Transient cortical blindness after caesarean hysterectomy for placenta percreta

International Journal of Obstetric Anesthesia (2004) 13, 291–299
2004 Elsevier Ltd. All rights reserved.

CORRESPONDENCE

doi:10.1016/j.ijoa.2004.03.010

tive, blind and randomized survey with a rigorously applied protocol can resolve the present dilemma.

Prophylactic epidural blood patch (PEBP) in obstetrics: yes or no?

Ray J. Defalque Birmingham, AL, USA E-mail: [email protected]

Prophylactic epidural blood patch (PEBP) involves the injection of autologous blood through an epidural catheter that was re-sited and used successfully for labor and delivery following an initial accidental dural puncture. It is infrequently used,1–3 despite its advantages. The technique saves time, money and patient discomfort and avoids a potential second accidental dural puncture, but the experts disagree in their recommendations.4,5 The main point of contention is the lack of irrefutable evidence demonstrating the effectiveness of the procedure. Of the four surveys carried out with controls,6–9 three7–9 were prospective randomized studies but each had only a small number of patients (40 to 50). Only one study8 had a blinded observer, and two8,9 had small discrepancies in the grouping of their patients. None of these studies had a rigorously applied protocol. The three prospective, randomized surveys7–9 reached contradictory conclusions: (a) Colonna-Romano and Shapiro,7 who studied 39 patients, found a statistically significant difference in the incidence of post dural puncture headaches (PDPH) between their patients treated with a PEBP (16%) and those untreated (84%). Thus in their patients with accidental dural puncture (ADP), PEBP was apparently unnecessary in 16% and ineffective in another 16% but 68% of their patients benefited from PEBP. (b) Lowenwirt et al.8 studied 49 patients and reported a similar success: 12% of their prophylactically treated patients had a moderate to severe PDPH vs. 84% of their untreated controls, a statistically significant difference. Thus in their treated patients, the PEBP was apparently unnecessary in 16% and ineffective in 12%, but 72% benefited from PEBP. (c) Mandell and Ramanathan9 however, studied 44 patients and obtained different results: their prophylactically treated patients had a 38% incidence of significant PDPH vs. a rate of 40% in their untreated controls. The difference was not statistically significant. In this study, PEBP was apparently unnecessary in 53% and ineffective in 38% of their treated patients, i.e., it had only helped 9% of the parturients. It is clear that an anesthesiologist at this time cannot give a reliable estimate of the success rate of PEBP to a parturient who has experienced ADP. Thus, one must agree with Sudlow and Warlow10 that, because of the multiple factors involved in the incidence of PDPH and in the success of EBP, only a very large, prospec-

REFERENCES 1. Sajjad T, Ryan T D R. Current management of inadvertent dural taps occurring during the siting of epidurals for pain relief in labour. Anaesthesia 1995; 50: 156–161. 2. Berger C W, Crosby E T, Grodecky W. North American survey of the management of dural puncture occurring during labour epidural analgesia. Can J Anaesth 1999; 45: 110–114. 3. Vasdex G M, Southern P A. Postdural puncture headache: the role of prophylactic epidural blood patch. Curr Pain Headache Rep 2001; 5: 281–283. 4. Duffy P J, Crosby E T. The epidural blood patch. Resolving the controversies. Can J Anaesth 1999; 46: 878–886. 5. Norris M C. Obstetric Anesthesia. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 731. 6. Palahniuk R J, Cumming M. Prophylactic blood patch does not prevent post-lumbar puncture headache. Can Anaesth Soc J 1979; 26: 132–133. 7. Colonna-Romano P, Shapiro B E. Unintentional dural puncture and prophylactic epidural blood patch in obstetrics. Anesth Analg 1989; 69: 522–523. 8. Lowenwirt I, Cohen S, Zephyr J, Hamer R, Hronkova B, Rovner J S. Treatment of accidental dural puncture in obstetric patients:prophylactic vs. therapeutic blood patch. Anesthesiology 1988; 88: A38. 9. Mandell G, Ramanathan S. Effectiveness of prophylactic patches in laboring parturients. A prospective study. Anesth Analg 1996; 82: S291. 10. Sudlow C, Warlow C. Epidural blood patching for preventing and treating post-dural puncture headache. Cochrane Database Syst Rev 2002; 2: CD001791.

doi:10.1016/j.ijoa.2004.05.002

Transient cortical blindness after caesarean hysterectomy for placenta percreta Postoperative cortical blindness is a dramatic and frightening event characterised by the inability to see in the presence of occipital cortical infarction or after transient brain ischaemia. A 31-year-old para 3 (two prior caesarean deliveries) parturient presented to our delivery room in week 33 of her fourth pregnancy with mild vaginal bleeding, uterine contractions and intact membranes. On ultrasound examination an anterior placenta praevia was diagnosed. According to department policy, the patient was admitted for further observation to the high-risk pregnancy 291

