolated unilateral oculomotor nerve palsy following accidental dural puncture after bilateral total knee replacement. Indian J Anaesth [serial online] 2019 [cited 2019 Jan 20];63:75-6. Available from: http://www.ijaweb.org/text.asp?2019/63/1/75/249791



Sir,

Combined spinal epidural anaesthetic technique is used commonly for bilateral total knee replacement. Accidental dural puncture is a known complication of epidural needle placement with incidence of 0.19–3.6%.[1] Cranial nerve palsy is a rare complication of dural puncture. Abducens nerve palsy following dural puncture has been reported.[2] We report a rare occurrence of transient oculomotor nerve palsy after an accidental dural puncture. The patient has reviewed the case report and has given written consent for the authors to publish the report.

A 53 year old lady with no comorbidities was posted for bilateral total knee replacement surgery. Her preoperative investigations were normal. Combined spinal epidural technique was planned with needle through needle technique using 18 G epidural Tuohy's needle and 29 G Whitacre spinal needle. There was a dural puncture with the epidural needle with loss of resistance to air technique in the first attempt at L3–L4 space in the sitting position. Second attempt was successful in L2–L3 space. 3 ml of 0.5% bupivacaine heavy was injected intrathecally through the spinal needle. 8 ml of 2% lignocaine with adrenaline was given epidurally after 3 hours. She was haemodynamically stable throughout the surgery. Postoperative analgesia included continuous epidural infusion of 0.1% bupivacaine and 2 μg/ml of fentanyl at 5 ml/hr through elastometric pump.

On the first postoperative day, she complained of blurred vision in the right eye. There was no headache, tinnitus or vomiting. On examination, she had ptosis of the right upper eye lid, right anisocoria of 2 mm sluggishly reacting to light, limitation of adduction and infraduction of right eye indicating oculomotor nerve palsy [Figure 1]. There was no papilloedema. Neurological examination of other cranial nerves, higher mental functions, motor and sensory systems were normal. Magentic resonance imaging (MRI) of the brain was normal. Immunological markers for various immunological disorders were negative. Thyroid function tests were normal. Intravenous steroid (methylprednisolone 250 mg bd) was used to decrease neural oedema. On second postoperative day, pupils were of equal size and extra ocular movements were normal. There was persistent mild ptosis of right eye [Figure 2]. On third postoperative day, she complained of bilateral frontal headache which aggravated in the sitting position and decreased in the recumbent position, characteristic of post-dural puncture headache (PDPH). She was treated conservatively with bed rest, plenty of fluids, analgesics and oral steroids. Headache subsided completely in next 48 hrs. Right eye ptosis resolved completely over next 1 week.
Figure 1: Postoperative day 1 showing ptosis of right eye

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Figure 2: Postoperative day 2 showing persistent mild ptosis of right eye

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Accidental dural puncture while performing epidural anaesthesia causes low cerebrospinal fluid (CSF) pressure and loss of hydraulic suspension of brain. This results in traction or possibly compression of the cranial nerve by surrounding structures with subsequent local ischaemia and nerve dysfunction.[2]

As per review of diplopia after dural puncture by Nishio et al., extraocular muscle palsy can manifest from first day to 3 weeks after dural puncture. Spontaneous recovery is observed in 80% of the patients within 2–8 months after the onset of diplopia.[3] Majority of these findings reverse completely following resolution of the CSF leak.[4] The typical MRI findings of intracranial hypotension are pachymeningeal enhancement, subdural fluid collections, pituitary enlargement and downward displacement of brainstem.[5] In our patient, MRI brain was normal despite the history of dural puncture and the occurrence of PDPH. Previous case reports have shown that absence of pachymeningeal enhancement on brain MRI does not exclude the diagnosis of symptomatic intracranial hypotension.[6]

The common causes of isolated oculomotor nerve palsy are aneurysms, ischaemia, tumours, trauma, immunological disorders and myasthenia gravis.[3] MRI brain ruled out aneurysm, tumour, encephalitis and trauma in our patient. Myasthenia gravis usually spares the pupil. Our patient did not have any of the risk factors for micro-vascular infarcts such as diabetes, hypertension and smoking. About 60% of patients with micro-vascular infarcts will have orbital pain, and pupil will be spared in 75% of them.[4] Serological markers for various immunological disorders were also negative.

Previously reported cranial nerve palsies after dural puncture have mostly involved abducens nerve. Our case is different from the previous reports, as it involved oculomotor nerve, occurred on first postoperative day, was transient, had no characteristic MRI findings and resolved within a week. Reassurance of the patient is important as most of the cranial nerve palsies after dural puncture resolve in a week-to-month time.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Sudhakar P, Trobe J, Wesollowski J. Dural puncture induced intracranial hypotension causing diplopia. J NeuroOpthalmol 2013;33:106-12.  Back to cited text no. 1
    
2.
Arcand G, Girard F, McCormack M, Chouinard P, Boudreault D, Williams S. Bilateral sixth cranial nerve palsy after unintentional dural puncture. Can J Anesth 2004;51:821-3.  Back to cited text no. 2
    
3.
Nishio I, Williams BA, Williams JP. Diplopia: A complication of dural puncture. Anesthesiology 2004;100:158-64.  Back to cited text no. 3
    
4.
Zada G, Solomon Tc, Giannotta S. A review of ocular manifestations in intracranial hypotension. Neurosurg Focus 2007;23:1-5.  Back to cited text no. 4
    
5.
Ruso A, Tessitore A, Cirillo M, Giordano A, Micco RD, Bussone G, et al. A transient third cranial nerve palsy as presenting sign of spontaneous intracranial hypotension. J Headache Pain 2011;12:493-6.  Back to cited text no. 5
    
6.
Mokri B, Atkinson JL, Dodick DW, Miller GM, Piepgras DG. Absent pachymeningeal gadolinium enhancement on cranial MRI despite symptomatic CSF leak. Neurology 1999;53:402-4.  Back to cited text no. 6
    


    Figures

  [Figure 1], [Figure 2]



 

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