Laser lithotripsy of vesical calculi in tetraplegic subjects with long-term urinary catheters is fraught with complications because of bladder wall oedema, infection, fragile urothelium, bladder spasms, and autonomic dysreflexia. Severe haematuria should be anticipated; failure to institute measures to minimise bleeding and prevent clot retention can be catastrophic. We present an illustrative case.
A tetraplegic patient underwent laser lithotripsy of vesical stone under general anaesthesia. During lithotripsy, severe bladder spasms and consequent rise in blood pressure occurred. Bleeding continued post-operatively resulting in clot retention. CT revealed clots within distended but intact bladder. Clots were sucked out and continuous bladder irrigation was commenced. Bleeding persisted; patient developed repeated clot retention. Cystoscopy was performed to remove clots. Patient developed abdominal distension. Bladder rupture was suspected; bed-side ultrasound scan revealed diffuse small bowel dilatation with mild peritoneal effusion; under-filled bladder containing small clot. Patient developed massive abdominal distension and ileus. Two days later, CT with oral positive contrast revealed intra-peritoneal haematoma at the dome of bladder with perforation at the site of haematoma. Free fluid was noted within the peritoneal cavity. This patient was managed by gastric drainage and intravenous fluids. Patient's condition improved gradually with urethral catheter drainage. Follow-up CT revealed resolution of bladder rupture, perivesical haematoma, and intra-peritoneal free fluid.
If bleeding occurs, bladder irrigation should be commenced immediately after surgery to prevent clot retention. When bladder rupture is suspected, CT of abdomen should be done instead of ultrasound scan, which may not reveal bladder perforation. It is debatable whether laparotomy and repair of bladder rupture is preferable to nonoperative management in tetraplegics. Anti-muscarinic drugs should be prescribed prior to lithotripsy to control bladder spasms; aspirin and ibuprofen should be omitted. If significant bleeding occurs during lithotripsy, procedure should be stopped and rescheduled. Percutaneous cystolithotripsy using a wide channel could be quicker to clear stones, as larger fragments could be retrieved; lesser stimulant for triggering autonomic dysreflexia, as it avoids urethral manipulation. But in patients with small, contracted bladder, and protuberant abdomen, percutaneous access to urinary bladder may be difficult and can result in injury to bowels.
Spinal cord injury; Tetraplegia; Neuropathic urinary bladder; Vesical calculus; Laser lithotripsy; Complications; Bladder perforation
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.
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.
Anterior sacral root stimulation combined with sacral posterior rhizotomy restores bladder function in spinal cord-injured patients suffering from hyperactive bladder. After successful implantation of bladder stimulator, urinary infection rate decreases, and patients are able to get rid of indwelling urinary catheters, which in turn reduce the risks for vesical malignancy. We present a spinal cord injury patient with non-functioning Brindley sacral anterior root stimulator, who developed carcinoma of urinary bladder.
A Caucasian male, who was born in 1943, sustained paraplegia at T-4 (ASIA-B) in 1981. This patient underwent implantation of sacral anterior root stimulator in September 1985. The bladder stimulator started giving trouble since 1996 and the patient went back to using indwelling urethral catheter. In August 2006, this patient passed blood in urine after a routine change of indwelling catheter. Cystoscopy showed unhealthy bladder mucosa. Bladder biopsy revealed carcinoma, which was infiltrating bundles of muscularis propria. Many of the nests showed evidence of squamous differentiation, while others could be transitional or squamous. This patient underwent cystectomy with lymphadenectomy in March 2007 in a hospital nearer his home. Histology showed three nodes involved. This patient has been doing well since the operation.
Occurrence of vesical malignancy in this patient with non-functioning bladder stimulator is a timely reminder to all health professionals, and health care managers that concerted efforts should be made to rectify a non-functioning sacral anterior root stimulator as soon as possible. Otherwise, facilities should be made available in the community for the spinal cord injury patient to use intermittent catheterisation and thereby, avoid permanent indwelling catheter, vesical calculi and urine infections, which are risk factors for bladder cancer.
Indwelling urethral catheter is often used in male spinal cord injury patients to provide drainage to neuropathic bladder. If the balloon of a Foley catheter is inflated in urethra or, when a properly inserted Foley catheter is later pulled and thereby, the Foley balloon comes to lie in urethra, an excessive length of catheter will remain outside the penis. This sign is termed "long catheter sign". Long catheter sign will also be positive when Foley catheter slips out of urinary bladder in situations where Foley balloon is ruptured by a spiky vesical calculus or deflated due to a defective valve.
