Any new clinical data, whether positive or negative, generated about a medical device should be published because health professionals should know which devices do not work, as well as those which do. We report three spinal cord injury patients in whom urological implants failed to work. In the first, paraplegic, patient, a sacral anterior root stimulator failed to produce erection, and a drug delivery system for intracavernosal administration of vasoactive drugs was therefore implanted; however, this implant never functioned (and, furthermore, such penile drug delivery systems to produce erection had effectively become obsolete following the advent of phosphodiesterase type 5 inhibitors). Subsequently, the sacral anterior root stimulator developed a malfunction and the patient therefore learned to perform self-catheterisation. In the second patient, also paraplegic, an artificial urinary sphincter was implanted but the patient developed a postoperative sacral pressure sore. Eight months later, a suprapubic cystostomy was performed as urethral catheterisation was very difficult. The pressure sore had not healed completely even after five years. In the third case, a sacral anterior root stimulator was implanted in a tetraplegic patient in whom, after five years, a penile sheath could not be fitted because of penile retraction. This patient was therefore established on urethral catheter drainage. Later, infection with Staphylococcus aureus around the receiver block necessitated its removal. In conclusion, spinal cord injury patients are at risk of developing pressure sores, wound infections, malfunction of implants, and the inability to use implants because of age-related changes, as well as running the risk of their implants becoming obsolete due to advances in medicine. Some surgical procedures such as dorsal rhizotomy are irreversible. Alternative treatments such as intermittent catheterisations may be less damaging than bladder stimulator in the long term.
A 22-year-old male sustained C-6 tetraplegia in 1992. In 1993, intravenous pyelography revealed normal kidneys. Suprapubic cystostomy was performed. He underwent open cystolithotomy in 2004 and 2008. In 2009, computed tomography revealed bilateral renal calculi. Coagulum pyelolithotomy of left kidney was performed. Pleura and peritoneum were opened. Peritoneum could not be closed. Following surgery, he developed pulmonary atelectasis; he required tracheostomy and mechanical ventilation. He did not tolerate nasogastric feeding. CT of abdomen revealed bilateral renal calculi and features of proximal small bowel obstruction. Laparotomy revealed small bowel obstruction due to dense inflammatory adhesions involving multiple small bowel loops which protruded through the defect in sigmoid mesocolon and fixed posteriorly over the area of previous intervention. All adhesions were divided. The wide defect in mesocolon was not closed. In 2010, this patient again developed vomiting and distension of abdomen. Laparotomy revealed multiple adhesions. He developed chest infection and required ventilatory support again. He developed pressure sores and depression. Later abdominal symptoms recurred. This patient's general condition deteriorated and he expired in 2011.
Conclusion. Risk of postoperative complications could have been reduced if minimally invasive surgery had been performed instead of open surgery to remove stones from left kidney. Suprapubic cystostomy predisposed to repeated occurrence of stones in urinary bladder and kidneys. Spinal cord physicians should try to establish intermittent catheterisation regime in tetraplegic patients.
A 29-year-old man developed paraplegia at T-10 level due to road traffic accident in 1972. Both kidneys were normal and showed good function on intravenous urography. Division of external urethral sphincter was performed in 1973. In 1974, cystogram showed retrograde filling of left renal tract, which was hydronephrotic. Left ureteric reimplantation was performed. Following surgery, cystogram revealed marked retrograde filling of left renal tract as before. Penile sheath drainage was continued. In 1981, intravenous urography revealed bilateral severe hydronephrosis. Left ureteric reimplantation was performed again in 1983. Blood pressure was 220/140 mm Hg; this patient was prescribed atenolol. Cystogram showed gross left vesicoureteral reflux. Intermittent catheterisation was commenced in 2001. In 2007, proteinuria was 860 mg/day. This patient developed progressive renal failure and expired in 2012. In a spinal cord injury patient with vesicoureteral reflux, the treatment should focus on abolition of high intravesical pressures rather than surgical correction of vesicoureteric reflux. Detrusor hyperactivity and high intravesical pressures are the basic causes for vesicoureteral reflux in spinal cord injury patients. Therefore, it is important to manage spinal cord injury patients with neuropathic bladder by intermittent catheterisations along with antimuscarinic drug therapy in order to abolish high detrusor pressures and prevent vesicoureteral reflux. Angiotensin-converting enzyme inhibitors or angiotensin-receptor-blocking agents should be prescribed even in the absence of hypertension when a spinal cord injury patient develops vesicoureteral reflux and proteinuria.
