- Email: [email protected]
EPISIOTOMY AND THIRD-DEGREE TEARS
760
while the brainstem and spinal cord neurons are the most resistant.’-" The clinical correlate of these pathological alterations is the rostrocaudal deterioration of function that typically occurs in hypoglycaemia-a phenomenon so often seen with metabolic insults to the CNS. Moreover, it is noteworthy that a similar rostrocaudal gradient exists at the biochemical level, with protein synthesis decreasing most in the cortex and basal ganglia and least in the brainstem in hypoglycaemic animals." This clinical pattern may be partially dependent on selective sensitivity of neurotransmitters in different areas of the brain; selectivity has been shown for some cholinergic neurons.I2 However, it is difficult to explain the hemiparesis on this basis. Perhaps localised impairment of blood supply to one hemisphere or pyramidal tract, as the result of arterial damage, could account for this. While there is experimental evidence for loss of autoregulation of cerebral blood flow to some parts of the brain but not others during hypoglycaemia, there is no 3 support for the concept of unilateral abnormality. 13 Conversely, there is no pathological evidence of arterial insufficiency in man to account for unilateral signs,and structural abnormalities in a localised part of the cerebrovascular system seem an improbable cause of hemiparesis in children or in patients whose paralysis is on different sides in different hypoglycaemic episodes. Maybe unilateral localised loss of autoregulation and spasm does account for this surprising phenomenon after all; positron emission tomography might well help to clarify the pathophysiology if technology and patient ever met at an opportune time. The peripheral nervous system is seldom affected by hypoglycaemia. Many workers believe that the rare case of muscle atrophy and weakness following hypoglycaemia is due to necrosis of the anterior horn cells and that true neuropathy does not occur. 14 However, many hypoglycaemic patients have sensory symptoms (and occasionally signs) in all four extremities, suggesting a peripheral neuropathic component.I There are also occasional reports of axonal dystrophy affecting both sensory and motor nerve fibres. 16,17 Presumably the peripheral nerve is much less vulnerable than the CNS because it is not solely dependent on oxidative metabolism of glucose for its energy source. The diagnosis of metabolic coma is notoriously difficult but one should be alert to the possibility of hypoglycaemia since its catastrophic CNS effects can be totally reversible if glucose is given in time. Provided the patient fulfils all the Brown AW, Meldrum BS. The nature and time course of the neuronal alteration resulting from oligaemia and hypoglycaemia in the brain of Maccaca mulatta. Brain Res 1971; 25: 483-99. 8. Richardson JC, Chambers BR, Heywood PM. Encephalopathies of anoxia and hypoglycemia. Arch Neurol 1959; 1: 178-90. 9. Agardh C-D, Kalimo H, Olsson Y, Siesjo BK. Hypoglycaemic brain injury. Acta Neuropath 1980; 50: 31-41. 10. Brierley JB, Graham DJ. Hypoxia and cerebrovascular disorders of the central nervous system. In: Adams JH, Corsellis JAN, Duchen LW, eds. Greenfield’s neuropathology. London: Edward Arnold, 1984: 150-52. 11. Kiessling M, Yaxia X, Kleihues P. Regionally selective inhibition of cerebral protein synthesis in the rat during hypoglycemia and recovery. J Neurochem 1984; 43: 1507-14. 12. Ghajar JBG, Gibson GE, Duffy TE. Regional acetylcholine metabolism in brain during acute hypoglycemia and recovery. J Neurochem 1985; 44: 94-98. 13. Siesjo BK, Ingvar M, Pelligrino D. Regional differences in vascular autoregulation in the rat brain in severe insulin induced hypoglycemia. J Cerebr Blood Flow Metab 1983; 3: 478-85. 14. Harrinson MJG. Muscle wasting after prolonged hypoglycaemic coma: Case report with electrophysiological data. J Neurol Neurosurg Psychiatry 1976; 39: 465-70. 15. Ziegler DK. Neurologic signs and symptoms following insulin coma therapy. J Nerv Ment Dis 1954; 120: 75-78 16 Mulder DW, Bastron JA, Lambert EH. Hypoglycaemic neuropathy Neurology 1956, 6: 627-35. 17. Jaspan JB, Wollman RL, Berstein L, Rubenstein AH. Hypoglycemic peripheral neuropathy in association with insulinoma. Medicine 1982; 61: 33-44. 7.
