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A UNIQUE COMPLICATION OF URETEROSIGMOIDOSTOMY: A CHANCE ENCOUNTER WITH A RECTAL STONE
Sir,
A 47-year-old man who had bilateral uretero-sigmoidostomies carried-out for ectopia vesicae as an infant, was referred to the urology clinic. There had been no long-term follow-up and he presented with symptoms of rectal bleeding and change in bowel habit. Renal function blood tests and an IVU were normal. Prior to flexible sigmoidoscopy, digital rectal examination revealed a large calculus within the rectum. Manual removal of the stone failed due to its size (5 X 7cm). Removal under a general anaesthetic was facilitated using Rampleys forceps and the calculus was sent for biochemical analysis. This revealed a triple phosphate calculus suggesting an aetiology related to the urinary diversion procedure. Sigmoidoscopy identified the ureteric orifices and polyp consisting of transitional epithelium. At follow-up he remained symptom-free and had consented to regular endoscopic surveillance.
Complications such as metabolic disturbance, renal function deterioration and malignant change following ureterosigmoidostomy are well-recognised.1,2
Indeed, the first patient undergoing this procedure 150 years ago died as a result of calcium deposits occluding both ureters. Currently, regular followup and life-long annual endoscopic surveillance are recommended following uretero-sigmoidostomy in providing optimal management.3 In this report we present what appears to be a unique complication from ureterosigmoidostomy whilst highlighting the importance of regular endoscopy in picking up pre-malignant and malignant changes at the site of uretero-sigmoid anastomoses.
Further reading:
1. Hall MC, Koch MO,
McDougal WS. Metabolic
consequences of urinary
diversion through intestinal
segments. Urol Clin North
Am 1991; 18: 725-35.
2. Wear JBJ, Barquin OP.
Ureterosigmoidostomy.
Long-term results. Urology
1973; 1: 192-200.
3. Husmann DA, Spence HM.
Current status of tumor
of the bowel following ureterosigmoidostomy: a
review. J Urol 1990; 144: 607-10
Mr D.A. Payne & Mr H.N. Blackford
Correspondence to: Mr D. A. Payne, Department of Surgery, Clinical Sciences Building, Leicester Royal Infirmary, Welford Road, Leicester, LE7 2LX, U.K.
Sir,
Re: “An alternative approach to fishbone extraction” by R. Viney and A. Reid J R Coll Edinb 2002; 47:515
I note with interest the method for removal of fishbones from the lingual tonsil described in recent article by R. Viney and A. Reid, J R Coll Edinb 47.2.
I am concerned about the potential danger of aspiration with the method described in the article. During the act of swallowing no visual control of the described manipulation is possible as the palate and the tongue base will obstruct the view through the nasal endoscope. This could potentially result in the dislodgement of the foreign body and its aspiration during the described procedure. It would be safer to perform the removal under a general anaesthetic but, if it is not possible or successful with instrumentation under a local anaesthetic and constant direct or endoscopic visual control.
The authors state that the removal of most impacted foreign bodies in the upper aero-digestive tract is possible with instrumentation via the buccal cavity. I find the term buccal cavity confusing, as it is nor described in the common texts on the anatomy of the mouth and could be mistaken for the oral vestibule. I assume the authors meant the oral cavity.
Further reading:
1. Viney R, Reid A. An
alternative approach to
fishbone extraction.
J R Coll
Surg Edinb
2002;
47:
515
2 Proops DW. (1997) The mouth
and related faciomaxillary
structures. In Scott-Brown’s
Otolaryngology (Volume 1,
Basic Sciences). Pp 1/8/1-4. Butterworth Heinemann,
Oxford
3. McMinn R M H. (1994) Mouth
and hard palate. In Last’s
Anatomy, pp 476-7. Churchill
Livingstone, Edinburgh
Mr D.C. Wild
Leicester Royal Infirmary
Sir,
I write in response to Mr. Wild’s letter expressing concern over potential aspiration of a fishbone lodged in the lingual tonsil during nasendoscopic extraction.1 It is true that swallowing during the manoeuvre briefly obstructs the view of the nasendoscope, but fortunately, the act of swallowing inhibits inhalation and also mechanically protects the airway making aspiration very unlikely.
Further reading:
1. Viney R, Reid A. An alternative approach to fishbone extraction. J R Coll Surg Edinb 2002; 47: 515
Mr R. Viney
West Midlands, U.K.