A male tetraplegic patient with, who had been taking warfarin, developed haematuria. Ultrasound scan revealed no masses, stones, or hydronephrosis. Urinary bladder had normal configuration with no evidence of masses or organised haematoma. Urine cytology revealed no malignant cells. Four months later, CT urography revealed an irregular mass at the base of urinary bladder. Cystoscopic biopsy revealed moderately differentiated adenocarcinoma, which contained goblet cells and pools of mucin showing strongly positive immunostaining for prostatic acid hosphatase and patchy staining for prostate specific antigen. Computed Tomography revealed multiple hypodense hepatic lesions and several osteolytic areas in femoral heads and iliac bone. With a presumptive diagnosis of prostatic carcinoma, leuprorelin acetate 3.75 mg was prescribed. This patient expired a month later. Conclusion. (i) Spinal cord injury patient, who passed blood in urine while taking warfarin, requires repeated investigations to look for urinary tract neoplasm. (ii) Anti-androgen therapy should be prescribed for 2 weeks prior to administration of gonadorelin analogue to prevent tumour flare causing bone pain, bladder outlet obstruction, uraemia, and cardiovascular risk due to hypercoagulability associated with a rapid increase in tumour burden. (iii) Spinal cord physicians should adopt a caring and compassionate approach while managing tetraplegic patients with several co-morbidities, as aggressive diagnostic tests and therapeutic procedures may lead to deterioration in the quality of life.
Condom catheters are indicated in spinal cord injury patients in whom intravesical pressures during storage and voiding are safe. Unmonitored use of penile sheath drainage can lead to serious complications.
A 32-year old, male person, sustained complete paraplegia at T-11 level in 1985. He had been using condom catheter. Eleven years after sustaining spinal injury, intravenous urography showed no radio-opaque calculus, normal appearances of kidneys, ureters and bladder. Blood urea and Creatinine were within reference range. A year later, urodynamics revealed detrusor pressure of 100 cm water when detrusor contraction was initiated by suprapubic tapping. This patient was advised intermittent catheterisation and take anti-cholinergic drug orally; but, he wished to continue penile sheath drainage. Nine years later, this patient developed bilateral hydronephrosis and renal failure. Indwelling urethral catheter drainage was established. Five months later, ultrasound examination of urinary tract revealed normal kidneys with no evidence of hydronephrosis.
Spinal cord injury patients with high intravesical pressure should not have penile sheath drainage as these patients are at risk for developing hydronephrosis and renal failure. Intermittent catheterisation along with antimuscarinic drug should be the preferred option for managing neuropathic bladder.
Urological complications are the major cause of ill health in patients with spina bifida. Urinary sepsis accounted for the majority of admissions in patients with spina bifida. As the patient grows older, changes occur in the adult bladder, leading to increases in storage pressure and consequent risk of deterioration of renal function, which may occur insidiously.
A 34-year-old male spinal bifida patient had been managing neuropathic bladder by penile sheath. Intravenous urography revealed normal kidneys. This patient was advised intermittent catheterisations. But self-catheterisation was not possible because of long, overhanging prepuce and marked spinal curvature. This patient developed repeated urine infections. Five years later, ultrasound examination of urinary tract revealed hydronephrotic right kidney with echogenic debris within the collecting system. There was no evidence of dilatation of the ureter near the vesicoureteric junction. The left kidney appeared normal. There was no evidence of calculus disease seen in either kidney. Indwelling urethral catheter drainage was established.
Two years later, MAG-3 renogram revealed normal uptake and excretion by left kidney. The right kidney showed little functioning tissue. Following a routine change of urethral catheter this patient became unwell. Ultrasound examination revealed hydronephrotic right kidney containing thick hyper-echoic internal septations and debris in the right renal pelvis suspicious of pyonephrosis. Under both ultrasound and fluoroscopic guidance, an 8 French pig tail catheter was inserted into the right renal collecting system. 150 ml of turbid urine was aspirated immediately. This patient developed large left pleural effusion, collapse/consolidation of the left lower lobe, a large fluid collection in the abdomen extending into the pelvis and expired twenty days later because of sepsis and respiratory failure.
Although penile sheath drainage may be convenient for a spina bifida patient and the carers, hydronephrosis can occur insidiously. With recurrent urine infections, hydronephrotic kidney can become pyonephrosis, which is life-threatening. Therefore, every effort should be made to carry out intermittent catheterisations along with antimuscarinic drug therapy.
Some tetraplegic patients may wish to undergo urological procedures without anaesthesia, but these patients can develop autonomic dysreflexia if cystoscopy and vesical lithotripsy are performed without anaesthesia.
We describe three tetraplegic patients, who developed autonomic dysreflexia when cystoscopy and laser lithotripsy were carried out without anesthesia.
In two patients, who declined anaesthesia, blood pressure increased to more than 200/110 mmHg during cystoscopy. One of these patients developed severe bleeding from bladder mucosa and lithotripsy was abandoned. Laser lithotripsy was carried out under subarachnoid block a week later in this patient, and this patient did not develop autonomic dysreflexia.
The third patient with C-3 tetraplegia had undergone correction of kyphoscoliotic deformity of spine with spinal rods and pedicular screws from the level of T-2 to S-2. Pulmonary function test revealed moderate to severe restricted curve. This patient developed vesical calculus and did not wish to have general anaesthesia because of possible need for respiratory support post-operatively. Subarachnoid block was not considered in view of previous spinal fixation. When cystoscopy and laser lithotripsy were carried out under sedation, blood pressure increased from 110/50 mmHg to 160/80 mmHg.
