Traumatic vertebro-jugular arteriovenous fistula successfully treated by percutaneous embolization

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ANZ J. Surg. (2001) 71, 688–692

CASE REPORT CASE REPORT

TRAUMATIC VERTEBRO-JUGULAR ARTERIOVENOUS FISTULA SUCCESSFULLY TREATED BY PERCUTANEOUS EMBOLIZATION WALID MOHABBAT,* MICHAEL CRAWFORD,* GEOFFREY PARKER,† KERWIN SHANNON* AND GEOFFREY H. WHITE* Departments of *Surgery and †Radiology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia Key words: arteriovenous fistula, embolization, neck, penetrating wounds, trauma.

INTRODUCTION The management of penetrating neck trauma remains controversial. Some authors advocate mandatory surgical exploration, arguing that most neck wounds cause significant injury; some potentially lethal injuries can only be diagnosed at operation and delays in operative treatment increase morbidity and mortality.1 Others, however, advocate selective neck exploration, arguing that this is a safe and more cost-effective approach with a much lower negative exploration rate.2–5 Furthermore, it has been argued that a large number of injuries discovered in asymptomatic patients can be safely managed non-operatively.5 A patient is reported who was managed non-operatively, who developed an arteriovenous fistula and was successfully treated by embolization. A brief overview of the recent literature on penetrating neck trauma is also presented.

CASE REPORT A 44-year-old woman presented to Royal Prince Alfred Hospital within 1 h of a stab injury to the right neck. The self-inflicted wound was made with broken glass and was at the junction of zones 2 and 3 (i.e. at the level of the angle of the mandible) over the right sternocleidomastoid muscle. In the emergency department her vital signs were stable with a pulse rate of 91 b.p.m., blood pressure of 148/104, respiratory rate 12 per min, oxygen saturation 99% on room air and Glascow coma score (GCS) of 15/15. The patient was otherwise asymptomatic and in particular had no dyspnoea or respiratory distress, haemoptysis, hoarseness, haematemesis, dysphagia nor odynophagia. On examination of the neck there was superficial bruising over the right upper neck with a 1.5-cm laceration over the anterior border of the sternocleidomastoid muscle. There was no evidence of active bleeding, expansile or pulsatile haematoma, vascular bruit or thrill, air bubbling through the wound nor subcutaneous emphysema. The patient had no neurological signs. A chest X-ray revealed no abnormality. A computed tomography (CT) scan of the neck was performed and this was reported as showing evidence of swelling of the right sternocleidomastoid muscle with fat stranding in the subcutaneous fat and anterior and posterior cervical spaces but no evidence of vascular or visceral injury. There was a suggestion of distension of the internal jugular vein (Fig. 1). Correspondence: Dr W. Mohabbat, 15 Northview Place, Mount Colah, NSW 2079, Australia. Email: [email protected] Accepted for publication 7 July 2001.

The patient was admitted to hospital, fasted and given supportive care in the form of intravenous fluids, antibiotics and analgesics. A psychiatry consultation was arranged and the patient was observed overnight. The following morning the patient complained of hearing her ‘heart beat’ and on auscultation a loud machinery murmur was heard over the right neck wound extending both up towards the ear and across the midline to the left neck. There was no haemodynamic compromise. Cerebral angiography was performed which revealed a fistula between the right vertebral artery and the right internal jugular vein. It also revealed good collateral circulation to the right vertebral artery via the circle of Willis (Fig. 2). Rigid pharyngo-oesophagoscopy was also performed and this detected no abnormalities. The following day, after informed consent and a further 24 h of intravenous antibiotics, the arteriovenous fistula was successfully embolized without complication. Via a right femoral approach a Tracker 18 microcatheter (Boston Scientific Corp., Botany, NSW, Australia) was placed in

Fig.1. Contrast-enhanced computed tomography (CECT) scan of the neck demonstrating thickening of the soft tissue spaces of the right side of the neck with fat stranding in the anterior and posterior cervical spaces.