Sir,
Re: “Wandering spleen: case report and literature review” Satyadas et al. J R Coll Edinb 2002; 47: 512-514
We read with interest the casereport by Satyadas et al concerning the management of a ‘wandering spleen’. Their decision to undertake an elective splenectomy is, however, curiously at odds with their own recommendation for splenic preservation in the form of a splenopexy.1 The authors cite their patient’s refusal to consider blood transfusion as a significant influence on their decision to abandon such conservatism, but singularly fail to provide a morbidity measure for the splenic relocation surgery which they appear to be so hesitant of. In fact, the published data that does exist fails to support the presumed assumption that splenopexy is associated with a significant risk of haemorrhage.
Whilst we would agree that a suture placed through the splenic capsule is more suited to an infant age-group (where it is both more resilient and better defined) a splenopexy need not carry with it any significant risk of post-operative haemorrhage - especially if capsular sutures are avoided. Our own preference is to relocate the detorted spleen into a mesh pouch and secure it in the left upper quadrant - a technique which avoids the placement of sutures in the capsule. We have previously reported the technique and the patient concerned remains well and symptom free at 5 years. It is our belief that this intervention would have served the author’s patient well and would have avoided the additional risk of sepsis which the individual concerned now undoubtedly faces as a consequence of her splenectomy.
Mr T. Lane
Queen Mary Westfield School of
Medicine and Dentistry,
London, U.K.
Ms M. South
The Maidstone Hospital,
Kent, U.K.
Sir,
The case report “Wandering spleen” (vol 47 Number 2 April 2002) is an interesting one. I note that the ultrasound scan of the abdomen and pelvis was apparently reported as showing a mass with a vascular pedicle in the lower abdomen suggestive of a wandering spleen. This is a robust report for a soft tissue mass with no characteristic features, as shown in the CT scan. The ultrasound scan has an arrow on a normal kidney and there is no apparent evidence of a soft tissue mass or the vascular pedicle.
Is this not rather a confusing image for a surgical journal and I wondered what the average radiological opinion would be. My opinion is that this is a normal kidney in the ultrasound scan and the CT image does show a nonspecific soft tissue mass in the pelvis.
I would be interested to hear your views on this ultrasound image.
Mr C.E. Mackintosh
Harley Street,
London, U.K.
There is no response from Satyadas et al to the letters submitted in response to their article Wandering spleen: case report and literature review Satyadas et al. J R Coll Edinb 2002; 47: 512-514
Sir,
Re: “Fireworks injury: temporal bone penetration and a wooden intra-cranial foreign body” by A. Al Mulla, M. Purva and A. Behbehani, J R Coll Surg Edinb Re: “Predictors of excessive blood 46.4 249-251
We read with interest the article published in the August 2001 edition of the Journal of The Royal College of Surgeons of Edinburgh. However, it seems to us that the authors made two mistakes.
Firstly, they say that a firework is a low velocity missile. This term is correct in the sense that the firework travels at a velocity below the speed of sound. However, a more contemporary approach would be to refer to the energy transfer, in this case the energy transfer was high as a temporary cavity is likely to have formed as the brain tissue moved away from the firework fragment and the temporal bone was fractured.
Secondly, they state that the diabetes insipidus occurred within a few hours of the surgery going on to suggest that this was a syndrome of inappropriate vasopressin (anti-diuretic hormone) secretion, typical of a severe head injury. Surely the injury the girl sustained caused damage to the hypothalamus, which in turn led to a deficiency of antidiuretic hormone as its production, or secretion was impaired. Consequently, neurogenic diabetes insipidus ensued. This in turn would have caused the hypernatraemia, polyuria and production of dilute urine, which they correctly describe as diabetes insipidus, but which they believe was caused by inappropriate anti-diuretic hormone (SIADH) secretion.
SIADH secretion is associated with head injuries, but because of the relative excess of anti-diuretic hormone the features are opposite to those they describe. It would seem to us that these two distinct conditions have been confused.
Mr C. McLean & Mr J. Bernard
Department of Orthopaedics,
Mayday
University Hospital,
London Road,
Thornton Heath,
Croydon, U.K.
Sir,
Predictors of excessive loss during operative treatment of hip fractures” Odumala et al. J R Coll Edinb 2002; 47: 552-556
We read your article with interest but we would like to raise some issues regarding it:
Estimation of platelet count and coagulation function do not feature in your article. Many patients who are ASA grade III / IV will have deranged coagulation systems and the measurement of these is likely to be a more sensitive predictor of blood loss.
The multivariate analysis identified those patients with ischaemic heart disease and cerebrovascular disease as being particularly “at risk”. This group of patients are invariably taking anticoagulant medication and, therefore, are more likely to experience greater blood loss. While this has not been assessed in your article it is a well-known observation that anti-coagulated patients bleed more.