These cases show that tetraplegic patients are likely to develop autonomic dysreflexia during cystoscopy and vesical lithotripsy, performed without anaesthesia. Health professionals should educate spinal cord injury patients regarding risks of autonomic dysreflexia, when urological procedures are carried out without anaesthesia. If spinal cord injury patients are made aware of potentially life-threatening complications of autonomic dysreflexia, they are less likely to decline anaesthesia for urological procedures. Subrachnoid block or epidural meperidine blocks nociceptive impulses from urinary bladder and prevents occurrence of autonomic dysreflexia. If spinal cord injury patients with lesions above T-6 decline anaesthesia, nifedipine 10 mg should be given sublingually prior to cystoscopy to prevent increase in blood pressure due to autonomic dysreflexia.
The Manchester Triage System is commonly used as the triage system in emergency departments of the UK. As per the Manchester Triage System, patients presenting with retention of urine to the accident and emergency department are categorized to yellow, which denotes that the ideal maximum time to first contact with a treating clinician will be 60 min. Cervical spinal cord injury patients, in whom urinary catheter is blocked, may develop suddenly headache, sweating, high blood pressure, cardiac dysrhythmia, convulsions, intracranial bleed, and acute neurogenic pulmonary oedema as a result of autonomic dysreflexia due to a distended bladder.
A 46-year-old male with C-6 tetraplegia developed urinary retention because of a blocked catheter. He was seen immediately on arrival in the spinal injuries unit. The blocked catheter was removed and a new catheter was about to be inserted. Then this patient said that the ceiling lights were very bright and glaring. Five milligrams of Nifedipine was given sublingually. This patient started having fits involving his head, face, neck and shoulders with loss of consciousness. A 14-French silicone Foley catheter was inserted per urethra without any delay and 300 ml of clear urine was drained. This patient recovered consciousness within 5 min. Computed tomography of the brain revealed no focal cerebral or cerebellar abnormality. There was no intra-cranial haemorrhage.
This case illustrates that spinal cord injury patients with lesion above T-6, who develop retention of urine because of a blocked catheter, may look apparently well, but these patients can develop suddenly life-threatening autonomic dysreflexia. Therefore, spinal cord injury patients, who present to the accident and emergency department or spinal units with a blocked urinary catheter, should be seen urgently although their vital signs may be stable on arrival. Increasing the awareness of staff in emergency departments regarding autonomic dysreflexia as well as education of the patient and carers will be useful in preventing this complication in persons with spinal cord injury.
Although complications related to suprapubic cystostomies are well documented, there is scarcity of literature on safety issues involved in long-term care of suprapubic cystostomy in spinal cord injury patients.
A 23-year-old female patient with tetraplegia underwent suprapubic cystostomy. During the next decade, this patient developed several catheter-related complications, as listed below: (1) Suprapubic catheter came out requiring reoperation. (2) The suprapubic catheter migrated to urethra through a patulous bladder neck, which led to leakage of urine per urethra. (3) Following change of catheter, the balloon of suprapubic catheter was found to be lying under the skin on two separate occasions. (4) Subsequently, this patient developed persistent, seropurulent discharge from suprapubic cystostomy site as well as from under-surface of pubis. (5) Repeated misplacement of catheter outside the bladder led to chronic leakage of urine along suprapubic tract, which in turn predisposed to inflammation and infection of suprapubic tract, abdominal wall fat, osteomyelitis of pubis, and abscess at the insertion of adductor longus muscle
Suprapubic catheter should be anchored securely to prevent migration of the tip of catheter into urethra and accidental dislodgment of catheter. While changing the suprapubic catheter, correct placement of Foley catheter inside the urinary bladder must be ensured. In case of difficulty, it is advisable to perform exchange of catheter over a guide wire. Ultrasound examination of urinary bladder is useful to check the position of the balloon of Foley catheter.
When urethral catheterisation is difficult or impossible in spinal cord injury patients, flexible cystoscopy and urethral catheterisation over a guide wire can be performed on the bedside, thus obviating the need for emergency suprapubic cystostomy. Spinal cord injury patients, who undergo flexible cystoscopy and urethral catheterisation over a guide wire, may develop potentially serious complications. (1) Persons with lesion above T-6 are susceptible to develop autonomic dysreflexia during cystoscopy and urethral catheterisation over a guide wire; nifedipine 5–10 milligrams may be administered sublingually just prior to the procedure to prevent autonomic dysreflexia. (2) Spinal cord injury patients are at increased risk for getting urine infections as compared to able-bodied individuals. Therefore, antibiotics should be given to patients who get haematuria or urethral bleeding following urethral catheterisation over a guide wire. (3) Some spinal cord injury patients may have a small capacity bladder; in these patients, the guide wire, which is introduced into the urinary bladder, may fold upon itself with the tip of guide wire entering the urethra. If this complication is not recognised and a catheter is inserted over the guide wire, the Foley catheter will then be misplaced in urethra despite using cystoscopy and guide wire.
It is well known in the literature that imaging has almost no value for diagnosis of superficial bladder cancer. However, wide gap exists between knowledge on diagnosis of bladder cancer and actual clinical practice.
