An unusual presentation of autonomic dysreflexia in a patient with cold abscess of cervical spine for anterolateral decompression.

A young female having complaints of quadriparesis along with bladder and bowel involvement, diagnosed to have osseous destruction of C4, C6, C7, T2 vertebral bodies with pre- and para-vertebral abscess, was taken up for anterolateral decompression and fusion of cervical spine. She presented with anxiety, agitation, sweating and headache and was in hypertensive crisis which was refractory to antihypertensives, anxiolytics and analgesics but showed a reasonable response to intravenous dexmedetomidine and finally responded dramatically to rectal evacuation. Autonomic dysreflexia was suspected with stimulus arising from distended rectum as all other causes of hypertension were ruled out.

INTRODUCTION

A patient with incomplete cervical cord injury,[12] taken up for cervical spine decompression and fusion surgery, developed hypertensive crisis in operation theatre which was refractory to routine antihypertensive measures. Anaesthesia and surgery proceeded when she reasonably responded to intravenous (IV) dexmedetomidine[3] only to have a rebound hypertension in the post-operative period which finally responded dramatically to rectal evacuation of impacted stool. Autonomic dysreflexia (AD), a potentially dangerous clinical syndrome occurs in spinal cord injury at or above the sixth thoracic vertebral level (T6)[4] resulting in acute uncontrolled hypertension due to over activity of sympathetic nervous system below the level of injury, triggered by an ascending sensory (noxious) stimulus usually an over distended bladder in almost 85% of cases and bowel distension due to impacted stools.[45]

CASE REPORT

A 35 year old female weighing 45 kg was having complaints of pain in the neck and weakness of all 4 limbs for 1 week. There were quadriparesis and a swelling on the left side of the neck along with tenderness in the cervical spine. Neurological examination revealed a power of 3/5 in bilateral upper and lower limbs and a sensory loss below C5 level with no bladder and bowel involvement. Rest of the clinical examination and baseline investigations were within normal limits. Based on fine needle aspiration cytology report of a caseating tubercular lesion, antitubercular treatment was started. X-ray spine showed mild cervical spondylosis with straightening of cervical curve. Magnetic resonance imaging of spine showed osseous destruction of C4, C6, C7, T2 vertebral bodies, pre- and para-vertebral abscess and mild tracheal compression at the level of C6–C7 [Figures 1 and 2]

Figure 1

Pre- and para-vertebral abscess with extension into B/L paraspinal muscles, anterior and posterior epidural space leading to significant compression of thecal sac and cervical spinal cord

Figure 2

Osseous destruction of C4, C6, C7, T2 vertebral bodies

An awake fiberoptic bronchoscopy ruled out any airway compromise. She was planned for an elective cervical spine decompression and fusion surgery under the American Society of Anesthesiologists Grade 1. However, a sudden bladder and bowel involvement called for immediate surgery.

The patient was extremely anxious, agitated, was sweating and complained of headache with pain in the neck even after a premedication of midazolam 1 mg IV. Monitors showed a heart rate (HR) of 150/min and a blood pressure (BP) of 188/110 mmHg. She was given fentanyl 100 μg and midazolam 0.5 mg IV. After 5 min BP was 196/120 mmHg with HR 158/min and continued to rise to 200/124 mmHg with a HR 156/min. Morphine 6 mg IV was given at this juncture. The haemodynamics showed no improvement. Keeping in mind, the progressing neurological deficit, aggressive haemodynamic optimization was attempted with a loading dose of esmolol 1 mg/kg IV was followed by an infusion 0.2 mg/kg/min after securing an arterial line. The BP minimally reduced to 190/110 with HR 148/min. Remaining parameters such as percentage saturation of oxygen (SpO2) remained within normal limits. A peripheral central catheter was inserted for central venous pressure monitoring. Despite continuing esmolol infusion for 15 min, there was no further fall in BP and patient remained anxious and restless. Furosemide 20 mg IV was administered and central venous pressure closely monitored. Physician opinion was sought in view of refractory hypertension and sinus tachycardia. Sodium nitroprusside (SNP) or esmolol was recommended. SNP was not readily available with us, and a trial of esmolol had already been given. The persistent anxiety factor prompted us to utilise the α2 agonist dexmedetomidine in a loading dose of 1 μg/kg over 10 min followed by infusion of 0.2 μg/Kg/h. The HR dropped to 120/min over 10 min, and the BP came down to 140/94 mmHg and patient became anxiety free. Having achieved a relatively stable haemodynamics it was decided to proceed with the case. Anaesthesia was induced with propofol 80 mg IV. While maintaining a manual inline stabilisation, mask ventilation was assured and vecuronium bromide 5 mg IV administered. Although a difficult intubation trolley was kept ready, trachea could be easily intubated with a 7.5 mm cuffed endotracheal tube. Anaesthesia was maintained on oxygen, nitrous oxide (50:50) and 1% sevoflurane. Dexmedetomidine infusion was maintained at the rate of 0.2 μg/kg/h. Intraoperatively, the patient was haemodynamically stable. Bispectral index was maintained between 40 and 60. Intake and output were maintained. Extubation was planned in a deeper plane of anaesthesia. To obtund the haemodynamic reflexes at extubation, dexmedetomidine infusion rate was increased to 0.5 μg/kg/h. Extubation was smooth and uneventful, and the patient shifted to high dependency unit (HDU).

