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Year : 2014  |  Volume : 58  |  Issue : 4  |  Page : 502-504  

Cardiovascular manifestations of perioperative acute urinary bladder over-distension

Department of Anaesthesia and Intensive Care, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India

Date of Web Publication17-Aug-2014

Correspondence Address:
Dr. Smita Prakash
C 17 HUDCO Place, New Delhi - 110 049
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-5049.139033

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How to cite this article:
Prakash S, Kale S, Mullick P, Gogia AR. Cardiovascular manifestations of perioperative acute urinary bladder over-distension. Indian J Anaesth 2014;58:502-4

How to cite this URL:
Prakash S, Kale S, Mullick P, Gogia AR. Cardiovascular manifestations of perioperative acute urinary bladder over-distension. Indian J Anaesth [serial online] 2014 [cited 2021 May 10];58:502-4. Available from: https://www.ijaweb.org/text.asp?2014/58/4/502/139033


Bladder over-distension may lead to undesirable autonomic manifestations such as vomiting, bradycardia, hypotension, hypertension, cardiac dysrhythmias, or even asystole. [1] We report two clinically diverse cardiovascular presentations of acute bladder over-distension.

Case 1: A 64-year-old male, with no associated comorbidities, was scheduled for transurethral resection of the prostate (TURP). Spinal anaesthesia was administered (2 ml heavy bupivacaine 0.5% plus fentanyl 10 μg). T8 level of sensory blockade was achieved. The intraoperative period was uneventful. In the recovery room, the patient was stable, heart rate (HR) 84/min, blood pressure (BP) 126/80 mmHg, SpO 2 99% and sensory block at T8 level. One hour later, the patient became restless, anxious, and diaphoretic. HR was 44/min, BP 90/60 mmHg, SpO 2 98%. Atropine 0.6 mg intravenous (IV) was administered. Abdominal examination revealed a grossly distended bladder (up to umbilicus). The tri-way urinary catheter lumen draining the bladder was blocked (blood clots) while bladder irrigation with saline continued, resulting in acute bladder over-distension. Bladder irrigation was discontinued. Patency of the draining catheter was established, and 650 ml of urine/saline was drained. Level of block had regressed to T10. The patient experienced relief and became haemodynamically stable.

Case 2: A 45-year-old, female was scheduled for staging laparotomy for ovarian malignancy under general anaesthesia. Pre-anaesthetic evaluation was unremarkable. Standard anaesthetic technique was used. Intra-operatively, patient's vitals remained stable and but her urine output was only 30 ml at 1.5 h. Fluid administered was adequate, and the bladder was not distended. A fluid challenge (500 ml Ringer's lactate) was administered followed by furosemide (10 mg) IV. Otherwise, patient had received crystalloid (3000 ml), colloid (500 ml) and blood (one unit). Patient had lost one litre of blood intraoperatively. Surgery lasted 3.5 h. The patient remained haemodynamically stable (HR: 62-76/min, BP: 110/76-126/82 mmHg). While abdomen closure was in progress, HR increased from 62/min to 157/min, BP 158/114 mmHg, irregular pulse and multiple atrial ectopics. Per-abdomen examination revealed an over distended bladder due to blocked catheter. Following a saline flush, 500 ml urine was drained. Within seconds of bladder decompression, HR decreased from 150 to 60/min and BP was 117/65 mmHg. The patient made an uneventful recovery.

Urinary retention(UR) is common after anaesthesia and surgery with a reported incidence between 5% and 70%. [2] The risk factors for UR include anaesthetic (excessive fluid administration, opioids, anticholinergics, neuraxial blockade); surgical (hernia repair, rectal and urologic surgery, duration of surgery >2 h) and patient factors (previous history of UR, underlying neurologic dysfunction, age >60 years, pre-existing contracted bladder). [3]

Clot retention (catheter blockage) manifests itself with suprapubic distension, severe lower abdominal discomfort, decreased or no exit of fluid and leakage of fluid/urine around the catheter. Symptoms of pain and lower abdominal discomfort may be masked by regional anaesthesia where bladder filling perception is abolished, [2] as in case 1. However, decreased fluid exit and presence of leakage around the catheter should alert to presence of catheter obstruction in a post-TURP patient. Close monitoring for colour and consistency of bladder returns, patency of inflow/outflow tubing and rate of irrigation can prevent postoperative bladder distension.

