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Year : 2017  |  Volume : 11  |  Issue : 1  |  Page : 260-262  

Case of neurological complication following subarachnoid block in a patient with unsuspected coagulopathy

Department of Anaesthesia and Critical Care, Kannur Medical College, Kannur, Kerala, India

Date of Web Publication16-Feb-2017

Correspondence Address:
Dr. Arun Mathur
Department of Anaesthesia and Critical Care, Kannur Medical College, Anjarakandy P.O, Kannur - 670 612, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0259-1162.194563

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Subarachnoid block (SAB) is an extensively used regional anesthesia technique for many surgeries. Neurological complications are rare following spinal anesthesia. We are reporting neurological complication in a patient the following appendectomy under SAB with unsuspected coagulopathy. The complication was noticed early and managed conservatively with a high dose of intravenous steroid and improved drastically in a short period.

Keywords: International normalized ratio, methylprednisolone, postspinal neurological complication, thalassemia, vigilant monitoring

How to cite this article:
Mathur A, Nagappa C V. Case of neurological complication following subarachnoid block in a patient with unsuspected coagulopathy. Anesth Essays Res 2017;11:260-2

How to cite this URL:
Mathur A, Nagappa C V. Case of neurological complication following subarachnoid block in a patient with unsuspected coagulopathy. Anesth Essays Res [serial online] 2017 [cited 2020 Aug 13];11:260-2. Available from:

   Introduction Top

The incidence of neurologic complication in central neuraxial blockade is reported to be between 1/1000 and 1/1,000,000.[1] Cauda equina syndrome (CES) as a complication of spinal anesthesia is characterized by varying degree of saddle anesthesia, sphincter dysfunction resulting in fecal incontinence, urinary retention, and paraplegia.[1] Probable cause, in this case, may be neurotoxicity, hematoma, or trauma to nerves. Early diagnosis and intervention were ensured with better outcome and recovery.

   Case Report Top

A male patient aged 45 years was admitted to the Department of General Surgery with a complaint of acute abdomen, diagnosed as acute appendicitis and posted for an open appendectomy. During preoperative examination thalassemia trait was elicited, he was evaluated previously in an institute after his son was diagnosed as thalassemia major. Pedigree analysis was done following which wife and two other kids were also found to be suffering from thalassemia minor. Routine investigations showed Hb - 12 g/dL, platelet - 190 × 109/L (130–400 × 109/L), total leukocyte count - 16 × 109/L (4.0–10.0 × 109/L), neutrophil - 74%, renal function test were normal electrocardiogram (ECG)-within normal limits (WNL). The patient was kept fasted overnight and planned to proceed under subarachnoid block (SAB).

In the operation theater, routine monitors such as ECG, noninvasive blood pressure (BP), and pulse oximeter were attached. Preoperative vitals were BP - 130/84, pulse rate - 78/min, SpO2-98%. The patient was preloaded with Ringer lactate (15 ml/kg) after securing an intravenous cannula; SAB was tried in lateral position with quincke needle 23-gauge (B. Braun). During first attempt in L3–L4 interspace free flow of cerebrospinal fluid (CSF) was present but mixed with blood and not cleared off even after waiting for some time. Spinal needle was withdrawn and the second attempt tried in L2–L3 interspace after 4 min. The second attempt was successful with free flow of CSF, although blood tinged. Hyperbaric bupivacaine 0.5% 15 mg was given, surgery started once the sensory level to touch and cold reached T6 and T4, respectively. Intraoperative period of 45 min was uneventful. Forty-five minutes (starting time 9 am and finishing time 9.45 a.m.).

During evening, postoperative rounds at 8.30 p.m., the patient complained of severe back pain, radiating to both legs. It was found that power in the left lower limb (LL) 1/5 and right LL 2/5 [Table 1]. Immediate Coagulation profile was; international normalized ratio (INR) - 2.3; prothrombin time - 27.6 s, activated partial thromboplastin time - 42 s. Rests of the results were not altered. Spinal hematoma was probable diagnosis after exclusion of other probabilities. In the absence of neurosurgeon and functional magnetic resonance imaging (MRI), we decided to shift the patient to a higher center for further management. Meanwhile, we started injection methylprednisolone 1.8 g infusion over 30 min followed by 324 mg/h, injection tranexamic acid 600 mg over 5 min and injection Vitamin K 10 mg. Four units of fresh frozen plasma requested. Surprisingly, patient's power improved between 1/5 to 2/5 in the left LL and 2/5 to 3/5 in the right LL in 2 h of starting steroids. Within the next 4 h, power in both LLs increased to 4/5. As nearest higher referral center was 4 h drive, we managed patient conservatively in our hospital. Next morning, patient's bilateral LL powers became normal (5/5). While discharging after 3 days, we referred the patient to hematologist and neurosurgeon for further evaluation. The patient did not come for follow-up.
Table 1: Medical Research Council scale

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   Discussion Top

CES has been recognized as a rare, devastating complication of SAB since Ferguson and Watkins [2] focused attention on this syndrome in 1937. Damage to nerve roots of cauda equina following spinal anesthesia may occur due to compression caused by hematoma, inflammation, stretching due to abnormal position, direct trauma, and spinal ischemia or as a result of neurotoxicity of local anesthetics.[3] Spinal hematoma following lumber puncture is associated with clotting disorders, either acquired (anticoagulant treatment) or congenital (hemophilia) or bleeding from a tumor or vascular malformation within the spinal canal.

