Case Series
Volumetric Overload Shocks (VOS) Causing the Transurethral Resection of the Prostate (TURP) Syndrome: Case Reports
Khalid A Ghanem1, Nisha Pindoria2, Salma A Ghanem3 and Ahmed N Ghanem4*
1Mansoura University Hospital, Egypt
2North Middlesex University Hospital Sterling Way, London
3Barts & the Royal London NHS Trust, Royal London Hospital, London
4Consultant Urologist Surgeon, Egypt
*Corresponding author: Ahmed N Ghanem, Consultant Urologist Surgeon, No 1 President Mubarak Street, Mansoura, 35511, Egypt
Published: 25 Oct, 2018
Cite this article as: Ghanem KA, Pindoria N, Ghanem
SA, Ghanem AN. Volumetric
Overload Shocks (VOS) Causing the
Transurethral Resection of the Prostate
(TURP) Syndrome: Case Reports. Ann
Clin Case Rep. 2018; 3: 1551.
Abstract
Introduction and Objective: The TURP syndrome complicates 1.5% glycine absorption during
the TURP procedure. It presents as vascular shock previously reported as hyponatraemic shock.
However, it is commonly mistaken for haemorrhagic or septicaemic shock and is treated with
volume expansion causing lethal outcome. The first two case reports reported here represent this
practice. The remaining two cases report the concept of VOS causing TURP syndrome and the life
saving treatment of Hypertonic Sodium Therapy (HST).
Patient and Methods: Four case reports are presented. Two represent the old school of thinking
using volume expansion for treatment of TURP syndrome with lethal outcome. Two cases represent
the modern school advancing the concept of VOS for the patho-etiology of TURP syndrome and
using HST for treatment.
Results: The first two cases were mistaken for a recognized shock and treated with volume expansion;
both died. The remaining two cases were identified as VOS1 and treated with HST whose lives were
saved.
Conclusion: The concept of VOS identified in the patho-etiology of the TURP syndrome as VOS1
characterized with acute hyponatraemia allows using HST as life saving therapy. VOS2 is that
induced by saline-based fluids and has no such clear marker.
Introduction
The TURP syndrome is well known in urology [1,2]. It complicates 1.5% glycine absorption
during the TURP procedure. It presents as vascular shock previously reported as hyponatraemic
shock [2]. However, it is commonly mistaken for haemorrhagic or septicaemic shock and is treated
with volume expansion causing lethal outcome [3]. The first two case reports reported here represent
this practice.
Recently, however, the role of VOS in the patho-etiology of the TURP syndrome has been
recognized [4,5]. It clearly demonstrates that further volume expansion is absolutely contraindicated
in the treatment of the TURP syndrome, for which Hypertonic Sodium Therapy (HST)
is the correct life-saving treatment. The remaining two cases reported here represent this practice.
Case Reports
Case 1
At the end of a 2 hours TURP procedure on a fit 78 years old man suffered severe hypotension
shock and cardiac arrest on the operating table. He was resuscitated with 4 units of blood, one litre
of Haemaccel, one litre of Hartmann and 200 ml of sodium Bicarbonate after which his serum
sodium concentration was 124 mmol/L. He remained shocked, in coma, respiratory distressed
requiring Dopamine infusion and assisted ventilation. He was thought to remain hypovolaemic
and volume expansion policy aiming at elevating his Central Venous Pressure (CVP) continued;
further infusion of 5 units of blood and 10 litres of colloids and crystalloids were given in 24 hours
and failed to elevate his pressures. Although fluid restriction and peritoneal dialysis were started on the 5th post operative day he became progressively oedematous
wit bilateral plural effusions. Progressive cerebral, renal, cardiac,
respiratory and gastro-intestinal failures led to his death on the 21th
post operative day. He had sterile cultures of urine and blood. Post
mortem examination was not done.
Case 2
Three hours after TURP with resection of 127 grams of tissue
on a previously fit 74 year old man under spinal anaesthetic, he
became unconscious, shocked and suffered respiratory arrest.
His blood pressure dropped to 79/40 mm hg, pulse to 36 beats per
minute and CVP to -1 cm saline. His serum sodium concentration
dropped to 103 mmol/L. He was given 6 units of blood and 3 litres
of colloids and crystalloids after which his serum sodium was raised
to 123 mmol/L. He was intubated, ventilated and received supportive
measures on ICU. He underwent further infusions of 21 units of
blood, 3 litres of colloids and 4 litres of crystalloids but his pressures
remain persistently low. Fourteen hours later severe catheter bleeding
required open packing of the prostatic cavity. Gastric and wound
capillary bleeding occurred despite normal coagulation screen and
repeated platelet infusions. It became clear he was fluid overloaded.
Although fluid restriction and peritoneal dialysis were started on
the 2nd day progressive cerebral, cardiovascular, respiratory, renal
and hepato-biliary failure occurred and culminated in his death on
the 6th postoperative day. His serum sodium and osmolality prior
to death were 130 and 321 respectively. Increased cardiac enzymes
activity suggested myocardial infarction [Creatinine kinase 16 (< 8
U/L), Hydroxybuterate dehydrogenase 557 (< 120 U/L) and Aspartate
Transferase (< 40 U/L).