Briefly JB,
requirements of Whipple’s triad (low blood glucose with typical symptoms relieved by glucose administration) the diagnosis of hypoglycaemia is made. There are said to be over one hundred causes for hypoglycaemia in man, and the clinician then has to decide which patient. It can be a difficult task.
one
is present in the
EPISIOTOMY AND THIRD-DEGREE TEARS
widely varying incidences for the use of episiotomy reported in the English language’ suggest that, like circumcision, episiotomy has often more to do with custom and ritual than medical necessity or advisability. But, in addition to enlarging the exit from the birth canal, episiotomy does straighten out the lower end of the curve of Carus and provide more space for the performance of obstetric manipulations. Only an armchair accoucheur might cavil THE
with its use in operative deliveries or other difficult births such as those caused by a persistent posterior position of the occiput or the extended legs of a frank breech presentation. Among the less secure indications for episiotomy are the "rigid perineum" and "button-holing" beloved of the midwives who conduct the vast majority of vaginal deliveries in Britain. These expressions are quaintly risible but underlying them is the real fear of allowing the patient to sustain a third-degree tear, which will put a blot on the midwife’s professional copybook. True, if expertly sutured, the tear will usually heal by first intention; but, should it fail to do so, infection is invariable and several months will usually elapse before a successful "cold" repair becomes feasible, the patient sometimes requiring colostomy in the meantime. A mediolateral episiotomy is therefore performed to deflect any perineal damage from the anus and rectal
sphincters. Beukens and colleagues2 have studied the relation between episiotomy and third-degree perineal tear in a survey of 21 278 singleton deliveries in ten Belgian hospitals between 1974 and 1978. The incidence of episiotomy was 28-4%. Third-degree tears occurred in 1’ 4% of deliveries with episiotomy and 0’9% of deliveries without episiotomy; but, when a subsample of spontaneous occipito-anterior deliveries was studied, and after stratification for birth weight and parity, no relation between episiotomy and third-degree tear was found. A third-degree tear seems to have been defined as "any tear that extends to the anal sphincter, including those extending into the rectum" (the italics are ours). But what help has this study been to the midwife and doctor anxious to prevent damage to the patient’s rectal sphincter and mucosa during spontaneous childbirth? Perhaps this question can best be answered by another. Would a relation between mediolateral episiotomy and third-degree perineal laceration have been shown if episiotomy had been 99% successful in preventing this complication in any number of patients correctly diagnosed to be at risk without it? The answer underlines the intrinsic limitations of surveys to assess the value of obstetric interventions. Solutions, sweet or sour, require randomisation of treatment; and it is cheering that so many midwives and obstetricians have shown themselves willing to submit to the discipline entailed by randomised controlled trials.3 1. Thacker SB, Banda HD. Benefits and risks of episiotomy: an interpretative review of the English language literature. 1960-1980. Obstet Gynecol Surv 1983; 38: 322-38 2. Beukens P, Lagasse R, Dramaix M, Wollast E. Episiotomy and third-degree teats. Br J Obstet Gynaecol 1985; 92: 820-23. 3. Sleep J, Grant A, Garcia J, et al. The West Berkshire perineal management trial. Br Med J 1984; 289: 587-90
while the brainstem and spinal cord neurons are the most resistant.’-" The clinical correlate of these pathological alterations is the rostrocaudal deterioration of function that typically occurs in hypoglycaemia-a phenomenon so often seen with metabolic insults to the CNS. Moreover, it is noteworthy that a similar rostrocaudal gradient exists at the biochemical level, with protein synthesis decreasing most in the cortex and basal ganglia and least in the brainstem in hypoglycaemic animals." This clinical pattern may be partially dependent on selective sensitivity of neurotransmitters in different areas of the brain; selectivity has been shown for some cholinergic neurons.I2 However, it is difficult to explain the hemiparesis on this basis. Perhaps localised impairment of blood supply to one hemisphere or pyramidal tract, as the result of arterial damage, could account for this. While there is experimental evidence for loss of autoregulation of cerebral blood flow to some parts of the brain but not others during hypoglycaemia, there is no 3 support for the concept of unilateral abnormality. 13 Conversely, there is no pathological evidence of arterial insufficiency in man to account for unilateral signs,and structural abnormalities in a localised part of the cerebrovascular system seem an improbable cause of hemiparesis in children or in patients whose paralysis is on different sides in different hypoglycaemic episodes. Maybe unilateral localised loss of autoregulation and spasm does account for this surprising phenomenon after all; positron emission tomography might well help to clarify the pathophysiology if technology and patient ever met at an opportune time. The peripheral nervous system is seldom affected by hypoglycaemia. Many workers believe that the rare case of muscle atrophy and weakness following hypoglycaemia is due to necrosis of the anterior horn cells and that true neuropathy does not occur. 14 However, many hypoglycaemic patients have sensory symptoms (and occasionally signs) in all four extremities, suggesting a peripheral neuropathic component.I There are also occasional reports of axonal dystrophy affecting both sensory and motor nerve fibres. 