A fifty-year-old Caucasian male with paraplegia at T-5 level had been managing neuropathic bladder by long-term indwelling urethral catheter. During his stay in spinal unit, the patient felt that there had been a tug on the drainage tube when he was being turned during night as part of the routine care for relief of pressure. Next morning, a health professional noticed that a long segment of catheter was lying outside penis. There was no bleeding from urethral meatus. Catheter continued to drain urine, which was yellowish in colour. Urine output was satisfactory. This patient did not develop any clinical feature of autonomic dysreflexia nor was he feeling unwell. In view of positive long catheter sign, radiological studies were performed to check the position of Foley catheter, which confirmed the clinical impression of incorrectly positioned Foley catheter. The catheter was removed; flexible cystoscopy was performed. A 16 Fr, 20 ml balloon Foley catheter was inserted over a 0.032" guide wire. Following this procedure, a considerably shorter length of Foley catheter remained outside the penis.
Positive long catheter sign indicates that the Foley catheter is placed incorrectly and needs repositioning urgently. Prompt recognition of long catheter sign and immediate repositioning of Foley catheter will help to prevent complications such as chronic distension of urinary bladder, urine infection, and pressure necrosis of urethra especially if Foley balloon remains inflated within urethra for a long period. In this patient, use of a Foley catheter with 20 ml balloon, and securing the drainage tube to thigh with two straps, helped to prevent inadvertent pull of Foley balloon into the urethra.
Silicone Foley catheters tend to become stiffer as size of the catheter increases. Whereas the tip of a size 12 French silicone, Foley catheter is soft and flexible, a size 24 French silicone, Foley catheter is distinctly stiff. Chronically inflamed neuropathic bladders are susceptible to perforation by the tip of a Foley catheter. We report a patient with multiple sclerosis and moderately severe chronic cystitis, in whom a size 22 French Foley catheter burrowed through the dome of urinary bladder.
A 55-year-old, Caucasian male suffering from multiple sclerosis underwent suprapubic cystostomy in January 2007. Initially, a size 16 Fr. silicone, Foley, catheter was inserted. During subsequent catheter changes, silicone Foley catheters of progressively increasing sizes were inserted and in July 2007, a size 22 Fr. catheter was used in order to prevent blockages and consequent bypassing of urine. In April 2008, he had an uneventful change of suprapubic catheter; but a week later, this patient developed profuse bypassing. On examination, suprapubic catheter contained fresh blood; there was hardly any urine in the leg bag, which was attached to suprapubic catheter. Cystogram showed localised extravasation of contrast on the superior aspect of urinary bladder around the tip of Foley catheter, which protruded beyond the dome of urinary bladder. The size 22 Fr. catheter was removed and a size 20 Fr silicone, Foley, catheter was inserted ensuring that the tip of catheter pointed towards bladder neck. This patient received gentamicin intravenously and he was prescribed ciprofloxacin for five days. He did not develop temperature or other features of sepsis. Bypassing stopped completely.
In this patient, bladder biopsy had shown moderately severe chronic inflammation and congestion. We learn from this case that we should have used a smaller size catheter, which has a softer texture and changed the catheter at shorter intervals rather than insert a larger bore catheter, and run the risk of perforation of neuropathic bladder by the tip of a stiff Foley catheter.
The spontaneous rupture of an infected renal cyst is a rare event. Spontaneous rupture with drainage to the exterior through a surgical scar has not been reported previously.
A 49-year-old male with tetraplegia had undergone extended right pyelolithotomy in 1999. Deroofing and marsupialisation of a cyst in the upper pole of the right kidney was performed in 2003. Subsequently there was recurrence of a thick-walled cystic space-occupying lesion in the upper pole of the right kidney. Thick pus was aspirated from the renal cyst on six occasions between September 2003 and November 2004. In March 2006, ultrasound examination revealed a cyst measuring 6.2 cm in diameter in the upper pole of the right kidney. Aspiration was planned when the renal cyst reached 7.5 cm in diameter. However, 11 months later, the cyst ruptured spontaneously and drained through the previous surgical scar in the flank, while the patient was recovering from a severe chest infection in the spinal unit. Ultrasound examination showed a fistulous tract running between the renal cyst and the abdominal wall. Repeated minor trauma sustained during turning, hoisting and chest physiotherapy all may have contributed to the rupture of the infected renal cyst and drainage through a weak spot in the abdominal wall.
In hindsight, we might have prevented rupture of the renal cyst had we considered aspiration of the renal cyst before it reached 7.5 cm in diameter, although this 7.5 cm diameter, as the threshold for percutaneous aspiration, is an arbitrary setting. This patient could have been advised to wear an abdominal corset to protect the right flank from pressure applied unintentionally during turning, hoisting or assisted coughing.
Increased spasms in spinal cord injury (SCI) patients, whose spasticity was previously well controlled with intrathecal baclofen therapy, are due to (in order of frequency) drug tolerance, increased stimulus, low reservoir volume, catheter malfunction, disease progression, human error, and pump mechanical failure. We present a SCI patient, in whom bladder calculi acted as red herring for increased spasticity whereas the real cause was spontaneous extrusion of catheter from intrathecal space.