Delay in diagnosis of bladder cancer in a male person with tetraplegia occurred because of reliance on negative flexible cystoscopy and single biopsy, negative ultrasound examination of urinary bladder, and computerised tomography of pelvis. Difficulties in scheduling cystoscopy also contributed to a delay of nearly ten months between the onset of haematuria and establishing a histological diagnosis of vesical malignancy in this patient. The time interval between transurethral resection and cystectomy was 42 days. This delay was mainly due to scheduling of surgery.
We learn from this case that doctors should be aware of the limitations of negative flexible cystoscopy and single biopsy, cytology of urine, ultrasound examination of urinary bladder, and computed tomography of pelvis for diagnosis of bladder cancer in spinal cord injury patients. Random bladder biopsies must be considered under general anaesthesia when there is high suspicion of bladder cancer. Spinal cord injury patients with lesions above T-6 may develop autonomic dysreflexia; therefore, one should be extremely well prepared to prevent or manage autonomic dysreflexia when performing cystoscopy and bladder biopsy. Spinal cord injury patients, who pass blood in urine, should be accorded top priority in scheduling of investigations and surgical procedures.
Spinal cord injury; Urinary bladder; Carcinoma; Suprapubic cystostomy; Cystoscopy
Never Events are serious, largely preventable patient safety incidents that should not occur if the available preventative measures have been implemented. We propose that a list of “Never Events” is created for spinal cord injury patients in order to improve the quality of care. To begin with, following two preventable complications related to management of neuropathic bladder may be included in this list of “Never Events.” (i) Severe ventral erosion of glans penis and penile shaft caused by indwelling urethral catheter; (ii) incorrect placement of a Foley catheter leading to inflation of Foley balloon in urethra. If a Never Event occurs, health professionals should report the incident through hospital risk management system to National Patient Safety Agency's Reporting and Learning System, communicate with the patient, family, and their carer as soon as possible about the incident, undertake a comprehensive root cause analysis of what went wrong, how, and why, and implement the changes that have been identified and agreed following the root cause analysis.
Neuropathic urinary bladder is often colonised by multidrug-resistant bacteria. We report a 64-year-old male spinal cord injury patient with paraplegia, who received gentamicin on empirical basis before undergoing suprapubic cystostomy, as antibiotic sensitivity report of urine was not available. This patient developed fulminate septicaemia. Although appropriate antibiotic therapy (meropenem) was started when this patient manifested features of sepsis, acute renal failure occurred and he expired. Inappropriate initial antimicrobial therapy was the major contributory factor for this patient's mortality. Learning points from this case are (1) never do a cystostomy without prior urine culture and appropriate antibiogram; (2) in a chronic spinal cord injury patient, full blood count, liver function tests, albumin level, and albumin to globulin ratio should be performed before any surgical procedure.
Following spinal cord injury, prostate undergoes atrophy probably due to interruption of neuro-hormonal pathways. The incidence of carcinoma of prostate is lower in patients with spinal cord injury above T-10 than in those with lesion below T-10.
A Caucasian male sustained T-4 paraplegia in 1991 at the age of 59-years. He had long-term indwelling urethral catheter. In May 1995, routine blood test showed prostate-specific antigen to be 17.7 mg/ml. Prostate biopsy revealed moderately differentiated primary adenocarcinoma of prostate; Gleason score was 3+3. Bone scans showed no evidence of metastatic bone disease. Bilateral orchidectomy was performed in September 1995. MRI of pelvis revealed no evidence of spread beyond prostatic capsule. There was no pelvic lymphadenopathy. In October 1996, this patient got chest infection and recovered fully after taking amoxicillin. In February 2001, he developed pneumonia and was prescribed cefuroxime intravenously. In March 2001, cystoscopy and electrohydraulic lithotripsy of vesical calculi were carried out. In August 2001, this patient was admitted to spinal unit for management of pressure sores. He expired on 28 June 2002 in local hospital. Cause of death was recorded as acute ventricular failure, congestive heart failure, chronic respiratory failure and spinal cord injury.
Although prostate gland undergoes atrophy in men who sustained spinal cord injury in early age, physicians should be vigilant and look for prostatic diseases particularly in men, who have sustained spinal cord injury during later period of life. Patients with cervical and upper dorsal lesions are at risk of developing potentially life-threatening chest complications after major surgical procedures including radical prostatectomy. Therefore, it may be advisable to consider chemoprevention of prostate cancer with Finasteride, especially in men, who sustained cervical and upper dorsal spinal cord injury during later part of their life.
Spinal cord injury patients are at risk for developing unusual complications such as autonomic dysreflexia while changing suprapubic cystostomy. We report a male patient with spina bifida in whom the Foley catheter was placed in the urethra during change of suprapubic cystostomy with serious consequences.
