Correspondence
In conclusion, we report a case where the use of
TEA in combination with antihypertensive therapy
may have caused a serious adverse event. Several lessons can be learned from this case report: firstly, in
patients with hypertension, starting two antihypertensive drugs at the same time may be dangerous. In
our patient, this was justified because of the severity
of the hypertension in combination with the urgent
need for the operation. However, starting two drugs
at the same time may influence BP too much, so it
seems prudent to start a beta-blocker first and eventually add an ACE-inhibitor later. Secondly, caution
should be taken when resuming antihypertensive
therapy in patients with TEA. In the absence of literature evidence, our recommendations in patients
on epidural analgesia are to resume antihypertensive
therapy only if the mean BP is within 20% of the
preoperative BP. Finally, in the direct postoperative
period, frequent BP recordings are very important,
in particular in patients with epidural analgesia.
B. G. Fikkers, J. Damen, G. J. Scheffer
Department of Anaesthesiology
Radboud University Nijmegen Medical Centre
Nijmegen, The Netherlands

895

H. C. Kruithof
Department of Geriatrics
Centre of Mental Health Care GGZ Oost Brabant
Oss, The Netherlands

References
1. Klungel OH, de Boer A, Paes AH, Nagelkerke NJ,
Seidell JC, Bakker A. Estimating the prevalence of hypertension corrected for the effect of within-person variability
in blood pressure. J Clin Epidemiol 2000; 53: 1158–1163.
2. Liu S, Carpenter RL, Neal JM. Epidural anaesthesia and analgesia. Their role in postoperative outcome. Anesthesiology
1995; 82: 1474–1506.
3. Cashman JN, Dolin SJ. Respiratory and haemodynamic
effects of acute postoperative pain management: evidence
from published data. Br J Anaesth 2004; 93: 212–223.
4. Stenseth R, Bjella L, Berg EM, Christensen O, Levang OW,
Gisvold SE. Effects of thoracic epidural analgesia on pulmonary function after coronary artery bypass surgery. Eur J
Cardiothorac Surg 1996; 10: 859–865.
5. Hopf HB, Schlaghecke R, Peters J. Sympathetic neural
blockade by thoracic epidural anaesthesia suppresses renin
release in response to arterial hypotension. Anesthesiology
1994; 80: 992–999.
6. Jaeger JM, Madsen ML. Delayed subarachnoid migration
of an epidural Arrow FlexTip Plus catheter. Anesthesiology
1997; 87: 718–719.

Hyponatraemic convulsions and fatal head injury secondary
to desmopressin treatment for enuresis
EDITOR:
Desmopressin analogues (DDAVP) are licensed for the
treatment of enuresis and are commonly prescribed by
general practitioners and urologists for patients with
nocturnal enuresis which is unresponsive to alternative
treatments. Although generally well tolerated, these
agents may have serious side-effects such as hypotonic
hyponatraemia. DDAVP-induced hyponatraemia has
been reported in adults treated for bleeding disorders
and in children treated for enuresis but to date there
have been few reports of symptomatic hyponatraemia
developing in adults treated with DDAVP for enuresis. We describe a case of desmopressin-induced severe
hyponatraemia in an adult being treated for nocturnal

Correspondence to: Vivienne Larney, Department of Anaesthesia, St. Georges’
Hospital, Blackshaw Road, London, SW17 OQT, UK. E-mail: vivienne_larney@
hotmail.com; Tel: ⫹44 208 6721255; Fax: ⫹44 208 7253135
Accepted for publication 16 April 2006 EJA 3717

enuresis which led to the development of seizures
and a subsequent fatal traumatic brain injury.
A 27-year-old male was transferred to our neurosurgical intensive care unit (ICU) for management of
a traumatic brain injury. He had developed seizures
at home and subsequently fell off a chair injuring his
head. His seizures continued and on admission to a
local hospital he was fitting and deeply comatose
with a Glasgow Coma Score (GCS) of 4. Intravenous
diazepam and phenytoin were administered, his trachea was intubated, and an urgent computed tomography (CT) brain scan was performed. This showed a
left fronto-temporal contusion with mass effect, and a
small subdural haematoma (Fig. 1). Of note, he was
hyponatraemic on admission with a serum sodium of
116 mmol L⫺1 and a calculated serum osmolality of
254 mosm kg⫺1. He was subsequently transferred to
our neurosurgical ICU for further management.
His family revealed that he had been treated with
desmopressin nasal spray for enuresis for the previous

© 2006 Copyright European Society of Anaesthesiology, European Journal of Anaesthesiology 23: 890–898

896

Correspondence

Figure 1.
CT brain showing a left fronto-temporal contusion with mass effect
and a small subdural haematoma.

