Atonic bladder

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  1. Normal bladder emptying is controlled by three segmental motor mechanisms
    1. sacral parasympathetic cell column in the lateral part of the intermediate gray of S2-4; emerges from S2-4 ventral rami as the pelvic splanchnic nerves which course through the inferior hypogastric ganglia to end on postganglionic neurons in the urinary bladder wall (a.k.a. the detrusor muscle) causing bladder contraction as well as relaxation of the internal sphincter
      1. these same nerves also produce erection and the peristaltic defecation
    2. sympathetic bladder center at T11-L2 of the intermediate cell column
      1. must be inhibited to relax the involuntary smooth muscle sphincters of the bladder base and urethra
      2. treatment of overactive internal sphincter may be done with alpha adrenergic blockade such as phenoxybenzamine
    3. S2-4 somatic motor neurons of the pudendal nerve nucleus (this is NOT part of autonomic nervous system)
      1. Controls voluntary external sphincter urethra muscle and must be inhibited
        1. Overactive external sphincter may be treated with any class of spasmolytic such as baclofen, benzodiazepines or dantrolene (dantrolene decreases the release of Ca from the endoplasmic reticulum)
      2. Also innervates bulbospongiosus and external anal sphincter
      3. Pudendal nerve lies under the gluteus maximus muscle and over the levator ani muscle
        1. Pudendal nerve divides into the perineal nerve, inferior rectal nerve, dorsal nerve of the penis, and posterior scrotal nerves
  2. Pressure afferents from the bladder wall bring sensation of bladder fullness into the spinal cord through parasympathetic fibers of the inferior hypogastric ganglia and pudendal nerve
    1. pressure afferents excite the parasympathetics to the detrusor muscle
  3. Pain afferents from the bladder return mostly with sympathetic innervation
  4. Pain and pressure afferents ascend bilaterally in all white columns and terminate on:
    1. pontine tegmentum reticular formation bladder center
    2. cortical detrusor center of the medial aspect of the frontal lobe (anterior cingulated gyrus)
    3. other less specific limbic and cortical areas
  5. from the cortical detrusor center, descending autonomic pathways activate the pontine tegmentum bladder center which in turn sends descending autonomics bilaterally into the lateral white columns to cause activation of the S2-4 parasympathetic cell column and inhibit the sympathetic bladder center and pudendal nucleus
    1. descending autonomics also inhibit the pressure afferents’ tendency to cause reflex activation of the detrusor parasympathetics
    2. if descending autonomics are destroyed by bilateral lateral white column disease or spinal cord transection, when bladder pressures reach a threshold level they will cause an uncontrolled reflex contraction of the bladder against the sphincters which do not relax normally resulting in a spastic or reflex bladder; treat with propantheline (a muscarinic antagonist) or oxybutynin (Ditropan) and external collection of urine
      1. detrusor hyperreflexia with sphincter areflexia is a rare disorder seen in myelomeningocoele and sacral cord lesions; this will result in urinary tract infections, hydronephrosis, and nephrolithiasis
    3. if bladder afferents are affected by diabetes or syphilis, there is no sensation of bladder fullness, but patients are still able to voluntarily empty the bladder – a sensory neurogenic bladder condition
    4. if lower motor neurons are affected in the sacral cord, cauda equina, or peripheral S2-4 there will be normal sensation but no voluntary or reflex motor function (an atonic, areflexic or motor paralytic bladder); treat this condition with bethanecol (a cholinergic drug)
  6. during the immediate after effects of acute spinal cord injury, there is a state of spinal shock; during spinal shock the patient has a flaccid paralysis below the level of the spinal lesion; no reflexes are obtained, sensation is not perceived and the bladder loses its capacity to contract and is in a state of retention overflowing when fully stretched; this is an atonic bladder and may last for days, weeks or months
    1. this occurs because the inhibiting effects of the higher central nervous system has been cut off from the lower cord
    2. as spinal shock passes off, reflexes return (flexor reflexes of skeletal muscle return first in 3 days to 3 weeks following injury) and become hyperactive; spasticity sets in and the bladder begins to show evidence of contractions even when the bladder isn’t full
  7. summary of treatment for bladder afferent/efferent pathology:
    1. parasympathetic pathology causing spastic detrusor muscle – muscarinic antagonist such as oxybutynin (Ditropan) or propantheline
    2. sympathetic pathology causing spastic internal sphincter – alpha blocker such as phenoxybenzamine (noncompetitive alpha blocker)
    3. S2-4 motor pathology (central spasticity) – baclofen or dantrolene
    4. S2-4 motor pathology (peripheral weakness) – bethanecol (cholinergic)
  8. bladder evaluation
    1. cystometrogram – measures intravesicular pressure and detrusor reflex
      1. normally the external urinary sphincter is tonically activated until about two seconds prior to emptying contraction when it is inhibited; during the two seconds prior to inhibition of the external urinary sphincter, intracystic pressure rises to about 130 cm H2O with a slight rise in pulse rate and blood pressure and opening of the bladder neck; urination occurs between a rising intracystic pressure of 40 and a falling pressure of 20; the external urinary sphincter gradually regains its sustained tonic contraction after that
      2. normally, the volume of urine in the bladder builds until it reaches around 400 cc – at that point the pressure in the bladder goes up markedly
        1. in a sensory paralytic bladder and a motor paralytic bladder, changes in volumes over 400 cc do not cause any increase in the pressure inside the bladder
        2. in a reflex neurogenic bladder there are sudden spikes and dips in pressure due to uninhibited contractions that appear with small changes in bladder volume
    2. EMG – voluntary sphincter contration tests supraspinal innervation
    3. voiding cystourethrogram (VCUG) – structural study
  9. Neurogenic bladder (a.k.a. neuropathic bladder)
    1. includes disorders of voiding, bladder control, and the attendant complications of infection, stone formation, and renal failure
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