Ibopamlne substitution in a dopamine. dependent patient
SIR--We report a patient who was weaned off intravenous dopamine after substitution of the new oral dopamine agonist ibopamine, t A 63-year-old, previously healthy m a n with intra-abdominal sepsis, who required n u m e r o u s laparotomies, developed intravenous dopamine dependence during a 165-day stay on our intensive care unit. No signs of sepsis were present at that time and he was normovolaemic, with a central venous pressure of 8 m m Hg. Several attempts to stop the dopamine resulted in hypotension, with a drop in intra-arterially measured blood pressure from 115/65 to 78/50 m m Hg, and oliguria, with a fall in diuresis from 120 m L / h o u r to less than 20 m L / h o u r . H e required a m i n i m u m dose of 8 gg/kg per m i n u t e of dopamine. We substituted the dopamine with ibopamine via a duodenal feeding tube at an initial dose of 100 m g three times daily. T h i s allowed a reduction of the dopamine infusion to 4 pg/kg per minute. D u r i n g the next 24 hours, the ibopamine dose was increased to 200 m g three times daily and the dopamine stopped. H e remained stable with a blood pressure of 105/60 m m Hg, a n d maintained an appropriate diuresis of at least 50 m L / h o u r . All other aspects of treatment remained unchanged. Arterial and central lines were removed and the patient was discharged to a general ward. I b o p a m i n e 200 m g three times daily was continued. Blood samples were taken o n four occasions, from a cannula in the radial artery, to measure plasma catecholamines and epinine, the active metabolite of ibopamine (table). High concentrations of catecholamines during dopamine infusion were reduced after stopping the dopamine.
tl t2 t3 t4 Normal values
Noradmnallne Adrenaline (nmol/L) (nmol/L)
44.5 8'2 5L4 3"9
862 242 15'5 32'9
1.5 not detectable 0"2 0 4 0.07-0-4
t l = during infusionof dopamine8 pg/kg per rain;t2 = 20 rainafter stopping dopamine; t3 = 30 rainafter administrationof ibopamine 100 rag;t4 = 30 rain after administrationof ibopamine200 mg Table: Plasma concentrations
Ibopamine substitution in our relatively stable patient allowed discontinuation of the intravenous dopamine infusion and earlier referral to a ger~eral ward. Although time-related effects may be responsible for this observation, we believe that this is unlikely, since repeated previous attempts to stop the intravenous dopamine failed and there were no other changes in clinical condition and/or treatment.
--t 2 2 3 bp
Figure: PCR amplification of VZV DNA in temporal bone sections Lanes 1 and 10 = 7 2 - 1 3 5 3 bp markers (Haelll ~X174, IBI-Kodak); 2, 4. 6, and 7 = 223 bp fragment amplified from VZV genome; and 3, 5, 8, and 9 : no amplification. Geniculate ganglion: affected side (lane 2 = c a s e 1. 6 =case 2) and unaffected side (lanes 4 and 8, respectively). Spiral ganglion, Scarpa's ganglion, organ of Corti. and macule of seccule (case 2): affected side (lane 3 =case 1, 7 =case 2) and unaffected side (lane 5 = c a s e 1, 9 = c a s e 2),
by Ramsay H u n t included disease affecting: the sensory portion of the facial nerve producing periauricular pain and cutaneous vesicular eruption; the sensory a n d m o t o r divisions of the facial nerve producing pain and facial paralysis; the sensory and motor parts of the facial nerve with hearing loss; and the sensory and motor divisions of the facial nerve with both hearing loss and vertigo. W e tested the hypothesis that herpes varicella-zoster viral (VZV) D N A is present in the geniculate ganglion of the facial nerve, as well as in the auditory and vestibular ganglia of patients with Ramsay H u n t syndrome (herpes zoster oticus). Archival h u m a n temporal bone sections from 2 patients with Ramsay H u n t syndrome, 10 normal controls, a n d 5 Bell's palsy patients were studied. D N A was extracted from unstained adjacent 25 p m sections t h r o u g h the geniculate ganglion and t h r o u g h the mid-modiolar region, s Primers ( 5 ' - C G T C A C ATATTATGCAAACATG-3' and 5'-CGTTTTTAATA T T A C A A A T C C C G C - 3 ' ) for a 223 base-pair (bp) fragment of V Z V genomic D N A were used and the resulting polymerase chain reaction product (figure) was confirmed by sequence analysis. I n patient 1, who h a d facial paralysis, periauricular pain, and vesicles without hearing loss, the V Z V f r a g m e n t was detected in the geniculate ganglia of the affected a n d unaffected sides. I n patient 2, who had facial paralysis, periauricular pain, and vesicles with sudden hearing loss, the V Z V fragment w a s detected in the geniculate ganglion and the mid-modiolar sections containing the auditory and vestibular ganglia o f the affected side. N o V Z V D N A was identified in the geniculate ganglion of the unaffected side of patient 2, n o r in any o f the control or Bell's palsy sections. T h e s e data suggest that the aetiology of Ramsay H u n t syndrome is recrudescence of latent V Z V located in the affected geniculate ganglia, and in the affected auditory and vestibular primary afferent ganglia of some patients.
Anthony R Milner, Jan H Zwaveling, Armand R J Girbes Department of Surgery, Intensive Care Unit, University Hospital Groningen, 9713 EZ Groningen, Netherlands
Phi/lip A Wackym, Paul Popper, Marc M Kerner, Wayne W Grody Section of Otology, Neuro-otologyand Skull Base Surgery, Division of Head and Neck Surgery; and Deoartmentof Pathology and Laboratory Medicine, UCLASchool of Medicine, Los Angeles, CA 90024, USA
1 Girbes ARJ, Van Veldhuisen DJ, Smit AJ. Dopamine agonists: a new perspective in cardiovascular therapy. Neth J &led 1991; 39: 6 5 - 71.
Varicella-zoster DNA in temporal bones of patients with Ramsay Hunt syndrome S I R - - I n 1907, oticus resulted contemporary sents neuritis encephalitis. 2~
J Ramsay H u n t suggested that herpes zoster from geniculate ganglionitis; t however, m a n y authors believe that this disorder repreor polycranial neuropathy following focal T h e original four classifications of the disease
Vo1342 • December 18/25, 1993
1 Hunt JR. On herpetic inflammations of the geniculate ganglion, a new syndrome and its complications. J Nerv Ment Dis 1907; 34: 73-96. 2 Payten RJ, Dawes DDK. Herpes zoster of the head and neck. J Laryngol Oto11972; 86: 1031-55. 3 Goldberg-M6Uer J, Olsen S, Kettel K. Histopathology of the facial nerve in herpes zoster oticus. Arch Otolaryngo11959; 69: 266--75. 4 Aviel A, Marshak G. Ramsay Hunt syndrome: a cranial polyneuropathy. Am J Otolaryngol 1982; 3: 61-66. 5 Wachym PA, Simpson TA, Gantz BJ, Smith RJH. Polymerase chain reaction amplification of DNA from archival celloidin-embedded human temporal bone sections. Laryngoscope 1993; 103: 583-88. 1555