A male patient, born in 1972 with spina bifida and paraplaegia, underwent suprapubic cystostomy in 2003 because of increasing problems with urethral catheter. The patient would come to spinal unit for change of suprapubic catheter every four to six weeks. Two days after a routine catheter change in November 2009, this patient woke up in the morning and noticed that the suprapubic catheter had come out. He went straight to Accident and Emergency. The suprapubic catheter was changed by a health professional and this patient was sent home. But the suprapubic catheter did not drain urine. This patient developed increasing degree of pain and swelling in suprapubic region. He did not pass any urine per urethra. He felt sick and came to spinal unit five hours later. About twenty ml of contrast was injected through suprapubic catheter and X-rays were taken. The suprapubic catheter was patent; the catheter was not blocked. The Foley catheter could be seen going around in a circular manner through the urinary bladder into the urethra. The contrast did not opacify urinary bladder; but proximal urethra was seen. The tip of Foley catheter was lying in proximal urethra. The balloon of Foley catheter had been inflated in urethra. When the balloon of Foley catheter was deflated, this patient developed massive bleeding per urethra. A sterile 22 French Foley catheter was inserted through suprapubic track. The catheter drained bloody urine. He was admitted to spinal unit and received intravenous fluids and meropenem. Haematuria subsided after 48 hours. The patient was discharged home a week later in a stable condition.
This case shows that serious complications can occur during change of suprapubic catheter in patients with neuropathic bladder. After inserting a new catheter, health professionals should observe spinal cord injury patients for at least thirty minutes and ensure that (1) suprapubic catheter drains clear urine; (2) patients do not develop abdominal spasm or discomfort; (3) symptoms and signs of sepsis or autonomic dysreflexia are absent.
In female patients with neuropathic bladder, the urethra is closed permanently in order to avoid urine leak. Then Benchekroun hydraulic ileal valve is attached to urinary bladder, thus providing a continent stoma for performing intermittent catheterisations.
We present a female patient with spina bifida who underwent Benchekroun continent vesicostomy in 1993. This patient developed severe stenosis of Benchekroun stoma and stones in urinary bladder. Dilatation of stoma and vesicolithotomy were carried out in 1995. Vesical calculi recurred; suprapubic cystolithotomy was performed in 1999. In March 2000, catheterisation of stoma was not possible and emergency suprapubic cystostomy was done. In April 2000, endoscopy was attempted through Benchekroun stoma. It was not possible to insert ureterorenoscope beyond two inches. The track was completely blocked. In November 2001, X-ray of abdomen showed several vesical calculi; suprapubic cystolithotomy was performed.
In March 2005, this patient developed pain in abdomen. X-ray of abdomen showed a large vesical calculus. In June 2005, suprapubic catheter was removed and a cystoscope was introduced in to the bladder. Then electrohydraulic lithotripsy was performed. In 2007, this patient was concerned about the increasing swelling in lower abdomen. Computed tomography of abdomen revealed midline, lower abdominal wall hernia, which contained several loops of small bowel and ileal cystoplasty. The large hernia was uncomfortable and tender on coughing, but did not cause obstructive bowel symptoms. Surgical repair of hernia was considered. But this patient would require alternative way of urinary diversion because the current location of suprapubic catheter would almost lead to infection of prosthetic material used in reconstruction of the anterior abdominal wall. After discussing risks of operative procedures with patient and her husband, it was decided not to proceed with surgery.
This case is a poignant reminder to spinal cord physicians that novel surgical techniques should be viewed cautiously, and patients should be informed of potential complications of surgical procedures some of which could be irreversible.
We report infection of Brindley sacral anterior root stimulator in a spinal cord injury patient, who ultimately required removal of the implant. The consequences of failed implantation were severe constipation, and loss of reflex penile erection and bladder emptying.
A male patient, born in 1973, fell off the balcony while on holidays in Crete in 1993 and developed complete tetraplegia at C-5 level. In 1996, deafferentation of sacral nerve roots 2, 3 and 4 were carried out bilaterally. Brindley sacral anterior root stimulator was implanted. On eleventh post-operative day, blood stained fluid came out of sacral wound. Microbiology of exudates showed growth of Pseudomonas aeruginosa, sensitive to gentamicin. As discharge of serosanguinous fluid persisted, sacral wound was explored. In March 1997, induration and craggy swelling were noted at the site of receiver. There was discharge from the surgical wound in the back. Wound swab grew Pseudomonas aeruginosa. The receiver was taken out. Cables were retrieved and tunnelled in left flank. Laminectomy wound was left open. In May 1997, cables were removed from left flank through the laminectomy wound. Grommet was sliced down as much as possible without producing leak of cerebrospinal fluid. Histoacryl glue was used over the truncated grommet as a sealing agent. Microbiology of end of S-2 and S-3 cables showed growth of Pseudomonas aeruginosa, which was sensitive to gentamicin. End of S-4 cable showed scanty growth of Pseudomonas aeruginosa and Klebsiella aerogenes. Review of this patient in January 1999 revealed presence of sinuses in dorsal wound exuding purulent material. The wound was explored; grommet and electrodes were removed. The consequences of failed implantation were severe constipation and loss of reflex penile erection and bladder emptying. This patient had to spend increasing amount of time for bowels management. Faecal incontinence limited his mobility. The problem with his bowels was affecting his confidence in doing anything, as the slightest movement could cause his bowels to work. The inconvenience and embarrassment of a bowel accident caused distress to the patient and to his mother.