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Fig. 2. Right ( ) and left ( ) vertebral artery angiograms showing a direct arteriovenous fistula from the right vertebral artery at the C1–2 level to ( ) the right internal jugular vein. The fistula fills from the right vertebral artery both below and above the fistula due to retrograde flow from the left side. The point of fistularization is shown ( ) with filling of the right internal jugular vein ( ) and vertebral venous plexus ( ).

Fig. 3. Right ( ) and left ( ) vertebral angiograms following microcatheter placement of ( ) 15-fibred platinum microcoils in the right vertebral artery from above and across to below the fistula. There was complete cessation of flow through the fistula.

the right vertebral artery from below with the catheter tip in the artery above the point of fistularization. A total of 15 fibred platinum microcoils (Boston Scientific Corp., Botany, NSW, Australia) were placed in the arterial lumen, taking particular care to completely occlude the vertebral artery above the fistula to prevent retrograde filling from the left vertebral artery, before occluding the artery at and below the fistula. The right posterior inferior cerebellar artery was preserved (Fig. 3). One day after the embolization the patient underwent duplex scanning of her neck which confirmed the right vertebral artery was occluded and there was normal flow in the right internal

jugular vein. Following psychiatric consultation the patient was discharged home. At follow up 4 months later the patient remained asymptomatic and a repeat duplex ultrasound scan revealed no evidence of the arteriovenous fistula.

DISCUSSION Neck trauma accounts for 5–10% of all serious traumatic injuries and has a mortality rate of 2–6%.6–8 The majority of serious penetrating neck trauma involves the anterior triangle of the neck,

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which contains most of the major vascular and visceral structures and the airway. For clinical purposes the neck is partitioned into three zones and the majority of neck trauma involves zone 2, which covers the midportion of the neck between the cricoid cartilage and the angle of the mandible.9–10 But serious injuries in zone 1 and 3 can more easily go unrecognized and can often necessitate special operative exposure (e.g. sternotomy for zone 1 injuries). Up to 30% of penetrating neck injuries as a whole will have sustained serious vascular injury.11 There has been a trend towards a more selective approach in the management of penetrating neck injuries in recent years; although obvious significant injuries warrant immediate repair. So called ‘hard signs’ mandate operative exploration and include severe active bleeding, shock not responding to fluids, absent radial pulse, air bubbling through the wound, bruit on admission, airway compromise, evolving stroke and expanding or pulsatile haematoma.2–6 The second principle of the selective approach is that initially stable but symptomatic patients should be further investigated according to the zone of injury and the symptomatology and all should have a chest X-ray and cervical spine films.2–7,12 Such patients with zone 1 or 3 violation are at particular risk of vascular injury because proximal or distal control may be difficult, and the vascular injury may not be obvious on initial evaluation. Angiography is helpful in predicting the need for unusual operative exposure and it allows the surgeon to plan the repair of vascular injuries that may be unexpected. For zone 3 injuries, therapeutic embolization or occlusion of the harmed vasculature remains the best option.13 This point was illustrated by the present case in which fistularization had occurred at the C1–2 level and operative access would have been difficult, hence making therapeutic embolization a more attractive option. Colour flow Doppler ultrasound has also been proposed as a non-invasive alternative to angiography.4 Angiography would be reserved for patients with a bruit because of the possibility of therapeutic embolization of a false aneurysm or arteriovenous fistula, or those with colour flow Doppler abnormalities requiring further investigation. More recent comparison of helical CT angiography with conventional angiography has shown a high sensitivity and specificity of helical CT angiography for detection of arterial occlusion, pseudoaneurysm, and arteriovenous fistula.14 Although conventional angiography is considered to be gold standard for diagnosing arterial injuries, it does carry a risk of procedure-related complications. These complications include haematoma at the puncture site, thrombosis of the vessel used to access the arterial system, distal embolization of atheromatous plaques and thrombi, arterial spasm and ischaemia and intimal dissection. The reported frequency of these complications varies from 0.16 to 2.00%.14 In the major arteries of the neck these complications may lead to ischaemic events in the central nervous system, sometimes with catastrophic results and permanent neurological sequele. Patients with symptomatology suggestive of aerodigestive tract trauma should have one or more of contrast swallow studies, endoscopy (rigid is superior to flexible), laryngoscopy, bronchoscopy and/or CT.2–5,12 Zone 2 injuries are considered separately in most studies because injuries in this zone are easier to diagnose and are relatively simple to explore. Hence some authors believe that these patients should be explored immediately with adjuvant diagnostic testing only if there was a question of zone 1 violation or a transcervical gunshot wound.2

