Delayed Manifestation of T ransurethral Syndrome as a Complication of T ransurethral Prostatic Resection

Published Quarterly

Mangalore, S outh India

ISSN 0972-5997

Vol ume 2; Issue 4; October-December

Case report

Delayed Manifestation of T ransurethral Syndrome as a Complication of

T ransurethral Prostatic Resection

Praveen Jadhav, Honorary Physician

Meera Jadhav, Honorary Surgeon

Pratibha Patel, Honorary Anaesthetist

Sunita Paithankar, Vivek Magdum, Medical Officers

Jairam Hospital and Research Center, Nashik R oad, Nashik 422101.

E-mail [email protected]

Citation: Jadhav P, Jadhav M, Patel P, Paithankar S, Magdum V. Delayed

Manifestation of T rans urethral Syndrome as a Complication of T rans urethral Prostatic

Resection. Online J Health Allied Scs. 2003; 4: 6

URL: http: //www.ojhas.org/issue8/2003-4-6.htm

Open Access Archive: http: //cogpr ints.ecs.s oton.aa uk/vi ew/s ubj ects /OJHAS. html

Abstract

Metabolic encephalopathy as a part of
‘transurethral syndrome’ is an immediate
complication following trans urethral resection of
prostate. It occurs during or few hours after the
s urgery. (1) However, delayed manifestation of
this complication is rare. It is also possible that
pretreatment with diuretics can exaggerate this
problem by predisposing the patient to
electrolyte abnormalities. Here we present a
report of such a patient who manifested with
neurological complications six days after the
prostate surgery.

Case Report

S eventy four year old male was operated for
prostate enlargement. He was a known case of
hypertens ion and ischemic heart disease and
was on regular treatment with nifedipine,
atenolol, indapamide, nitrates, nicorandil and
low dose aspirin. T ransurethral prostatic
resection was done and bladder wash was given
us ing 6 liters of glycine. Post-operative course
was uneventful and patient was discharged four
days later in a stable condition on pre-existing
treatment, antibiotics (cefixime) and doxazocin.

Two days later patient was brought with 7-8
hours history of increasing dr ows iness,
uneas iness, chest discomfort, hiccups and
vomiting. He had tachycardia (heart rate of 1 04
per minute), blood pressure of 150/90 mmHg,
and normal chest signs. He was drowsy, had no
focal neurological deficit and had bilateral
ex tens or plantar s . His drowsiness increased over
the next 4- 5 hours, from being alert to
responding sluggishly to verbal commands. He
had a generalized tonic convulsion, with up
rolling of eyeballs and incontinence. His
abdomen gradually distended with only sluggish
peristalsis being audible.

His initial investigations revealed serum sodium
of 130 meq/lit, potassium of 2.9 meq/lit,
chlorides of 92 meq/lit, calcium of 7.8 mg/dl,
magnesium of 1 .4 mg/dl, and phos phor us of 2.5
mg/dl . His renal and hepatic parameters,
hemoglobin, clotting profile and CT scan were
normal . There was neutrophilic leucocytos is
(WBC count of 12,400 per cubic mm).
Electrocardiogram showed generalized T wave
inversion.

He was started on replacement therapy with
potassium drip. T hough calcium replacement
could have further dropped the potassium
levels , decision was taken to replace the
depleted levels of calcium with 10 ml of calcium
gluconate intravenously for the first day.
Phenytoin was started for preventing further
convuls ions and antibiotics for preventing
infections . He was kept nil by mouth with
continuous aspiration of gastric contents.

Repeated electrolyte examinations were
performed. T hough potassium levels returned to
normal , hyponatremia manifested on the second
day after    admission (129 meq/lit).

Correspondingly,      abdominal      distension

decreased and peristalsis reappeared. However,

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