292 International Journal of Obstetric Anesthesia unit and two 12 mg doses of betamethasone were given intramuscularly over 48 h. Three days after admission she developed massive bleeding and was taken for emergency caesarean section. Upon entering the operating room her blood pressure was 130/80 mmHg, pulse 110 beats/min and oxygen saturation 98% on room air. She received 2 L of Ringer’s lactate solution before induction of anaesthesia through two large (17-gauge) peripheral intravenous lines placed in cubital veins. A combined spinal-epidural was sited at L3-4, hyperbaric bupivacaine 8 mg and fentanyl 15 lg were given intrathecally and the epidural catheter was flushed with 2 mL of 2% lidocaine. The caesarean delivery was performed through the previous Pfannenstiel scar. On exposure of the uterus, the placenta was clearly seen to invade the lower parametrium adjacent to the lower uterine segment. Although performed with extreme caution, the uterine incision transected the anterior placenta and excessive bleeding occurred. After delivery of a healthy baby boy, the blood pressure dropped gradually to 70/40 mmHg and the heart rate rose to 140 beats/min. This state of haemodynamic instability concurrent with continued bleeding lasted for 5 min, despite intensive intravenous fluid replacement and administration of ephedrine 50 mg and phenylephrine 100 lg. As part of the resuscitation general anaesthesia was induced with ketamine 75 mg, propofol 50 mg and suxamethonium 100 mg using a rapid sequence technique. At this point, in order to control the bleeding the surgeons were forced to perform a hysterectomy. The patient was transfused with 5 units of packed red cells, one unit of fresh frozen plasma, 12 units of cryoprecipitate, 6 units of platelets and 5000 mL of crystalloid. After correction of the original hypotensive episode, the systolic pressure ranged from 110 to 120 mmHg and the heart rate was between 110-120 beats/min. Anaesthesia was maintained with repeated doses of midazolam (total 8 mg) and fentanyl (total 150 lg). The urine output was 340 mL and the estimated blood loss at surgery alone was 4000 mL. By the end of the operation, which lasted 2 h 15 min, the surgeons had managed to control the bleeding and the patient was stable with a haemoglobin of 10 mg/ dL and platelet count of 218 · 109/L. Fibrinogen, fibrinogen degradation products and electrolytes were within the normal range. An hour later the patient awakened in the recovery room and the tracheal tube was removed. She immediately complained of complete blindness. An extensive evaluation was carried out. This included ophthalmological, neurological and psychiatric examination followed by computerised tomography of the brain, all of which revealed no abnormal findings. The patient was kept under close observation in the recovery room with a diag-

nosis of hypotension-induced cortical blindness. Twenty-four long hours after the surgery the patient’s vision gradually returned, but during the following 24 h the patient complained of recurring episodes of bilateral complete blindness, each lasting a few seconds. Forty-eight hours later, the patient’s vision was, and remained, completely normal. Cortical blindness is characterised by an inability to see in the presence of an intact anterior visual pathway. This blindness is most often binocular and results from an insult to the occipital cortex. The occipital cortex is especially sensitive to ischaemia and systemic hypoxia because of its relatively distal location from the central cerebral vasculature. Computerised tomography helps to exclude the presence of intracranial haemorrhage or a neoplastic process, but is not diagnostic. Magnetic resonance imaging is the recommended technique of choice in these patients.1 This investigation is not available in our hospital. Previous reports of transient cortical blindness in pregnancy have focused largely on patients with preeclampsia or eclampsia,2-4 cardiogenic shock or after haemorrhage from an incomplete abortion.5 Some case reports have included retinal artery embolism.6 The prognosis of cortical blindness depends on the aetiology,7-8 severity and duration of the initiating event, as well as the speed of initial recovery. Bilateral cortical blindness with occipital abnormalities on MRI is associated with a poor prognosis5 and in this situation cortical blindness may be the result of an insult to the visual associated cortex (Anton’s syndrome). In cases of massive peripartum blood loss, cortical blindness is a complication that should not be disregarded. Although our patient had bilateral blindness associated with hypotension, she recovered completely. This further emphasises the importance of shock prevention and aggressive resuscitation in patients with placenta percreta. A. M. Ioscovich, D. J. Nyman, A. Briskin Department of Anaesthesia S. Grisaru-Granovsky Department of Obstetrics and Gynaecology Shaare Zedek Medical Centre, Jerusalem, Israel E-mail: [email protected]

REFERENCES 1. Conghlin W F, McMurdo S K, Reeves T M R. Imaging of postpartum cortical blindness. J Comput Assist Tomogr 1989; 13: 572–576. 2. Cunningham F G, Fernandez C O, Hernandes C. Blindness associated with preeclampsia and eclampsia. Am J Obstet Gynecol 1995; 172: 1291–1298.

