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is not possible, a single-lumen tracheal tube with a bronchial blocker should be considered. The use of a single-lumen tube in the manner described in our case was an expeditious solution to an unexpected dif®cult situation, and is not recommended. In conclusion, CDH in an adult is a diagnostic and anaesthetic challenge. The diagnosis should be considered in any patient presenting with an acute abdomen and respiratory distress.
References 1 Merin RG. Congenital diaphragmatic hernia from the anesthesiologist viewpoint. Anesth Analg 1966; 45: 44±52 2 Durham TM, Green JG, Hodges ED, Nique TA. Congenital diaphragmatic hernia: implications for nitrous oxide use in dentistry. Spec Care Dentist 1993; 13: 107±9 3 Cullen MI, Klein MD, Philippart AI. Congenital diaphragmatic hernia. Surg Clin North Am 1985; 11: 1115±38 4 Williams R. Congenital diaphragmatic hernia: a review. Heart Lung 1982; 11: 532±40 5 Munizaga J, Allison MJ, Aspillaga E. Diaphragmatic hernia associated with strangulation of the small bowel in an Atacamena mummy. Am J Phys Anthropol 1978; 48: 17±20 6 Creighton RE, Whalen JS, Conn AW. The management of congenital diaphragmatic hernia. Can Anaesth Soc J 1966; 13: 124±9 7 Berman L, Stringer DA, Ein S, Shandling I. Childhood diaphragmatic hernias presenting after the neonatal period. Clin Radiol 1988; 39: 237±44 8 Dietrich CL, Smith CE. Anaesthesia for Caesarean delivery in a patient with an undiagnosed traumatic diaphragmatic hernia. Anesthesiology 2001; 4: 1028±31 9 Katz RI, Belenker SL, Poppers PJ. Intraoperative management of a patient with a chronic, previously undiagnosed traumatic diaphragmatic hernia. J Clin Anesth 1998; 10: 506±9
British Journal of Anaesthesia 90 (1): 98±100 (2003)
DOI: 10.1093/bja/aeg021
Postpartum cerebral ischaemia after accidental dural puncture and epidural blood patch M. Mercieri1*, A. Mercieri2, S. Paolini3, R. Arcioni1, D. Lupoi4, F. Passarelli4, G. Pinto1 and D. Celleno4 1
UniversitaÁ di Roma `La Sapienza', Ospedale S. Andrea, Rome, Italy. 2Ospedale S. Isidoro, Trescore, Bergamo, Italy. 3Ospedale S. Maria, Terni, Italy. 4Ospedale Fatebenefratelli, Isola Tiberina, Rome, Italy *Corresponding author: Via Pavia 124, I-00161 Rome, Italy. E-mail:
[email protected] Puerperal women are reported to have a rate of cerebral infarction 13 times greater than nonpregnant females. We report a case of cerebral ischaemia in a 30-yr-old healthy parturient after epidural analgesia for labour, complicated by dural puncture treated with two epidural blood patches. Investigations showed the development of cerebral ischaemia on postpartum
Ó The Board of Management and Trustees of the British Journal of Anaesthesia 2003
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will con®rm the presence of bowel loops in the thoracic cavity. Once the diagnosis has been established, urgent surgical correction is required. Anaesthetic management of CDH presenting acutely in the adult is poorly described, but the principles resemble management of late-diagnosed traumatic diaphragmatic herniae.9 Large-bore i.v. access should be gained and ¯uid resuscitation commenced. Invasive arterial and central venous pressure monitoring should be considered, but if the patient is in extremis, these should not delay commencement of surgery. The patient is at high risk of aspiration because of gastrointestinal obstruction, and therefore antacid premedication should be given, and a nasogastric tube should be inserted and aspirated if possible before rapid sequence induction with cricoid pressure. If dif®cult intubation is anticipated, awake ®breoptic intubation or tracheostomy under local anaesthesia should be considered. If the patient is haemodynamically unstable, induction should be in theatre with the surgeon ready to operate immediately. Agents less likely to decrease MAP (etomidate and fentanyl) should be used. Expansion of the viscera is likely to worsen the mass effect and impair circulation and respiration. Face-mask ventilation, with potential gastric insuf¯ation; and nitrous oxide anaesthesia should therefore be avoided. In theory, positive-pressure ventilation might preferentially ventilate the normal lung rather than the collapsed lung. However, any re-expansion of the collapsed lung may exacerbate the mass effect, with rapid and disastrous worsening of the circulation. The collapsed lung should therefore be isolated and ventilation of the normal lung started with small tidal volumes and pressures, using a double-lumen tube, until the affected hemithorax has been decompressed. If this
Cerebral ischaemia after dural puncture
