Nephrol Dial Transplant (1996)
11:
885-886
Case Report
NephrologyDialysisTransplantation
Acute renal failure
in the
setting
of
the neuroleptic malignant syndrome
Z. Korzets,
E.
Zeltzer
and J.
Bernheim
Dept.
of
Nephrology, Meir Hospital, Kfar Saba
and the
Sackler School
of
Medicine, Tel Aviv University, Tel Aviv, Israel
Key words: acute renal failure; neuroleptic malignantsyndrome; rhabdomyolysis
Introduction
Neuroleptic malignant syndrome
(NMS) is a
rare
but
potentially fatal reaction associated with neuroleptic
drugs.
It is
characterized
by
hyperthermia, muscularrigidity, changes
in
mental status
and
autonomicdysfunction
[1]. The
diffuse muscle rigidity leads
to
myonecrosis with resultant rhabdomyolysis
and the
possible production
of
myoglobinuric renal failure.In this report
we
present
a
patient with
NMS
aftertreatment with haloperidol,
who
developed acute renalfailure
due to
rhabdomyolysis.
The
clinical features
of
NMS,
their pathophysiology,
and the
associationbetween
the
syndrome
and
rhabdomyolysis-inducedacute renal failure
are
discussed.
As the
presence
of
renal failure
in NMS
confers
a
worse prognosis
[1,2],
physician awareness
is
mandatory
for
rapid diagnosisof NMS
and the
early institution
of
aggressive treat-ment modalities.Case
Report
An 83-year-old Caucasian female was initially admittedto
our
hospital because
of
ascending cholangitis.Relevant past history included the presence of coronaryheart disease with repeated hospitalizations
for pul-
monary oedema.
The
patient
had
also been diagnosedas suffering from
an
organic brain syndrome.Laboratory data showed
a
leukocytosis
of
11500/ul,serum urea 73 mg/dl, creatinine
1.6mg/dl,
aspartateaminotransferase
316 IU/1 (N
7-37), alanine amino-transferase
319 IU/1 (N
0-40), y-glutamyl transferase868 IU/1
(N
7-49), alkaline phosphatase
559
IU/1
(N
53-128),
and a
bilirubin
of
4.3 mg/dl (2.5 mg/dl
direct).
Total protein
was 7.7 g/dl
with
an
albuminlevel
of 4.3 g/dl,
calcium
10
mg/dl, phosphorus3.6 mg/dl
and
creatinine phosphokinase
(CPK) 170
Correspondence
and
offprint requests
to:
Prof. J.
Bernheim, Dept.
of
Nephrology, Meir Hospital, Kfar Saba, Israel.
IU/1
(N
15-170). Treatment with intravenous fluidsand broad-spectrum antibiotics
led to a
rapid improve-ment, with resolution
of the
patient's fever
and
jaun-
dice.
However,
she
became extremely agitated
and
restless
and
was prescribed haloperidol
2
mg daily fromthe third hospital
day. In a
much calmer
and
sedate state,
she was
discharged after
7
days with
a
recommendation
to
continue haloperidol
at a
doseof
1
mg/day.Twelve days later,
the
patient
was
readmittedbecause
of the
onset
of
extreme pyrexia. Physicalexamination revealed
an
obese woman
in a
highlydisoriented
and
confused state. Body temperature
was
41.5°C, pulse
150
b.p.m.,
and
blood pressure variedwidely between 130/80
and
60/40 mmHg. Significantgeneralized body rigidity
was
evident. Laboratoryinvestigations this time showed
a
haemotocrit
of
26%,leukocytes
19 400/(xl
with
a
shift
to the
left, thrombo-cytes 91000/ul, serum sodium
161
mEq/1,
potassium3.5
mEq/1,
urea 217 mg/dl, creatinine
6.4
mg/dl,
cal-
cium
3.8
mg/dl, phosphorus 26 mg/dl, albumin 3
g/dl,
and bicarbonate
21
mEq/1.
CPK
values peaked
at
15200 IU/1 with
a
lactate dehydrogenase
of
2830
IU/1
(range 230-460). Aminotransferases, alkaline phos-photase,
and
bilirubin were within normal limits. Urineoutput was 200 ml/day with urinalysis being unremark-
able.
Urine myoglobin
was
negative.
A
chest X-raywas without abnormality. Repeated blood
and
urinecultures were negative. Cerebrospinal fluid was normal.Aggressive supportive measures (notably without
dia-
lysis) were initiated
in
addition
to
empiric treatmentwith bromocriptine mesylate 5
mg
thrice daily. Withinthe next
9
days
the
patient's condition improved
con-
siderably.
Her
fever abated,
she
became orientated,and blood pressure stabilized
at
130/70 mmHg.
She
entered
a
polyuric phase with
a
decline
of
serumcreatinine
to
her baseline value
of 1.6
mg/dl.
In
parallel,CPK values decreased
to 1119
IU/1, calcium increasedto
7.8
mg/dl,
and
phosphorus returned
to a
normal
3.1
mg/dl. However, despite this dramatic improve-ment,
she
suddenly died
on the 12th
hospital
day.
Discussion
The entity known
as NMS was
first described
in 1960
by Delay
et al.
[3]
during
the
early clinical trials
of
© 1996 European Dialysis
and
Transplant Association-European Renal Association
Leave a Comment