In the HDU, the BP and HR showed a rising trend. A team discussion and case analysis led to suspicion of AD. Urinary bladder catheterization was in situ. A per rectal examination revealed impacted hard stools which was then evacuated. In the next 60-90 min, the BP came down to 140/84 mmHg and HR settled to 100/min. Antihypertensives could be tapered and finally stopped. The patient was observed for the next 48 h with strict instructions of bowel care by enema. Her stay in HDU remained uneventful thereafter.

DISCUSSION

Our patient presented with incomplete cervical cord injury[12] without any associated comorbidity but developed rapid neurological deficit with bladder and bowel involvement. On the operation table, she developed hypertensive crisis which was refractory to the conventional treatment, but responded somewhat to the cocktail of α2 agonist dexmedetomidine, opioid, beta blocker, diuretic and inhalation anaesthetic[67] which helped us to tide over the intraoperative period only to have a rebound hypertension in the immediate post-operative period. Since we were dealing with a lesion at the cervical level with relatively intractable hypertension in a young patient with no previous history of hypertension, AD[4] was considered as a possible cause, which led us to search for a focus of stimulation. The urinary bladder was already catheterised so any stimulus arising from bladder was ruled out. A per rectal examination revealed impacted hard stools. A remarkable response occurred after 60–90 min of stool evacuation.

AD is a potentially dangerous clinical syndrome that develops in spinal cord injury at or above the T6 vertebra,[4] resulting in acute, uncontrolled hypertension due to widespread reflex activity of sympathetic nervous system below the level of injury, triggered by an ascending sensory (usually noxious) stimulus either an over distended bladder, in almost 85% of cases, or bowel distension due to impacted stools,[45] due to isolation of spinal cord below the injury from normal regulation by vasomotor centres in the brainstem.[8] Pressure sores, ingrowing toenails, pregnancy and labour are also known to trigger AD. Release of catecholamines causes severe vasoconstriction with skin pallor, piloerection and a sudden rise in BP usually accompanied by a headache. Rise in BP is sensed by baroreceptors in the aortic arch and carotid bodies resulting in parasympathetic activity and compensatory bradycardia (via the vagus nerve).[458]

Our patient had a unique presentation for several reasons. Firstly, though it is a known occurrence in spinal cord injury, very few cases have been reported in non-traumatic causes. However, causes like spinal cord tumours or post-neurosurgery above T6, secondary to medical conditions such as multiple sclerosis[9] are also known.

Secondly, our patient presented with tachycardia contrary to the much common presentation of bradycardia[9] in these patients. However, it has been observed that tachycardia is not an uncommon finding especially in patients with cervical lesion as was our patient.[57] Thirdly, only 27% of patients with incomplete lesions present with AD (in comparison to 91% of complete lesions)[5] as was in our patient. Because of all the above factors, we considered it wise to rule out all other possibilities of such a presentation before concluding on AD as the cause.

To rule out common causes of hypertension in a young female, a thorough history and examination were followed by a repeat routine laboratory tests along with special tests such as fundoscopy, thyroid profile, renal Doppler, ultrasound kidney, ureter, bladder, echocardiography, serum cortisol and vanillylmandelic acid.[10] Since all were within normal range, we zeroed down to a diagnosis of AD.

CONCLUSION

We want to emphasize that while dealing with a cervical cord injury, traumatic or atraumatic, complete or incomplete, the element of AD should be kept in mind, which should prompt us to eliminate any focus of stimulus below the level of injury. Catheterization of the urinary bladder and bowel evacuation with enema are the pearls of the preoperative preparation of such cases.

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Conflicts of interest

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