day 14. A transcranial Doppler ultrasonography showed vasospasm of the left middle cerebral artery still present at 3-month follow-up. At 1-yr follow-up, the patient had homonymous hemianopsia. We discuss the possible causative mechanism of the cerebral ischaemia in relation to the dural puncture and epidural blood patch. Br J Anaesth 2003; 90: 98±100 Keywords: analgesia, obstetric; brain, cerebral ischaemia; complications, dural puncture Accepted for publication: July 24, 2002
Case report A 30-yr-old gravida 2 para 1 woman was admitted to hospital in active labour. She had no history of neurological or haematological disease, migraine, lupus, malignancy or infection, except for pulmonary tuberculosis treated medically 2 yr before admission. She had no oedema, proteinuria, hyperuricaemia or hypertension. She took no medication, did not use alcohol or tobacco and reported no allergies. Epidural analgesia was required when the cervical dilatation was 5 cm. During the attempt at epidural needle placement at L3±4, a dural puncture occurred with a 16gauge Tuohy needle. After a new attempt at L2±3, the epidural catheter was correctly positioned and epidural analgesia for labour was conducted until the parturient delivered a healthy term infant. Seven hours after delivery, the patient suffered from a dull, throbbing headache, relieved only by supine positioning, but recurring immediately after sitting or standing. Headache was so severe that we performed an EBP, injecting 18 ml of autologous blood, at the same level of dural puncture. The procedure was effective in relieving headache; the patient felt well and started lactation without discomfort. On postpartum day 2, postural headache recurred and gradually became extremely severe and disabling. This prompted us to perform a second EBP on postpartum day 3, with injection of 20 ml of autologous blood at L3±4 level. After the procedure, she developed mental confusion and agitation. She still suffered with occipital headache, not relieved by recumbent position and not associated with other neurological symptoms, nausea or vomiting. Arterial pressure remained in the normal range throughout the puerperium. Because of the continuing headache, which
Table 1 Transcranial Doppler ultrasonography measurements. Data are mean ¯ow velocity (cm s±1) Days after symptom onset
Right MCA
Left MCA
BA
0 2 5 15 90 180
165 170 171 156 125 65
221 215 241 170 142 60
65 53 55 49 64 55
MCA=middle cerebral artery; BA=basilar artery.
99
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was no longer postural, a cranial computed tomography (CT) scan and, subsequently, a magnetic resonance imaging (MRI) were performed disclosing no abnormalities. In particular there was no sign of subarachnoid blood. No medication, such as ergotamine or bromocriptine, was administered to the patient. On postpartum day 9, she developed generalized seizures followed by right hemiparesis, mainly affecting the face and arm, associated with visual disturbances. Again a CT scan showed no abnormalities except for a subtle effacement of cortical sulci. A transcranial Doppler ultrasonography (TCD) showed a left middle cerebral artery (MCA) mean ¯ow velocity (Vm) of 221 cm s±1 and right MCA Vm of 165 cm s±1; normal Vm was found in basilar artery. Follow-up TCDs were performed by the same examiner at 2, 5, 15 days, and 3 and 6 months after symptom onset (Table 1). The patient was transferred to ICU; nimodipine and phenobarbital were commenced. Eventually, on postpartum day 14, a repeat MRI disclosed multiple hyperdense areas on T2-weighted images, involving the left internal capsule and the parieto-occipital white matter. These ®ndings were consistent with ischaemic lesions involving the left MCA territory. Conditions such as hereditary antithrombin III de®ciency, proteins C and S de®ciencies were excluded. Laboratory studies, including vasculitis screening, electroencephalography and echocardiography, were normal. At the time of discharge, the patient still showed right arm weakness and homonymous hemianopsia. One year after discharge, she had completely recovered from the motor de®cit but still had homonymous hemianopsia.
The incidence of ischaemic stroke in women of childbearing age is 3.5±18 per 100 000 per year in western countries.1 The risk is slightly increased during pregnancy, particularly during the postpartum period.1 Puerperal women are reported to have a rate of cerebral infarction that is 13 times greater than non-pregnant females.2 We report a case of postpartum cerebral ischaemia after epidural analgesia complicated by postdural puncture headache (PDPH) and epidural blood patch (EBP).