Would it be right to assume that ASA grading was carried out by the anaesthetist? What guideline or protocol was used to ensure standardisation when assessing co-morbid condition severity, and was this carried out by one individual or several?
You state a 36% transfusion rate in your population, which seems quite high. We are not certain that this mirrors the practice in the rest of the country. It would have been helpful if the criteria for transfusion used in your unit were specified. Current guidelines suggest transfusion only if haemoglobin levels are below 8g/dl, or the patients co-morbid conditions are exacerbated by anaemia.1
The 16 patients treated by cannulated screw fixation should have been excluded from the study from the outset. This group, quite clearly, will not sustain the same blood loss as open operations and then inclusion of these patients in the data merely biases the results.
A blood loss of 480mls, assuming a haematocrit of around 45% equates to only 216mls of cell loss, which equates to around 1g of haemoglobin. This is replaced intra-operatively with crystalloid, it being rare to require intra-operative blood during a hemiarthroplasty of DHS. The indication for cross matching a patient pre-operatively is if blood will be needed intra- or immediately postoperatively and it would be interesting to see at what point during your patients treatment the blood transfusion took place.
Also, your statement that patients at risk of cerebral myocardial ischaemia should be given blood if unresponsive to crystalloid infusions seems unclear; surely, it is standard practice to give blood to all surgical patients who develop “shock” secondary to blood loss, irrespective of their risk factors.
Using transfusion rates as markers of blood loss, unless indications for transfusion are standardised, will always give biased results and we, therefore, applaud your attempts to further define pre-operative factors predicting excessive blood loss. However, we feel there are some major confounding factors in your study, which make interpretation of the data difficult. As always, the patients must be treated on individual grounds after consideration of their own unique circumstances, but simple practice of pre-operative group and saving, with a post-operative haemoglobin check, and transfusion based on current guidelines saves unnecessary cost and wastage of blood products as well as avoiding the inherent risks in blood transfusion.
Further reading:
1. UK Blood Transfusion and Tissue Transplantation Guidelines, Handbook of Transfusion Medicine. Edition 3, Chapter 6.
Mr B.J. Davis & Mr B. Kapoor
Stoke-on-Trent,
U.K.
Sir,
We are grateful to Mr Davies and Mr Kapoor for their comments on our article published recently in your journal. We have carefully considered all the points they have raised.
We did not add the patient’s platelet count and coagulation status as an independent variable because we believe that this will be reflected in their ASA grade and “at risk status” of patients. In addition, we wanted to emphasise on clinical parameters and not on laboratory variables which usually have a high correlation with clinical independent variables. The ASA grade of the patients in this prospective study was carried out by the first author to avoid inter-observer variability and was based on the American College of Anaesthesiology guidlines.1
We agree that a transfusion rate of 36% is quite high, although similar rates been reported by some workers.2 This occurred because a higher transfusion trigger of 10gmdl (2/3 of all transfusions) was used by most of the consultants at the time of this study. The remaining one-third of our patients were transfused intra-operatively. This has since been revised down to the accepted guidelines of between 7-8gmdl after this study.
We disagree that the 16 patients treated with cannulated screws should be excluded from the study from the onset because this remains a type of operation for femoral neck fractures with surgical hip exposure similar to that of a 2 hole DHS. However, this group of patients was excluded from the statistical analysis because none of them lost more than 480mls. As for patients “at risk” who develop shock during operative procedures, the American College of Physicians (ACP) makes it clear that they should be only given blood if they remain unstable despite adequate crystalloid therapy.3 They reasoned that the emphasis should be on physiological responses such as: urine output, blood pressure, skin temperature, severity of lactic acidosis, an haemoglobin levels and of between 7-8gmdl.
We acknowledge that predicting increased blood loss in hip fractures is a complex subject but we have decided to study fewer independent variables and emphasise more clinical variables to avoid the possibilities of a type 1 error. We agree it would be desirable to look at laboratory parameters but we believe it would be more useful and accurate for blood loss to be measured by direct laboratory methods.
Further reading:
1. American College of
Anaesthesiology. New
classification of physical
status.
Anaesthesioogy
1963;
24:
111
2. Levi N. Blood Transfusion
requirements in Intracapsular
femoral neck fractures.
Injury
1996;
27:
709-11
3. Practice strategies for elective
red blood cell transfusion.
American College of
physicians. Ann Intern Med
1992; 116; 403-6
Mr A.O. Odumala
South Wales