- Email: [email protected]
The pelvic floor and incontinence
The
Figure: Coronary angiogram of proximal aneurysm of left anterior descending coronary artery
erythema chronicum migrans, neurological involvement, and oligoarthritis, with positive IgG ELISA for B burgdorferi. Echocardiography revealed a reduced left ventricular ejection fraction (26%), dilated aorta, aortic insufficiency II, and a huge aneurysm in the region of the left anterior descending coronary artery. Coronary angiography confirmed an aneurysm of the proximal left anterior descending coronary artery, measuring 1-2 cm in diameter (figure). A 46-year-old man presented with dilated cardiomyopathy (ejection fraction 36%) and typical stage III Lyme borreliosis acrodermatitis chronicaa (paraesthesias, atropicans, cardiovascular oligoarthritis, involvement, typical tick bite, and erythema chronicum migrans history plus positive IgG ELISA). Routine coronary angiography was done to 4
exclude ischaemic heart disease
as
the
of left showed an
source
ventricular dysfunction. Coronary angiography aneurysm of the proximal anterior descending coronary artery, measuring 1-0 cm in diameter, confirmed by
echocardiography. Coronary aneurysms have been reported secondary to vaculitis in Kawasaki syndrome, Takayasu syndrome, and late syphillis. 1-5 It is not unlikely that coronary artery aneurysms may result from spirochaetal infection following vascular inflammation in late Lyme borreliosis. Dilated cardiomyopathy and aortic dilation would also argue in favour of an inflammatory genesis of the coronary arterial aneurysms. Since echocardiography has a high sensitivity (100%) for proximal coronary aneurysms, this non-invasive technique could be routinely used to screen late Lyme disease patients for aneurysms. R Gasser, N Watzinger, B Eber, O Luha, E Reisinger, G Seinost, W Klein, on behalf of the Borreliosis Study Group Department of Medicine, University of Graz, 8036 Graz, Austria We thank the following members of the Borreliosis Study Group for their helpful contributions: I Wendelin, F Fruhwald, H Zebedin, and
J Bergloff. 1
2
Cox J, Krajden M. Cardiovascular manifestations of Lyme disease. Am Heart J 1991; 122: 1449-55. Gasser R, Dusleag J, Reisinger E, et al. Reversal by ceftriaxone of dilated cardiomyopathy in Borrelia burgdorferi infection. Lancet 1992;
339: 1174-75. 3 Prewitt TA. Syphilitic aortic insufficiency. JAMA 1970; 211: 637-43. 4 Capannari TE, Daniels SR, Meyer RA, Schwartz DC, Kaplan S. Sensitivity, specificity and predictive value of two-dimensional echocardiography in detecting coronary aneurysms in patients with Kawasaki disease. JACC 1986; 7: 355-60. 5 Gaida BJ, Gervais HW, Mauer D, Leyser KH, Eberle B, Dick W. Übersicht Takayasu-Syndrom. MedKlin 1991; 86: 367-73.