The most likely causes in our case could be hematoma, trauma or neurotoxicity to nerves leading to CES. As patient complained of back pain and leg pain postoperatively and examination revealed sensory and motor deficit. Transient neurologic syndrome as differential diagnosis ruled out as it is exclusively a pain syndrome, as pain was present prolonged effect of block was also negated.[4]

Abnormal INR, sign, symptoms, examination findings, and blood tinged CSF at repeated lumber punctures goes in favor of hematoma causing CES. As MRI was unavailable hematoma could not be confirmed.

The basic treatment for spinal hematoma is surgical decompression.[5],[6] However, there are cases reported in which the conservative treatment was satisfactory.[7],[8] The initial early improvement might be an indication for the institution of the conservative treatment.[9]

In our case, as soon as, we had suspected neurological complication, we started the patient on a high dose of injection methylprednisolone 30/mg/kg over 30 min followed by continuous infusion at the rate of 5.4 mg/kg/h.[8] In the meantime, during the discussion to shift the patient to higher center, we had found patient's power in both LL improved within an hour of starting infusion. As power came to 4/5 in both LL in 4 h, we had decided to wait till morning. Surprisingly, power in both limbs became 5/5 by morning.

It is unusual for a thalassemia minor patient to have deranged INR as they are mostly associated with hypercoagulable state and thromboembolic phenomenon.[10] The patient had increased total leukocyte count and neutrophils favors ongoing sepsis that may also affect coagulation profile. To rule out congenital clotting factor deficiency patient was referred to a higher referral center. Unfortunately, the patient did not come for follow-up. Thus, it is difficult to comment on exact diagnosis in this case.

   Conclusion Top

When spinal anesthesia or epidural anesthesia is administered, the possibility of neurological complications should always be considered especially if a patient on anticoagulant or multiple/traumatic puncture occurred. We suggest to follow standard regional anesthesia guidelines for a patient on anticoagulant or deranged coagulation profile. If blood tinged CSF comes after repeated attempt, it is advisable to proceed with general anesthesia for early diagnosis of neurological deficit if any.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Agarwal A, Kishore K. Complications and controversies of regional anaesthesia: A review. Indian J Anaesth 2009;53:543-53.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
Ferguson FH, Watkins KH. Paralysis of the bladder and associated neurological sequelae of spinal anesthesia (cauda equina syndrome). Br J Surg 1937;25:735-52.  Back to cited text no. 2
Traore M, Diallo A, Coulibaly Y, Guinto CO, Timbo SK, Thomas JT. Cauda equina syndrome and profound hearing loss after spinal anesthesia with isobaric bupivacaine. Anesth Analg 2006;102:1863-4.  Back to cited text no. 3
Cöcelli LP, Erkutlu I, Karakurum G, Avci N, Gül R, Oner U. Transient neurologic syndrome after spinal anesthesia with epidural steroid treatment. Curr Ther Res Clin Exp 2009;70:316-22.  Back to cited text no. 4
Castillo J, Santiveri X, Escolano F, Castaño J. Spinal cord compression caused by hematoma related to neuroaxial anesthesia in Spain. Rev Esp Anestesiol Reanim 2003;50:504-9.  Back to cited text no. 5
Lawton MT, Porter RW, Heiserman JE, Jacobowitz R, Sonntag VK, Dickman CA. Surgical management of spinal epidural hematoma: Relationship between surgical timing and neurological outcome. J Neurosurg 1995;83:1-7.  Back to cited text no. 6
La Rosa G, d'Avella D, Conti A, Cardali S, La Torre D, Cacciola F, et al. Magnetic resonance imaging-monitored conservative management of traumatic spinal epidural hematomas. Report of four cases. J Neurosurg 1999;91 1 Suppl: 128-32.  Back to cited text no. 7
Segabinazzi D, Brescianini BC, Schneider FG, Mendes FF. Conservative treatment of hematoma after spinal anesthesia: Case report and literature review. Rev Bras Anestesiol 2007;57:188-94.  Back to cited text no. 8
Kim T, Lee CH, Hyun SJ, Yoon SH, Kim KJ, Kim HJ. Clinical outcomes of spontaneous spinal epidural hematoma: A comparative study between conservative and surgical treatment. J Korean Neurosurg Soc 2012;52:523-7.  Back to cited text no. 9
Eldor A, Rachmilewitz EA. The hypercoagulable state in thalassemia. Blood 2002;99:36-43.  Back to cited text no. 10


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