8 years. Enuresis seems to have been a problem only
when he consumed alcohol. He had two previous
admissions to another hospital in the previous 3 years
with seizures associated with hyponatraemia. The first
of these occurred when after consuming alcohol and
cocaine he developed seizures and required tracheal
intubation and ICU admission for 2 days. His sodium
on this occasion was 112 mmol L⫺1 and a CT brain
was normal. A further admission for seizures occurred
a year later. Again alcohol had been consumed and he
was noted to be hyponatraemic (Na⫹ 117 mmol L⫺1).
A diagnosis of probable ‘alcohol-induced seizures’ was
made on that occasion and the patient was discharged.
The history of desmopressin use was not obtained
during these two previous admissions.
On arrival in our neurosurgical ICU an intracranial
pressure (ICP) monitor was inserted and his head
injury was managed according to our standard protocol aiming to maintain ICP ⬍20 mmHg and cerebral
perfusion pressure (CPP) ⬎60 mmHg. Further laboratory tests confirmed the presence of hypotonic
hyponatraemia. On clinical examination the patient
was euvolaemic and his hyponatraemia was felt to be
due to a combination of desmopressin treatment and
excess fluid intake. As cerebral oedema secondary to
traumatic brain injury is exacerbated by the presence
of hyponatraemia, correction of his low sodium was
imperative. Using a combination of hypertonic saline
and fluid restriction his sodium rose from
116 mmol L⫺1 to 130 mmol L⫺1 over 24 h. Despite
careful correction of his low sodium, and appropriate
management of his head injury, he developed severe
cerebral oedema and raised ICP necessitating a craniotomy and partial left frontal lobectomy. Postoperatively the patient continued to deteriorate, his ICP
continued to rise and he died 4 days after admission
from his head injury.

Desmopressin (DDAVP) is a synthetic structural
analogue of antidiuretic hormone (ADH) licensed for
the treatment of cranial diabetes insipidus, nocturia
associated with multiple sclerosis and primary nocturnal enuresis. Compared with ADH, desmopressin has
a longer lasting and more potent antidiuretic effect
and is devoid of vasopressor effects. When used for the
treatment of nocturnal enuresis, intranasal desmopressin can induce water intoxication with profound
hyponatraemia and resultant seizures if water intake
is not restricted.
There have been numerous case reports of
desmopressin-induced symptomatic hyponatraemia
in children treated for enuresis [1–6] but only a few
case reports of this complication occurring in
enuretic adults [7–9]. A recent review and metaanalysis of trials looking at the use of desmopressin
in older adults with nocturia found the pooled estimate for the incidence of hyponatraemia was 7.6%
[10]. This suggests that hyponatraemia as a complication of desmopressin treatment is relatively common. However in most cases the hyponatraemia is
mild and asymptomatic. In a large randomized trial
investigating desmopressin for long-term treatment
of nocturia in 249 patients, the incidence of hyponatraemia was 14% but was clinically significant in
only 0.8% [11].
The risk of developing hyponatraemia associated
with desmopressin therapy is higher in those patients
with above average fluid intake. In the case described
above, the use of desmopressin followed by excessive
alcohol intake precipitated a fall in serum sodium.
Although the patient’s demise was not directly due to
the presence of desmopressin-induced hyponatraemia,
it played a pivotal role leading to seizure activity and
a subsequent fall resulting in a traumatic brain injury.
The cerebral oedema which resulted was further exacerbated by the presence of hyponatraemia and ultimately proved fatal.
Due to the potential for serious adverse effects,
desmopressin should not be considered as the first
choice treatment for primary nocturnal enuresis.
Careful selection of patients who will comply with
instructions regarding restriction of fluid intake and
who understand the potential serious adverse effects is
necessary prior to commencing therapy with desmopressin. When therapy is commenced it is essential
to monitor the patient’s daily fluid intake and serum
sodium periodically. These measures may help to
prevent the development of this serious and potentially fatal iatrogenic condition.
V. Larney, R. Dwyer
Department of Anaesthesia and Intensive Care
Beaumont Hospital
Dublin, Ireland

© 2006 Copyright European Society of Anaesthesiology, European Journal of Anaesthesiology 23: 890–898