16,17 Presumably the peripheral nerve is much less vulnerable than the CNS because it is not solely dependent on oxidative metabolism of glucose for its energy source. The diagnosis of metabolic coma is notoriously difficult but one should be alert to the possibility of hypoglycaemia since its catastrophic CNS effects can be totally reversible if glucose is given in time. Provided the patient fulfils all the Brown AW, Meldrum BS. The nature and time course of the neuronal alteration resulting from oligaemia and hypoglycaemia in the brain of Maccaca mulatta. Brain Res 1971; 25: 483-99. 8. Richardson JC, Chambers BR, Heywood PM. Encephalopathies of anoxia and hypoglycemia. Arch Neurol 1959; 1: 178-90. 9. Agardh C-D, Kalimo H, Olsson Y, Siesjo BK. Hypoglycaemic brain injury. Acta Neuropath 1980; 50: 31-41. 10. Brierley JB, Graham DJ. Hypoxia and cerebrovascular disorders of the central nervous system. In: Adams JH, Corsellis JAN, Duchen LW, eds. Greenfield’s neuropathology. London: Edward Arnold, 1984: 150-52. 11. Kiessling M, Yaxia X, Kleihues P. Regionally selective inhibition of cerebral protein synthesis in the rat during hypoglycemia and recovery. J Neurochem 1984; 43: 1507-14. 12. Ghajar JBG, Gibson GE, Duffy TE. Regional acetylcholine metabolism in brain during acute hypoglycemia and recovery. J Neurochem 1985; 44: 94-98. 13. Siesjo BK, Ingvar M, Pelligrino D. Regional differences in vascular autoregulation in the rat brain in severe insulin induced hypoglycemia. J Cerebr Blood Flow Metab 1983; 3: 478-85. 14. Harrinson MJG. Muscle wasting after prolonged hypoglycaemic coma: Case report with electrophysiological data. J Neurol Neurosurg Psychiatry 1976; 39: 465-70. 15. Ziegler DK. Neurologic signs and symptoms following insulin coma therapy. J Nerv Ment Dis 1954; 120: 75-78 16 Mulder DW, Bastron JA, Lambert EH. Hypoglycaemic neuropathy Neurology 1956, 6: 627-35. 17. Jaspan JB, Wollman RL, Berstein L, Rubenstein AH. Hypoglycemic peripheral neuropathy in association with insulinoma. Medicine 1982; 61: 33-44. 7.
Briefly JB,
requirements of Whipple’s triad (low blood glucose with typical symptoms relieved by glucose administration) the diagnosis of hypoglycaemia is made. There are said to be over one hundred causes for hypoglycaemia in man, and the clinician then has to decide which patient. It can be a difficult task.
one
is present in the
EPISIOTOMY AND THIRD-DEGREE TEARS
widely varying incidences for the use of episiotomy reported in the English language’ suggest that, like circumcision, episiotomy has often more to do with custom and ritual than medical necessity or advisability. But, in addition to enlarging the exit from the birth canal, episiotomy does straighten out the lower end of the curve of Carus and provide more space for the performance of obstetric manipulations. Only an armchair accoucheur might cavil THE
with its use in operative deliveries or other difficult births such as those caused by a persistent posterior position of the occiput or the extended legs of a frank breech presentation. Among the less secure indications for episiotomy are the "rigid perineum" and "button-holing" beloved of the midwives who conduct the vast majority of vaginal deliveries in Britain. These expressions are quaintly risible but underlying them is the real fear of allowing the patient to sustain a third-degree tear, which will put a blot on the midwife’s professional copybook. True, if expertly sutured, the tear will usually heal by first intention; but, should it fail to do so, infection is invariable and several months will usually elapse before a successful "cold" repair becomes feasible, the patient sometimes requiring colostomy in the meantime. A mediolateral episiotomy is therefore performed to deflect any perineal damage from the anus and rectal
sphincters. Beukens and colleagues2 have studied the relation between episiotomy and third-degree perineal tear in a survey of 21 278 singleton deliveries in ten Belgian hospitals between 1974 and 1978. The incidence of episiotomy was 28-4%. Third-degree tears occurred in 1’ 4% of deliveries with episiotomy and 0’9% of deliveries without episiotomy; but, when a subsample of spontaneous occipito-anterior deliveries was studied, and after stratification for birth weight and parity, no relation between episiotomy and third-degree tear was found. A third-degree tear seems to have been defined as "any tear that extends to the anal sphincter, including those extending into the rectum" (the italics are ours). But what help has this study been to the midwife and doctor anxious to prevent damage to the patient’s rectal sphincter and mucosa during spontaneous childbirth? Perhaps this question can best be answered by another. Would a relation between mediolateral episiotomy and third-degree perineal laceration have been shown if episiotomy had been 99% successful in preventing this complication in any number of patients correctly diagnosed to be at risk without it? The answer underlines the intrinsic limitations of surveys to assess the value of obstetric interventions. Solutions, sweet or sour, require randomisation of treatment; and it is cheering that so many midwives and obstetricians have shown themselves willing to submit to the discipline entailed by randomised controlled trials.3 1. Thacker SB, Banda HD. Benefits and risks of episiotomy: an interpretative review of the English language literature. 1960-1980. Obstet Gynecol Surv 1983; 38: 322-38 2. Beukens P, Lagasse R, Dramaix M, Wollast E. Episiotomy and third-degree teats. Br J Obstet Gynaecol 1985; 92: 820-23. 3. Sleep J, Grant A, Garcia J, et al. The West Berkshire perineal management trial. Br Med J 1984; 289: 587-90