Correspondence 293 3. Do D V, Rismondo V, Nguyen Q D. Reversible cortical blindness in preeclampsia. Am J Ophthalmol 2002; 134: 916–918. 4. Boromeo C J, Blike G T, Wiley C W, Hirsch J A. Cortical blindness in a preeclamptic patient after a cesarean delivery complicated by hypotension. Anesth Analg 2000; 91: 609–611. 5. Argenta P A, Morgan M A. Cortical blindness and Anton syndrome in a patient with obstetric hemorrhage. Obstet Gynecol 1998; 91: 810–812. 6. Lara-Torre E, Lee M S, Wolf M A, Shah D M. Bilateral retinal occlusion progressing to long-lasting blindness in severe preeclampsia. Obstet Gynecol 2002; 100: 940–942. 7. Aldrich M S, Alessi A G, Beck R W, Gilman S. Cortical blindness: etiology, diagnosis and prognosis. Ann Neurol 1987; 21: 149–158. 8. Belden J R, Caplan L R, Pessin M S, Kwan E. Mechanisms and clinical features of posterior border-zone infarcts. Neurology 1999; 53: 1312–1318.

doi:10.1016/j.ijoa.2004.02.004

A high spinal or a subdural block? Subdural block occurs much more frequently than we recognize,1 but the recent case of a high block following 2.6 mL of hyperbaric bupivacaine described by Anand et al.2 hardly resembles a subdural block. These blocks are of slow gradual onset, usually with a delay of 20–35 min following bupivacaine.3 Their patient’s block was up to T6 three minutes after injection, C2 after 6 min and produced apnoea after about 8 min. This is not unusual with a high spinal block, which it almost certainly was. Delayed onset of total spinal blocks was well demonstrated by Evans, who published (in 1974) an unusual series of 100 cases of deliberate total spinal blocks (using mostly 1% lidocaine) for major intra-abdominal surgery and reported that the mean time for a spinal block to become total was 10 min, but varied widely from 30 s to 45 min.4 Recent anatomical work on the ultrastructure of the subdural space5 has revealed that it is not a potential space as previously thought, but a cavity or series of cavities within the arachnoid layer produced by trauma from needle or catheter insertion and subsequent injection. These studies combined with our own radiographic imaging1 suggest that there may be two types of subdural block, a superficial injection producing a very restricted or failed block and a deeper injection resulting in the extensive type of delayed block that Anand et al.2 suspected, incorrectly, in their patient. We would have to disagree with the authors that “subdural blocks may be diagnosed on clinical grounds alone”, and encourage our colleagues to seek radiological confirmation in patients who have a catheter in situ, as mistakes can be made and subdural injection may recur in the same patient with subsequent blocks, even years later!1 Modern contrast injection is very safe and straightforward and can be performed in any radiology department that has 10 minutes to spare.

Clive Collier Department of Anaesthetics Royal Hospital for Women Barker Street, Sydney, NSW, Australia E-mail: nfi@zip.com.au

REFERENCES 1. Collier C B. Accidental subdural injection during attempted lumbar epidural block may present as a failed or inadequate block; radiographic evidence. Reg Anesth Pain Med 2004; 29: 45–51. 2. Anand S, Gupta M, Singh B. A case of extensive block during spinal anaesthesia for caesarean delivery: is there room to go wrong? International Journal of Obstetric Anesthesia 2004; 13: 61–62. 3. Collier C B. Subdural block – four more cases, and a radiographic review. Anaesth Intensive Care 1992; 20: 215–232. 4. Evans T I. Total spinal anaesthesia. Anaesth Intensive Care 1974; 2: 158–163. 5. Reina M A, Casasola O D L, Lopez A, et al. The origin of the spinal subdural space: ultrastructure findings. Anesth Analg 2002; 94: 991–995.

doi:10.1016/j.ijoa.2004.05.004

In reply We thank Clive Collier for his interest in our report. We agree that subdural blocks are of slow and gradual onset, but in confirmed subdural blocks with bupivacaine the onset has been reported to be 1-45 min.1–3 Dr. Collier is of the opinion that the block in our patient was almost certainly a high spinal block. It is difficult to believe that just 2.6 mL of hyperbaric bupivacaine injected in the CSF at L3-4 with the patient in the sitting position, but put in the supine position immediately thereafter, would reach as high as C2. It is now well recognized that the subdural space is not a virtual space such as the interpleural space. In an anatomical study, Reina et al.4 demonstrated that the arachnoid membrane had a compact laminar portion covering the dural sac in its inner surface and a trabeculated portion that extended like a spider’s web to the pia mater of the spinal cord. The dura-arachnoid interface is occupied by neurothelial cells and some amorphous material. The subdural space can appear due to tearing of this interface mainly through the amorphous material because of mechanical forces such as air or fluid injection. Collier’s recent report5 suggests that the tearing may occur either circumferentially, which produces the typical sausage-shaped mass of contrast injection, or it may extend cephalad leading to a high subdural block with the classical railroad track appearance on contrast injection. With the present knowledge, it is difficult to comment about the factors that determine the manner of spread of the dye but we believe that in our case the dura-arachnoid interface opened up in the cephalad direction during injection supposedly