Post-mortem examination showed enlarged congested and
oedematous lung, liver, heart and kidneys. All tissues were laden with
water, 1,500 ml of blood stained fluid was found in the plural spaces
and 3 litres in the peritoneal cavity. The myocardium was oedematous
but there was neither infarction nor coronary artery disease.
Case 3
Six hours after endoscopic bladder tumour resection on 67
year old fit man, he became comatosed and hypotensive (BP
70/50 mm hg). He was thought to be in hypovolaemic shock and
was transfused with 5 units of blood and 3 litres of colloids and
crystalloids. His blood pressure remained below 90 mm hg and
CVP at-5 cm saline. He developed generalized convulsive fit, 12 hour
later a neurological assessment confirmed coma with fixed dilated
pupils and quadriplegia. He was thought to have suffered cerebrovascular
accident. At this time bladder perforation was diagnosed
and his serum sodium dropped to 110 mmol/L. He underwent a
rapid infusion of 500 ml 5% NeCl, followed by laparotomy and over
sewing of bladder perforation. Three litres of fluid was drained from
his peritoneal cavity. Postoperatively he passed 4.5 litres of urine
and recovered fully from coma and quadriplegia. He was discharged
home on the 14th postoperative day.
Case 4
During TURP on a fit 74 year old man, his BP raise temporarily
from 129/89 mm hg to 160/100 mm hg. He later became hypotensive
and developed brochospasm and pulmonary crepitations. Frusimide,
atropine and aminophylline were given. The patient had undergone
an infusion of 2 units of blood, one litre of Haemaccel and one litre
of Hartmann. On recovery from the anaesthetics, he suffered a
generalised convulsive fit and went into coma. Pulmonary oedema,
bronchospasm and cardiac dysrythmia re-occurred. He remained
socked, hypothermic, comatosed and annuric. His BP was 80/50
mm hg CVP ranging between -9 cm and -4 cm saline; giving an
impression of hypovolaemic shock. However, a volume of 5.5 litres
of the irrigating fluid 1.5% Glycine was calculated missing from the
returned fluid; remaining inside the patient’s body. His immediate
postoperative serum sodium concentration was 101 mmol/L and
serum osmolality was 270 mOsm/L. The osmolality further dropped
to 217 mOsm/L after 4 hours. Volumetric overload shock was realised
and a fluid restriction policy was adopted in spite of the low BP and
CVP. He was given a rapid infusion of 1.8% sodium chloride and 400
ml of 8.4% sodium bicarbonate, given in 200 ml increments and each
was followed by estimation of serum electrolytes and osmolality. Over
the next 24 hours he lost 5.1 litres of urine and 1.7 litres of gastric
aspirate leading to his full recovery. He was discharged home on the
6th postoperative day.
Discussion
Here we report 4 cases of the TURP syndrome of which two
died and two survived. The two who died are representative of most
previous reports on the TURP syndrome. Their conditions were
mistaken for one of the recognised shocks such as haemorrhagic or
septicaemic shock and were treated with further volume expansion.
Such practice should be made obsolete.
The remaining two case reports are representative of the modern
school of practice. In this school volume expansion is absolutely
contraindicated. The role of VOS in the patho-etiology of the TURP
syndrome has been reported [4,5].
It advances Hypertonic Sodium Therapy (HST) of 5% sodium
chloride or 8.4% sodium bicarbonate as the treatment of choice
which is life saving.
The advantage of recognising VOS is not only saving the lives of
the TURP syndrome identified as VOS1 patients but also paves the
way for recognising the condition induced by sodium-based fluids
identified as VOS2. The latter has no clear serum marker such as
hyponatraemia seen in VOS1 and is more difficult to identify. VOS2
presents with the Adult Respiratory Distress Syndrome (ARDS).
References
- Ghanem AN, Ward JP. Osmotic and metabolic sequelae of volumetric overload in relation to the TURP syndrome. Br J Urol. 1990;66:71-8.
- Harrison RH 3rd, Boren JS, Robinson JR. Dilutional hyponatraemic shock: another concept of the transurethral prostatic reaction. J Urol. 1956;75(1):95-110.
- Bertrand J, Gambini A, Cazalaa JB. Le syndrome de resection de la prostate (TURP) syndrome, mythe oy realite? Jour d’ Urologie. 1981;87:1-4
- Ghanem AN, Ghanem SA. Volumetric overload shocks: Why Is starling’s law for capillary interstitial fluid transfer wrong? the hydrodynamics of a porous orifice tube as alternative. Surgical Science. 2016;7(6):245-9.
- Ghanem SA, Ghanem KA, Ghanem AN. Volumetric overload shocks in the patho-etiology of the Transurethral Resection of the Prostate (TURP) syndrome and acute dilution hyponatraemia: the clinical evidence based on prospective clinical study of 100 consecutive TURP patients. Surg Med Open Access J. 2017:1(1);1-7.