This case illustrates that bacterial infection is a major problem in spinal cord injury patients who undergo implantation of medical devices. Further, this case underlines the need for honest discussion with spinal cord injury patients about possible complications of implantation of sacral anterior root stimulator and long-term consequences of an unsuccessful operation.
The consequences of spinal cord injury upon urinary bladder are readily recognised by patients and health care professionals, since neuropathic bladder manifests itself as urinary incontinence, or retention of urine. But health care professionals and persons with spinal cord injury may not be conversant with neuropathic dysmotility affecting the ureter and renal pelvis. We report an adult male patient with spinal cord injury, who developed bilateral hydronephrosis after he started managing neuropathic bladder by penile sheath drainage.
A male patient, born in 1971, sustained spinal cord injury following a motorbike accident in September 1988. In November 1988, intravenous urography showed normal upper tracts. He was advised spontaneous voiding with 2-3 catheterisations a day. In February 1995, this patient developed fever, chills and vomiting. Blood urea: 23.7 mmol/L; creatinine: 334 umol/L. Ultrasound revealed marked hydronephrosis of right kidney and mild hydronephrosis of left kidney. Bilateral nephrostomy was performed in March 1995. Right pyeloplasty was performed in May 1998. In July 2005, this patient developed urine infection and was admitted to a local hospital with fever and rigors. He developed septicaemia and required ventilation. Ultrasound examination of abdomen revealed bilateral hydronephrosis and multiple stones in left kidney. Percutaneous nephrostomy was performed on both sides. Subsequently, extracorporeal shock wave lithotripsy of left renal calculi was carried out. Right nephrostomy tube slipped out in January 2006; percutaneous nephrostomy was performed again. In June 2006, left ureteric antegrade stenting was performed and nephrostomy tube was removed. Currently, right kidney is drained by percutaneous nephrostomy and left kidney is drained by ureteric stent. This patient has indwelling urethral catheter.
It is possible that regular intermittent catheterisations along with anticholinergic medication right from the time of rehabilitation after this patient sustained paraplegia might have prevented the series of urological complications. Key components to successful management of external drainage of kidney in this patient are:  use of size 14 French pigtail catheter for long-term nephrostomy,  anchoring the catheter to skin to with Percufix catheter cuff to prevent accidental tug , replacing the nephrostomy dressing once a week by the same team in order to provide continuity of care, and  changing nephrostomy catheter every six months by a senior radiologist.
We review urological procedures performed on a spinal cord injury patient during three decades.
A 23-year-old male patient sustained T-12 paraplegia in 1971. In 1972, intravenous urography showed both kidneys functioning well; division of external urethral sphincter was performed. In 1976, reimplantation of left ureter (Lich-Gregoir) was carried out for vesicoureteric reflux. As reflux persisted, left ureter was reimplanted by psoas hitch-Boari flap technique in 1978.
This patient suffered from severe pain in legs; intrathecal injection of phenol was performed twice in 1979. The segment bearing the scarred spinal cord was removed in September 1982.
This patient required continuous catheter drainage. Deep median sphincterotomy was performed in 1984. As the left kidney showed little function, left nephroureterectomy was performed in 1986. In an attempt to obviate the need for an indwelling catheter, bladder neck resection and tri-radiate sphincterotomy were carried out in 1989; but these procedures proved futile. UroLume prosthesis was inserted and splinted the urethra from prostatic apex to bulb in October 1990. As mucosa was apposing distal to stent, in November 1990, second UroLume stent was hitched inside distal end of first. In March 1991, urethroscopy showed the distal end of the distal stent had fragmented; loose wires were removed. In April 1991, this patient developed sweating, shivering and haematuria. Urine showed Pseudomonas. Suprapubic cystostomy was performed. Suprapubic cystostomy was done again the next day, as the catheter was pulled out accidentally during night. Subsequently, a 16 Fr Silastic catheter was passed per urethra and suprapubic catheter was removed. In July 1993, Urocoil stent was put inside UroLume stent with distal end of Urocoil stent lying free in urethra. In September 1993, this patient was struggling to pass urine. Urocoil stent had migrated to bladder; therefore, Urocoil stent was removed and a Memotherm stent was deployed. This patient continued to experience trouble with micturition; therefore, Memotherm stent was removed. Currently, wires of UroLume stent protrude in to urethra, which tend to puncture the balloon of urethral Foley catheter, especially when the patient performs manual evacuation of bowels.
We failed to implement intermittent catheterisation along with anti-cholinergic therapy. Instead, we performed several urological procedures with unsatisfactory outcome; the patient lost his left kidney. We believe that honest review of clinical practice will help towards learning from past mistakes.
Distigmine, a long-acting anti-cholinesterase, is associated with side effects such as Parkinsonism, cholinergic crisis, and rhabdomyolysis. We report a spinal cord injury patient, who developed marked hydronephrosis and hydroureter after distigmine therapy, which led to a series of complications over subsequent years.
A 38-year-old male developed T-9 paraplegia in 1989. Intravenous urography, performed in 1989, showed normal kidneys, ureters and bladder. He was prescribed distigmine bromide orally and was allowed to pass urine spontaneously. In 1992, intravenous urography showed bilateral marked hydronephrosis and hydroureter. Distigmine was discontinued. He continued to pass urine spontaneously.