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Discussion
References
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1 Lamy C, Hamon JB, Coste J, Mas JL. Ischemic stroke in young women. Risk of recurrence during subsequent pregnancies. French study group on stroke in pregnancy. Neurology 2000; 25: 269±74 2 Wiebers DO. Ischemic cerebrovascular complications of pregnancy. Arch Neurol 1985; 42: 1106±13 3 Qureshi AI, Frankel MR, Ottenlips JR, Stern BJ. Cerebral hemodynamics in preeclampsia and eclampsia. Arch Neurol 1996; 53: 1226±31 4 Kittner SJ, Stern BJ, Feeser BR, et al. Pregnancy and the risk of stroke. N Engl J Med 1996; 335: 768±74 5 Naidu K, Moodley J, Corr P, Hoffmann M. Single photon emission and cerebral computerised tomographic scan and transcranial Doppler sonographic ®ndings in eclampsia. Br J Obstet Gynaecol 1997; 104: 1165±72 6 Bogousslavsky J, Despland PA, Regli F, Dubuis PY. Postpartum cerebral angiopathy: reversible vasoconstriction assessed by transcranial Doppler ultrasounds. Eur Neurol 1989; 29: 102±5 7 Lee KY, Sohn YH, Kim SH, Sunwoo IN. Basilar artery vasospasm in postpartum cerebral angiopathy. Neurology 2000; 54: 2003±5 8 Shearer VE, Jhaveri HS, Cunningham FG. Puerperal seizures after post-dural puncture headache. Obstet Gynecol 1995; 85: 255±60 9 Ganz JC, Hall C, Zwetnow NN. Cerebral blood ¯ow during experimental epidural bleeding in swine. Acta Neurochir 1990; 103: 148±57 10 Grif®ths AG, Beards SC, Jackson A, Horsman EL. Visualization of extradural blood patch for post lumbar puncture headache by magnetic resonance imaging. Br J Anaesth 1993; 70: 223±5 11 Boezaart AP. Effects of cerebrospinal ¯uid loss and epidural blood patch on cerebral blood ¯ow in swine. Reg Anesth Pain Med 2001; 26: 401±6
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To our knowledge, no report has documented the development of cerebral ischaemia after epidural analgesia complicated by PDPH and EBP, after a normal pregnancy. Most of the reported cases of peripartum cerebral ischaemia were associated with a history of eclampsia and pre-eclampsia.3 4 In our case, diffuse arterial vasospasm, shown by TCD, caused the cerebral ischaemia. In obstetrics, vasospasm has reportedly been associated with either eclampsia or postpartum cerebral angiopathy (PPCA).5±7 In our patient, however, eclampsia can be excluded. She was normotensive throughout pregnancy, labour and delivery, and the puerperium. PPCA is a rare clinical syndrome comprising headache, vomiting, seizure and focal neurological de®cits after a normal pregnancy. It has always been reported as a reversible syndrome.7 However, in our patient, vasospasm was still present at 3-month follow-up and homonymous hemianopsia was present at 1-yr follow-up. The patient refused any further diagnostic procedures. In our opinion, the sequence of events suggests a de®nite causal relationship between the development of vasospasm and what happened after the dural puncture. Whether the vasospasm was related to the dural puncture or to the subsequent EBP is unknown. Perhaps the cerebral vasospasm was caused by the lumbar puncture per se. Shearer and colleagues8 described eight women with postpartum PDPH who developed seizures and visual disturbances. Angiography performed in two of them revealed diffuse cerebral artery vasospasm. They concluded that cerebral vasoconstriction, possibly due to anatomical brain displacement, could provide an explanation for the development of both headache and seizures after dural puncture. However, our case is noteworthy for the severity of neurological impairment. Also, it is the ®rst to demonstrate de®nite MRI evidence of ischaemic lesions as a result of vasospasm after dural puncture. Alternatively, vasospasm could be primarily related to the EBP. Subdural and extradural haematomas are powerful stimuli for cerebral vasoconstriction.9 We may hypothesize that blood, spreading through the dura mater, could have caused cerebral vasoconstriction. Grif®ths and colleagues10 have shown a signi®cant subarachnoid spread of blood after EBP with MRI. In a recent study carried out in pigs,11 cerebral blood ¯ow (CBF) increased after removing 9 ml of cerebrospinal ¯uid (CSF) with a cisternal puncture. CBF returned to baseline after injecting 10 ml autologous blood in the lumbar epidural space and decreased, by as much as half the baseline value, after subdural injection of 10 ml autologous blood. Of note, three pigs had blood-stained CSF at puncture of cisterna, probably as a result of needle injury
of an epidural blood vessel, and CBF remained unchanged, after CSF drainage, in all three animals. The author suggested that EBP relieves PDPH through vasoconstriction caused by subarachnoid spread of the epidurally injected blood. In our case, the time elapsing between EBP and the onset of neurological symptoms matches the latency time after which typical post-subarachnoid haemorrhage vasospasm usually develops. In conclusion, this case is of considerable complexity and dif®cult interpretation. Our two hypotheses are not mutually exclusive. Nevertheless, neither of them alone can consistently give an explanation of the series of events and the long-lasting cerebral vasospasm that occurred in our patient. As a last option we could speculate that dural puncture and/ or EBP might have caused an irreversible case of PPCA where sustained cerebral vasospasm has been responsible for the development of cerebral ischaemia.