pelvic floor and incontinence
SIR-In his review of the aetiology of idiopathic faecal incontinence in women, Kamm (Sept 10, p 730) emphasises the notion that pregnancy and, especially, difficult childbirth as shown by the necessity for forceps delivery, can lead to several inter-related abnormalities in pelvic floor structures and sphincter muscles. These abnormalities include traumatic tears in external and sphincter musculature, damage to pelvic floor innervation leading to partial denervation and weakness of the striated musculature, and loss of ligamentous integrity. All these factors will lead to functional incompetence of the pelvic floor. However, there remains a difficulty in understanding the common selectivity of the development of faecal incontinence or stress urinary incontinence. The occurrence of tears in the anal sphincter muscle, although evidently important, cannot be the only factor’ since, as Kamm and his colleagues have pointed out, it is not present in all women with this form of faecal incontinence. In some women both faecal and urinary incontinence develop. Investigation of the extent of neurogenic damage in these functional disorders of continence has shown that stress urinary incontinence is associated with greater involvement of the perineal innervation of the pelvic floor than of the external anal sphincter, and faecal incontinence with greater involvement of the innervation of the external anal sphincter than of the anterior perineum, although these innervations are both branches of the pudendal nerve.2 Damage to these nerves will also result in sensory impairment which, as in any neuromuscular system, will be important in determining dysfunction.3 This is not the only factor, since not all women with incontinence show striking abnormalities in innervation, and the underlying mechanism of this selective incontinence remains Stress urinary incompletely understood. in incontinence can be described functional and anatomical terms, in relation to the pressure/flow abnormalities acting around the bladder neck that result in the inadvertent expulsion of urine, but the pathogenesis of these changes is controversial. Nonetheless, it seems likely that similar pathophysiological mechanisms underlie urinary and faecal incontinence. The unravelling of this puzzle should be the next task in understanding the complex events that lead to the devastating functional disorder of stress incontinence. Only then will prevention be attainable. Michael Swash Department of Neurology, Royal 1
2
3
London
Hospital, London E1 1BB, UK
Snooks SJ, Henry MM, Swash M. Faecal incontinence due to external anal sphincter division in childbirth is associated with damage to the innervation of the pelvic floor musculature: a double pathology. Br J Obstet Gynaecol 1985; 92: 824-28. Snooks SJ, Barnes PRH, Swash M, Henry MM. Damage to the innervation of the voluntary anal and periurethral striated sphincter musculature in incontinence: and electrophysiological study. J Neurol Neurosurg Psychiatry 1948; 47: 1296-73. Rogers J, Henry MM, Misiewicz JJ. Combined sensory and motor deficit in primary neuropathic faecal incontinence. Gut 1988; 29: 5-9.
Keratitis solaris after
long exposure to
photoflood spotlights SiR-Daxecker and colleagues (Sept 24, p 886) draw attention to the potentially damaging effect of corneal exposure to ultraviolet radiation from sunbeds. They also mention that halogen desk lamps are a potential source of keratitis solaris. We report keratitis solaris in a patient who was
exposed
to
very
bright floodlights during
a
photography
session.
1301
Figure: Coronary angiogram of proximal aneurysm of left anterior descending coronary artery
erythema chronicum migrans, neurological involvement, and oligoarthritis, with positive IgG ELISA for B burgdorferi. Echocardiography revealed a reduced left ventricular ejection fraction (26%), dilated aorta, aortic insufficiency II, and a huge aneurysm in the region of the left anterior descending coronary artery. Coronary angiography confirmed an aneurysm of the proximal left anterior descending coronary artery, measuring 1-2 cm in diameter (figure). A 46-year-old man presented with dilated cardiomyopathy (ejection fraction 36%) and typical stage III Lyme borreliosis acrodermatitis chronicaa (paraesthesias, atropicans, cardiovascular oligoarthritis, involvement, typical tick bite, and erythema chronicum migrans history plus positive IgG ELISA). Routine coronary angiography was done to 4
exclude ischaemic heart disease
as
the
of left showed an
source
ventricular dysfunction. Coronary angiography aneurysm of the proximal anterior descending coronary artery, measuring 1-0 cm in diameter, confirmed by
echocardiography. Coronary aneurysms have been reported secondary to vaculitis in Kawasaki syndrome, Takayasu syndrome, and late syphillis. 1-5 It is not unlikely that coronary artery aneurysms may result from spirochaetal infection following vascular inflammation in late Lyme borreliosis. Dilated cardiomyopathy and aortic dilation would also argue in favour of an inflammatory genesis of the coronary arterial aneurysms. Since echocardiography has a high sensitivity (100%) for proximal coronary aneurysms, this non-invasive technique could be routinely used to screen late Lyme disease patients for aneurysms. R Gasser, N Watzinger, B Eber, O Luha, E Reisinger, G Seinost, W Klein, on behalf of the Borreliosis Study Group Department of Medicine, University of Graz, 8036 Graz, Austria We thank the following members of the Borreliosis Study Group for their helpful contributions: I Wendelin, F Fruhwald, H Zebedin, and
J Bergloff. 1
2
Cox J, Krajden M. Cardiovascular manifestations of Lyme disease. Am Heart J 1991; 122: 1449-55. Gasser R, Dusleag J, Reisinger E, et al. Reversal by ceftriaxone of dilated cardiomyopathy in Borrelia burgdorferi infection. Lancet 1992;
339: 1174-75. 3 Prewitt TA. Syphilitic aortic insufficiency. JAMA 1970; 211: 637-43. 4 Capannari TE, Daniels SR, Meyer RA, Schwartz DC, Kaplan S. Sensitivity, specificity and predictive value of two-dimensional echocardiography in detecting coronary aneurysms in patients with Kawasaki disease. JACC 1986; 7: 355-60. 5 Gaida BJ, Gervais HW, Mauer D, Leyser KH, Eberle B, Dick W. Übersicht Takayasu-Syndrom. MedKlin 1991; 86: 367-73.