Correspondence

References
1. Beach PS, Beach RE, Smith LR. Hyponatraemic seizures
in a child treated with desmopressin to control enuresis.
Clin Pediatr 1992; 31: 566–569.
2. Yaouyanc G, Jonville AP, Yaouyanc-Lapalle H et al. Seizure
with hyponatremia in a child prescribed desmopressin for
nocturnal enuresis. Clin Toxicol 1992; 30: 637–641.
3. Kallio J, Rautava P, Huupponen R et al. Severe hyponatremia caused by intranasal desmopressin for nocturnal
enuresis. Acta Paediatr 1993; 82: 881–882.
4. Schwab M, Wenzel D, Ruder H. Hyponatraemia and cerebral convulsion due to short term DDAVP therapy for control of enuresis nocturna. Eur J Pediatr 1996; 155: 46–48.
5. Donoghue MB, Latimer ME, Pillsbury HL et al.
Hyponatremic seizure in a child using desmopressin for nocturnal enuresis. Arch Pediatr Adolesc Med 1998; 152: 290–292.
6. Apakama DC, Bleetman A. Hyponatraemic convulsion
secondary to desmopressin treatment for primary enuresis.
J Accid Emerg Med 1999; 16: 229–230.

897

7. Bernstein SA, Williford SL. Intranasal desmopressinassociated hyponatremia: a case report and literature review.
J Fam Pract 1997; 44: 203–208.
8. Odeh M, Oliven A. Coma and seizures due to severe
hyponatremia and water intoxication in an adult with
intranasal desmopressin therapy for nocturnal enuresis.
J Clin Pharmacol 2001; 41: 582–584.
9. Shindel A, Tobin G, Klutke C. Hyponatremia associated
with desmopressin for the treatment of nocturnal polyuria.
Urology 2002; 60: 344.
10. Weatherall M. The risk of hyponatremia in older adults
using desmopressin for nocturia: a systematic review and
meta-analysis. Neurourol Urodyn 2004; 23: 302–305.
11. Lose G, Mattiasson A, Walter S et al. Clinical experiences
with desmopressin for long-term treatment of nocturia.
J Urol 2004; 172: 1021–1025.

Total spinal anaesthesia following epidural test dose
in an ankylosing spondylitic patient with anticipated
difficult airway undergoing total hip replacement
EDITOR:
The use of regional anaesthesia in patients with a
recognized difficult airway does not solve the problem of difficult airway; the difficult airway is still
present. We report a case where giving regional
anaesthesia in a patient with difficult airway, required
emergency securing of the airway.
A 58-yr-old male patient (55 kg, 160 cm, ASA II)
suffering from ankylosing spondylitis for 25 yr was
scheduled for total hip replacement. Airway examination revealed interincisor distance of 4 cm, normal
dentition, and reduced mentosternal distance of
6 cm due to fixed flexion deformity of neck. X-ray
revealed ankylosis of spinous processes showing posterior joint involvement, resorption of the anterior
surfaces of the vertebral bodies and ossification of the
posterior ligaments and surrounding soft tissues.
Anaesthesia was planned with a combined spinal
epidural (CSE), separate needle technique, with difficult intubation cart ready. Premedication consisted
of diazepam 10 mg orally the previous night and oral
ranitidine 150 mg with metoclopramide 10 mg 2 h
before surgery. On arrival in the operating room,
routine monitoring was applied and an intravenous
(i.v.) line was secured. The epidural block was
Correspondence to: Yatindra Kumar Batra, Department of Anaesthesiology and
Intensive Care, Postgraduate Institute of Medical Education and Research,
Chandigarh-160012, India. E-mail: ykbatra@glide.net.in
Accepted for publication 15 April 2006 EJA 3788

attempted by the para-median approach through
L3–4 space with the patient in the sitting position
but the space could only be localized in the third
attempt. While threading the epidural catheter,
some initial resistance was met at the 10-cm mark
but was overcome. Later, multiple attempts were
made with 26-G Quinke’s needle to locate the subarachnoid space, but free flow of cerebrospinal fluid
could not be obtained and the procedure was abandoned. We decided to proceed with epidural block
alone. Before fixing the epidural catheter, basal readings of heart rate (HR) and blood pressure (BP) were
recorded and a test dose of lidocaine 2% 3 mL with
epinephrine 15 µg (1:200 000) was injected, after
negative aspiration, to confirm the position of catheter
in the epidural space. Soon after the test dose the
patient complained of dizziness and weakness. He
was asked to lie down in the supine position and
oxygen provided by face mask. Within a couple of
minutes the patient became unconscious, apnoeic
and BP dropped to 80/50 mmHg with severe bradycardia (heart rate ⬍ 36 min⫺1). Immediately atropine
0.6 mg and mephentermine 6 mg were given i.v. and
attempts at mask ventilation with 100% oxygen were
made. The patient’s HR increased but it was not
possible to mask-ventilate despite inserting an oral
airway. An attempt to intubate the trachea with
direct laryngoscopy also failed. By this time the
patient had started desaturating with SPO2 reading
80%. However, we were able to place a size 4 laryngeal

© 2006 Copyright European Society of Anaesthesiology, European Journal of Anaesthesiology 23: 890–898