A 44-year-old male sustained a fracture of C5/6 and incomplete tetraplegia at C-8 level. Medtronic Synchromed pump for intrathecal baclofen therapy was implanted 13 months later to control severe spasticity. The tip of catheter was placed at T-10 level. The initial dose of baclofen was 300 micrograms/day of baclofen, administered by a simple continuous infusion. During a nine-month period, he required increasing doses of baclofen (875 micrograms/day) to control spasticity. X-ray of abdomen showed multiple radio opaque shadows in the region of urinary bladder. No malfunction of the pump was detected. Therefore, increased spasticity was attributed to bladder stones. Electrohydraulic lithotripsy of bladder stones was carried out successfully. Even after removal of bladder stones, this patient required further increases in the dose of intrathecal baclofen (950, 1050, 1200 and then 1300 micrograms/day). Careful evaluation of pump-catheter system revealed that the catheter had extruded spontaneously and was lying in the paraspinal space at L-4, where the catheter had been anchored before it entered the subarachnoid space. A new catheter was passed into the subarachnoid space and the tip of catheter was located at T-8 level. The dose of intrathecal baclofen was decreased to 300 micrograms/day.
Vesical calculi acted as red herring for resurgence of spasticity. The real cause for increased spasms was spontaneous extrusion of whole length of catheter from subarachnoid space. Repeated bending forwards and straightening of torso for pressure relief and during transfers from wheel chair probably contributed to spontaneous extrusion of catheter from spinal canal in this patient.
Men with spinal cord injury (SCI) appear to have a greater incidence of bacterial colonisation of genital skin as compared to neurologically normal controls. We report a male patient with paraplegia who developed rapidly progressive infection of scrotal skin, which resulted in localised necrosis of scrotum (Fournier's gangrene).
This male patient developed paraplegia at T-8 level 21 years ago at the age of fifteen years. He has been managing his bladder by wearing a penile sheath. He noticed redness and swelling on the right side of the scrotum, which rapidly progressed to become a black patch. A wound swab yielded growth of methicillin-resistant Staphylococcus aureus (MRSA). Necrotic tissue was excised. Culture of excised tissue grew MRSA. A follow-up wound swab yielded growth of MRSA and mixed anaerobes. The wound was treated with regular application of povidone-iodine spray. He made good progress, with the wound healing gradually.
It is likely that the presence of a condom catheter, increased skin moisture in the scrotum due to urine leakage, compromised personal hygiene, a neurogenic bowel and subtle dysfunction of the immune system contributed to colonisation, and then rapidly progressive infection in this patient. We believe that spinal cord injury patients and their carers should be made aware of possible increased susceptibility of SCI patients to opportunistic infections of the skin. Increased awareness will facilitate prompt recourse to medical advice, when early signs of infection are present.
Memokath urethral sphincter stents are used to facilitate bladder emptying in patients with spinal cord injury, but long term follow-up has not been reported.
Case series of ten men with spinal cord injury who underwent insertion of Memokath stents and were followed for up to nine years.
Within four years, the stent had to be removed in nine out of ten patients because of: extensive mucosal proliferation causing obstruction to the lumen of the stent; stone around the proximal end of the stent, incomplete bladder emptying, and recurrent urinary infections; migration of the stent into the bladder related to digital evacuation of bowels; large residual urine; concretions within the stent causing obstruction to flow of urine, and partial blockage of the stent causing frequent episodes of autonomic dysreflexia. In one patient the stent continued to function satisfactorily after nine years.
The Memokath stent has a role as a temporary measure for treatment of detrusor-sphincter dyssynergia in selected SCI patients who do not get recurrent urinary infection and do not require manual evacuation of bowels.
We present a case to illustrate controversies in percutaneous drainage of infected, perinephric haematoma in a tetraplegic patient, who had implantation of baclofen pump in anterior abdominal wall on the same side as perinephric haematoma.
A 56-year-old male with C-4 tetraplegia had undergone implantation of programmable pump in the anterior abdominal wall for intrathecal infusion of baclofen to control spasticity. He developed perinephric haematoma while he was taking warfarin as prophylactic for deep vein thrombosis. Perinephric haematoma became infected with a resistant strain of Pseudomonas aeruginosa, and required percutaneous drainage. Positioning this patient on his abdomen without anaesthesia, for insertion of a catheter from behind, was not a realistic option. Administration of general anaesthesia in this patient in the radiology department would have been hazardous.
Results and Conclusion
Percutaneous drainage was carried out by anterior approach under propofol sedation. The site of entry of percutaneous catheter was close to cephalic end of baclofen pump. By carrying out drainage from anterior approach, and by keeping this catheter for ten weeks, we took a risk of causing infection of the baclofen pump site, and baclofen pump with a resistant strain of Pseudomonas aeruginosa. The alternative method would have been to anaesthetise the patient and position him prone for percutaneous drainage of perinephric collection from behind. This would have ensured that the drainage track was far away from the baclofen pump with minimal risk of infection of baclofen pump, but at the cost of incurring respiratory complications in a tetraplegic subject.