pelvic floor and incontinence
SIR-In his review of the aetiology of idiopathic faecal incontinence in women, Kamm (Sept 10, p 730) emphasises the notion that pregnancy and, especially, difficult childbirth as shown by the necessity for forceps delivery, can lead to several inter-related abnormalities in pelvic floor structures and sphincter muscles. These abnormalities include traumatic tears in external and sphincter musculature, damage to pelvic floor innervation leading to partial denervation and weakness of the striated musculature, and loss of ligamentous integrity. All these factors will lead to functional incompetence of the pelvic floor. However, there remains a difficulty in understanding the common selectivity of the development of faecal incontinence or stress urinary incontinence. The occurrence of tears in the anal sphincter muscle, although evidently important, cannot be the only factor’ since, as Kamm and his colleagues have pointed out, it is not present in all women with this form of faecal incontinence. In some women both faecal and urinary incontinence develop. Investigation of the extent of neurogenic damage in these functional disorders of continence has shown that stress urinary incontinence is associated with greater involvement of the perineal innervation of the pelvic floor than of the external anal sphincter, and faecal incontinence with greater involvement of the innervation of the external anal sphincter than of the anterior perineum, although these innervations are both branches of the pudendal nerve.2 Damage to these nerves will also result in sensory impairment which, as in any neuromuscular system, will be important in determining dysfunction.3 This is not the only factor, since not all women with incontinence show striking abnormalities in innervation, and the underlying mechanism of this selective incontinence remains Stress urinary incompletely understood. in incontinence can be described functional and anatomical terms, in relation to the pressure/flow abnormalities acting around the bladder neck that result in the inadvertent expulsion of urine, but the pathogenesis of these changes is controversial. Nonetheless, it seems likely that similar pathophysiological mechanisms underlie urinary and faecal incontinence. The unravelling of this puzzle should be the next task in understanding the complex events that lead to the devastating functional disorder of stress incontinence. Only then will prevention be attainable. Michael Swash Department of Neurology, Royal 1
2
3
London
Hospital, London E1 1BB, UK
Snooks SJ, Henry MM, Swash M. Faecal incontinence due to external anal sphincter division in childbirth is associated with damage to the innervation of the pelvic floor musculature: a double pathology. Br J Obstet Gynaecol 1985; 92: 824-28. Snooks SJ, Barnes PRH, Swash M, Henry MM. Damage to the innervation of the voluntary anal and periurethral striated sphincter musculature in incontinence: and electrophysiological study. J Neurol Neurosurg Psychiatry 1948; 47: 1296-73. Rogers J, Henry MM, Misiewicz JJ. Combined sensory and motor deficit in primary neuropathic faecal incontinence. Gut 1988; 29: 5-9.
Keratitis solaris after
long exposure to
photoflood spotlights SiR-Daxecker and colleagues (Sept 24, p 886) draw attention to the potentially damaging effect of corneal exposure to ultraviolet radiation from sunbeds. They also mention that halogen desk lamps are a potential source of keratitis solaris. We report keratitis solaris in a patient who was
exposed
to
very
bright floodlights during
a
photography
session.
1301