In 2006, intravenous urography showed moderate dilatation of both pelvicalyceal systems and ureters down to the level of urinary bladder. This patient was performing self-catheterisation only once a day. He was advised to do catheterisations at least three times a day. In December 2008, this patient developed haematuriawhich lasted for nearly four months.. He received trimethoprim, then cephalexin, followed by Macrodantin, amoxicillin and ciprofloxacin. In February 2009, intravenous urography showed calculus at the lower pole of left kidney. Both kidneys were moderately hydronephrotic. Ureters were dilated down to the bladder. Dilute contrast was seen in the bladder due to residual urine. This patient was advised to perform six catheterisations a day, and take propiverine hydrochloride 15 mg, three times a day. Microbiology of urine showed Klebsiella oxytoca, Pseudomonas aeruginosa, and Enterococcus faecalis. Cystoscopy revealed papillary lesions in bladder neck and trigone. Transurethral resection was performed. Histology showed marked chronic cystitis including follicular cystitis and papillary/polypoid cystitis. There was no evidence of malignancy.
Distigmine therapy resulted in marked bilateral hydronephrosis and hydroureter. Persistence of hydronephrosis after omitting distigmine, and presence of residual urine in bladder over many years probably predisposed to formation of polypoid cystitis and follicular cystitis, and contributed to prolonged haematuria, which occurred after an episode of urine infection. This case illustrates the dangers of prescribing distigmine to promote spontaneous voiding in spinal cord injury patients. Instead of using distigmine, spinal cord injury patients should be advised to consider intermittent catheterisation together with oxybutynin or propiverine to achieve complete, low-pressure emptying of urinary bladder.
Leakage of urine around a catheter is not uncommon in spinal cord injury patients, who have indwelling urethral catheter. Aetiological factors for leakage of urine around a catheter are bladder spasms, partial blockage of catheter, constipation, and urine infection. Usually, leakage of urine subsides when the underlying cause is treated. Leakage of urine around a suprapubic catheter is very rare and occurs in patients, in whom the urethra is closed due to severe stricture or previous surgery.
We describe a 35-year-old female patient with spina bifida and paraplegia, who had undergone suprapubic cystotomy followed by urethral closure for leakage of urine per urethra. She developed leakage of urine around suprapubic Foley catheter, which did not subside even after changing the catheter, ruling out vesical calculus, and ensuring that there was no kink in catheter or drainage tube. As a desperate measure, we punched a large hole at the tip of a Foley catheter and used this catheter for suprapubic drainage. Leakage of urine around suprapubic catheter stopped and the patient was greatly relieved.
Leakage of urine around a catheter requires prompt attention in spinal cord injury patients; otherwise patients can develop maceration of neuropathic skin and pressure sore. Management of spinal cord injury patients with leakage of urine around a suprapubic catheter should include (i) changing the catheter, (ii) prescribing anticholinergic drugs to control bladder spasm, (iii) treating constipation and urine infection when present, (iv) imaging studies or flexible cystoscopy to look for vesical calculus. If leakage of urine persists despite all these measures, use of a modified Foley catheter in which, a large hole has been made at the tip, is worth trying.
Suprapubic cystostomy is performed in spinal cord injury patients in order to prevent complications associated with long-term urethral catheter drainage. We report a patient in whom suprapubic catheter did not drain urine satisfactorily and imaging studies revealed hourglass bladder.
A female patient sustained paraplegia in a traffic accident in 1994 at the age of seventeen years. When she was discharged from spinal unit, she was performing self- catheterisations. In 1995, indwelling urethral catheter drainage was instituted, as she was not able to cope up with self-catheterisations. Intravenous urography, performed in 1994, 1997, 2000 and 2003 showed urinary bladder of normal shape. In 2004, this patient developed frequent blockages and bypassing of catheter; therefore, suprapubic cystostomy was performed. In 2005, she was leaking urine per urethra; therefore, an indwelling catheter was inserted; both suprapubic and urethral catheters drained urine. In 2008, suprapubic catheter failed to drain any urine. Cystogram revealed hourglass bladder. The balloon of suprapubic Foley catheter was located in the upper compartment of hourglass bladder whereas the urethral catheter was placed in the inferior compartment. Ultrasound examination of urinary bladder showed two compartments of hourglass bladder separated by a narrow waist. Computed tomography cystogram delineated smaller superior and larger inferior compartment of the hourglass bladder. At present this patient is happy to manage her bladder with suprapubic and urethral catheters.
When prompt replacement of a mal-functioning suprapubic catheter fails to rectify the problem, computer tomography cystography should be performed to check precise location of suprapubic catheter and structural abnormalities of urinary bladder. In this patient, cystogram revealed hourglass bladder. Possible reasons for development of hourglass bladder in spinal cord injury patients are: traction applied to dome of urinary bladder by Foley balloon when suprapubic catheter is taped tightly to anterior abdominal wall for several months; uncoordinated contractions of detrusor muscle; chronic cystitis leading to hypertrophy of bladder wall.
