In autonomic dysreflexia, which of the following symptoms do patients typically experience?
Autonomic dysreflexia is a life-threatening emergency which can occur in patients with spinal cord injuries (SCI) at or above T6. There is massive sympathetic discharge of the distal autonomous cord (i.e., below the level of the spinal cord injury) secondary to specific stimulus. Ordinarily the reflexes would be inhibited by output from the medulla but in SCI this does not happen and leads to autonomic dysreflexia.
The most common cause is bladder distension due to a blocked catheter, cystoscopy or urodynamics. Other causes include faecal loading, skin, and urine infections. Symptoms are flushing and sweating of skin above the level of injury, hypertension with reflex bradycardia and headache. The crucial step is to identify it, remove the offending stimulus, sit the patient up and administer 10 mg nifedipine to chew, not sublingually. Blood pressure must be monitored throughout.
An upper motor neurone lesion will usually comprise which of the following features?
In spinal cord injuries at or above the level of T10, the patient is most likely to have an upper motor neurone type injury with neurogenic detrusor overactivity and detrusor-sphincterdyssynergia (DSD). DSD is defined as involuntary contraction of the urethral and/or periurethral striated muscle simultaneously with a detrusor contraction. This is the result of loss of co-ordination by the pontine micturition centre. The typical appearance on a pressure-flow trace is drawn as shown in figure below.
Pressure/flow trace and EMG in a spinal cord injured patient with DSD. (From Hussain, M. et al., BJMSU, 5, 192–203, 2012.)
When considering metabolic changes in substitution cystoplasties using bowel, which of the following is CORRECT?
In the bowel lumen, sodium ions (Na+) are secreted in exchange for hydrogen ions (H+) and bicarbonate ions (HCO3 − ) in exchange for chloride ions (Cl−). Urine has high concentrations of ammonia (NH3), ammonium (NH4 + ), hydrogen and chloride – these substances are reabsorbed in bowel segments exposed to urine resulting in chronic acid load. Whether this results in significant metabolic acidosis depends on the patient (comorbidities), bowel segment used and the duration of contact of the bowel with urine.
A mild, subclinical hyperchloremic metabolic acidosis is encountered in all patients that undergo urinary diversion using bowel. ≤20% of these will have episodes of severe acidosis. 10% of patients with an ileal conduit have a clinically important metabolic acidosis after 1 year.
Renal wasting and secretion of potassium from the bowel results in hypokalaemia. In general, this will not have important clinical consequences. However, when metabolic acidosis is treated, potassium is exchanged with the intracellular space causing further potassium depletion, manifesting clinically as muscle weakness. Several cases of muscle weakness mistaken for GuillainBarré syndrome after ureterosigmoidostomy are reported. Therefore, when correcting acidosis also supplement potassium (potassium citrate 15 mEq or 1.6 g BD-QDS). Lifelong follow-up of patients with bowel substitutions is recommended, comprising bloods (FBC, U&E, bicarbonate, chloride, B12, folate) and USS KUB at regular intervals.
Which of the following is TRUE in spinal shock?
Spinal shock involves a spinal cord concussion, which usually involves a period of paralysis, hypotonia and areflexia. All reflex activity below the level of the lesion is abated. At its conclusion there may be hyperreflexia, hypertonicity and clonus. It can last for up to 12 weeks, but the time period is variable. Return of reflex activity below the level of injury indicates the end of spinal shock.
The bulbocavernosus reflex (anal sphincter contraction in response to squeezing the glans penis or tugging on the urethral catheter) involves the S2, S3 nerve roots and is a spinal cord mediated reflex. Initial management of spinal shock involves urethral catheterisation with the aim of converting the patient over to intermittent catheterisation (self or by carer) as soon as possible.
Be careful not to mix up spinal shock and autonomic dysreflexia.
Which of the following is TRUE regarding onabotulinum toxin A?
Onabotulinum toxin A was first used in 1988 for the treatment of detrusor-sphincter dyssynergia. The first report for neurogenic detrusor overactivity was by Schurch in 2000. It is a selective inhibitor of presynaptic vesicular acetylcholine release by cleaving the synaptosomal-associated protein 25 (SNAP-25). The effects are temporary lasting on an average of 6–9 months. Re-injections are equally effective. It is generally performed under local anaesthesia with a flexible cystoscope as a day case procedure. Whilst originally licensed in the UK for use in neurogenic detrusor overactivity, in 2019 it was licensed for use in idiopathic detrusor overactivity (NICE).
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