In case 2, furosemide was administered as urine output was less than optimal despite adequate fluid replacement, no response to a fluid challenge and after confirmation of a non-distended bladder by the surgeon during laparotomy. A blocked catheter resulted in bladder over-distension and consequent haemodynamic manifestations. Prior to administration of a diuretic, it is imperative that the patency of the urinary catheter (kinking/obstruction) and its correct position in the bladder be ascertained.

Normal adult bladder capacity ranges between 400 and 600 ml. [3] The first need to void is experienced at a bladder volume of 150 ml and the urge to void at 300 ml. [3] Dullness of the bladder to the level of the umbilicus provides a rough estimate of at least 550 ml of urine, but it can vary as much as 1000 ml with dullness extending above the umbilicus. [4] Spontaneous voiding of urine does not occur until after segmental sensory analgesia has regressed to S3.

Urinary bladder distension can cause cardiac dysrhythmias, most likely due to autonomic disturbances. [5],[6] Eggers and Baker [5] reported multifocal ventricular tachycardia attributed to a neurogenic reflex due to bladder over-distension. Yamaguchi et al. [6] described the appearance of bigeminy on distension of the bladder in a conscious 47 years old diabetic. The parasympathetic response to acute over-distension is possibly due to a vaso-vagal reflex (afferent impulse enters the spinal cord through the pelvic nerves, ascends via sacro-bulbar connection close to the vagal nuclei and the resultant vaso-vagal reflex). [7] A vesicovascular response to urinary bladder distension is mediated by sympathetic vasoconstrictor neurons that contribute to increased sympathetic outflow. [8]

Acute bladder over-distension is an important, but often unrecognised medical complication. Potentially harmful UR should be suspected in the presence of severe pain, restlessness, confusion, chills, bradycardia, hypotension or hypertension, cardiac dysrhythmias or vomiting.Failure to recognise acute over-distension of the bladder can lead to serious cardiovascular morbidity.

   References Top

1.Ishikawa T, Sato J, Nishino T. Acute changes in bladder volume produce minimal cardio-respiratory responses in lightly anesthetised humans. Can J Anaesth 2000;47:786-91.  Back to cited text no. 1
2.Baldini G, Bagry H, Aprikian A, Carli F. Postoperative urinary retention: Anesthetic and perioperative considerations. Anesthesiology 2009;110:1139-57.  Back to cited text no. 2
3.Lamonerie L, Marret E, Deleuze A, Lembert N, Dupont M, Bonnet F. Prevalence of postoperative bladder distension and urinary retention detected by ultrasound measurement. Br J Anaesth 2004;92:544-6.  Back to cited text no. 3
4.Kemp D, Tabaka N. Postoperative urinary retention: Part II - A retrospective study. J Post Anesth Nurs 1990;5:397-400.  Back to cited text no. 4
5.Eggers GW Jr, Baker JJ. Ventricular tachycardia due to distention of the urinary bladder. Anesth Analg 1969;48:963-7.  Back to cited text no. 5
6.Yamaguchi Y, Tsuchiya M, Akiba T, Yasuda M, Kiryu Y, Fuzishiro Y, et al. Action of autonomic nervous reflex arising from visceral organs upon the heart. Acta Neuroveg 1966;28:224-33.  Back to cited text no. 6
7.Yamaguchi Y, Tsuchiya M, Akiba T, Yasuda M, Kiryu Y, Hagiwara T, et al. Nervous influences upon the heart due to overdistension of the urinary bladder: The relation of its mechanism to vago-vagal reflex. Keio J Med 1964;13:87-99.  Back to cited text no. 7
8.Fagius J, Karhuvaara S. Sympathetic activity and blood pressure increases with bladder distension in humans. Hypertension 1989;14:511-7.  Back to cited text no. 8


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