Spinal cord injury produces multiple systemic and metabolic alterations. A decrease in micro vascular blood flow to liver, spleen and muscle has been described following spinal cord injury.
We present a 46-year-old male patient with C-4 complete tetraplegia, who developed a large stag horn calculus with branches in upper, middle and lower calyces of left kidney. This patient underwent Gil-Vernet extended pyelolithotomy and required intra-operative electrohydraulic lithotripsy and retrieval of stones from upper, middle and lower calyces using flexible cystoscope and stone basket. Computed tomography, performed eighteen days after surgery, showed multiple areas of non-enhancing cortex posteriorly and in the upper pole, suggestive of focal infarction. Magnetic resonance imaging of left kidney confirmed the presence of an area of infarction in middle third of posterior cortex, but there was no evidence of trauma to posterior division of renal artery. Therefore, we postulate that compression of renal parenchyma by Gil-Vernet retractors during surgery, and firm pressure that was applied over the middle of kidney for prolonged periods while several attempts were being made to retrieve fragments of calculi from renal calyces, led to ischaemia and subsequently, infarction of mid-third posterior cortex of left kidney.
This case illustrates importance of gentle handling of kidney during extended pyelolithotomy in order to prevent subtle renal trauma, which may be detected only by advanced imaging studies. Further, spinal cord physicians should take a pragmatic approach to management of stones located inside renal calyces. Both spinal cord injury patients and their physicians should remember that in our enthusiasm to achieve complete clearance of stones embedded deeply within renal calyces, we could produce irreversible injury to kidney, as indeed happened in this patient. Therefore, emphasis should be placed on prevention of struvite renal calculi by discarding indwelling urinary catheters and eliminating Proteus bacteriuria.
A 36-year-old male sustained fracture of first lumbar vertebra, splenic tear and paraplegia in a motorcycle accident in 2001; splenectomy was performed.
In 2008, he presented with temperature and feeling rough. With a diagnosis of urine infection, he was prescribed ciprofloxacin, followed by trimethoprim, amoxicillin, and gentamicin, as temperature did not subside. White cell count was 21.2 × 109/L; lymphocytes were 13.05 × 109/L (1.00 – 4.00). Therefore, computerised tomography (CT) of chest and abdomen was performed. Thrombus was present in pulmonary arteries bilaterally involving the lobar and segmental branches. Enlarged lymph nodes were seen in axillae, chest, abdomen and inguinal regions. Radiological diagnosis was lymphoma. Cell marker showed an excess of large granular lymphocytes and activated lymphocytes. The Glandular Fever Slide Test was positive. Subsequently, Paul Bunnell test was also positive. Epstein Barr virus serology was consistent with recent Epstein Barr virus infection. Antibiotic was omitted; enoxaparin was prescribed for pulmonary artery thrombosis.
Learning points from this case: (1) Although routine administration of antibiotic to a spinal cord injury patient with pyrexia may be acceptable in outpatient setting, other possibilities such as infection by multi-drug resistant organism, viral infection, venous or, arterial thrombosis should be considered if a patient does not respond promptly to antibacterial therapy. (2) When full blood count showed lymphocytosis (comprising > 50% of white blood cells) with atypical morphology, lymphocyte surface markers, Paul Bunnell test, and Epstein Barr virus serology should be performed. These tests would have led to a diagnosis of infectious mononucleosis, and abdominal imaging studies could have been avoided. (3) Lymphoid hyperplasia is the hallmark of infectious mononucleosis; therefore, we should have suspected glandular fever rather than lymphoma when CT scan revealed enlarged lymph nodes in abdomen, mediastinum, axillae and inguinal regions in this patient, who had lymphocytosis with atypical morphology. (4) A soft tissue mass, situated inferior to left hemidiaphragm in this asplenic patient, was misinterpreted as lymph nodes; review of CT led to the correct diagnosis of splenunculus. (5) Acute infection with Epstein Barr virus may lead to transient induction of anti-phospholipid antibodies, which can cause vascular thrombosis. (6) This case illustrates the value of reviewing test results and discussion with senior doctors, as these measures help to recognize medical errors and improve patient care.
We present a male tetraplegic patient, who developed stones in neuropathic bladder six times within a span of three years. Unusual features of this case are: (1) This patient started developing stones in urinary bladder thirteen years after sustaining spinal cord injury. (2) He was performing intermittent catheterisation and did not have an indwelling catheter. (3) The presenting symptom of vesical lithiasis was abdominal spasms and not urine infection. (4) The major component of the stones was calcium phosphate; magnesium ammonium phosphate was completely absent in the calculus on four occasions. (5) Proteus species were not grown from urine at any time. (6) This patient failed to acidify urine below a pH of 5.3 after taking simultaneously furosemide (40 mg) and fludrocortrisone (1 mg), which suggested incomplete renal tubular acidosis type 1.
We learn from this case that biochemical analysis of stones removed from urinary bladder may be useful. If the major component of vesical calculus is calcium phosphate, complete or incomplete renal tubular acidosis type 1 should be excluded, as it may be possible to reduce the risk of recurrence of calcium phosphate stones by oral potassium citrate therapy or, vegetable and fruit rich diet.