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The patient presented here was in fact asymptomatic initially and the vast majority of patients with penetrating neck trauma fall into this category. This is particularly true in Australia where the proportion of gunshot victims is low. The important observation to make in this population is whether there has been a zone 1 violation. If so then the injury must be regarded as high risk and all such patients should receive angiography as standard practice. The incidence of major vascular injury found at angiography in such patients varies in the literature from 0 to 32%.14 More recent views are to question the need to perform angiography on all such patients. One author found that if these asymptomatic patients have a normal physical examination combined with a normal chest X-ray then the chance of angiographically demonstrable vascular injury was 0% (0/36).15 That retrospective study15 was limited by the small number and lack of follow up. The danger of the selective management approach is to miss an occult injury that can lead to significant morbidity or mortality. The majority of penetrating neck trauma seen in Australia is likely to consist of stab wounds. One author found that, outside the USA in Toronto, knife wounds accounted for 65% of penetrating neck injuries and gunshot wounds accounted for only 8%.6 As illustrated in the present case, although the patient may present asymptomatic initially, they can go on to develop symptoms later. Hence multiple types of pathologies can remain undiagnosed following the initial evaluation including the following. Penetrating oesophageal injuries Over the past 50 years improved outcomes in the management of penetrating oesophageal injuries have been tied to early recognition and definitive surgical management, and delays have been associated with higher morbidity and mortality.16–19 A recent multicentre study by Asenio et al. looked at 405 patients with oesophageal injury.16 They found most patients had no symptoms or signs of oesophageal injury. Dysphagia was present in 7% and subcutaneous emphysema was present in 19%. The overall mortality rate was 19%; early deaths comprised 14.6% and late dates from either associated injuries or complications comprised 5.4%. Forty-nine per cent of these complications were deemed to be oesophageal related. Asenio et al. found a significant difference (P < 0.001) in the number of patients incurring oesophageal-related complications (wound infection, abscess, oesophageal fistula, tracheo-oesophageal fistula, mediastinitis, empyema), 41% for a group of patients investigated with oesophagoscopy, contrast studies ± CT scans (mean time from admission to operating theatre (OT): 13 h) compared to 19% for a second group of patients who had no preoperative evaluation (mean time from admission to OT: 1 h). They concluded that increased oesophageal-related morbidity is related to the diagnostic workup and its inherent delay in the operative repair of these injuries. Although they did not recommend that immediate operation be performed on every patient, the authors concluded that whatever method is chosen to evaluate patients (preoperative investigations vs immediate operation), it needs to be done expediently. The safety period in penetrating oesophageal injuries is likely to be < 8 h. Penetrating carotid injuries Although bright red bleeding from a neck wound suggests carotid injury, bleeding may not be initially present because the damaged vessel wall may be temporarily sealed by thrombus. When head injuries are also present, a neurological deficit may be due to the

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head injury, or from ischaemia secondary to partial or complete occlusion of the carotid artery. Acute carotid arteriovenous fistula may be impossible to diagnose clinically in the initial devaluation because the murmur may not be audible until several days after the injury.20 There is usually also a latent period between carotid artery injury and onset of neurological signs and symptoms as a result of clot embolization to intracranial arteries, usually the middle cerebral artery.20 Penetrating vertebral injuries The clinical presentation of patients with vertebral artery injuries is often benign.21 Because of the dual blood supply to the basilar artery, abrupt cessation of flow in one vertebral artery is readily compensated for by the contralateral vertebral artery. Unilateral vertebral artery occlusion seldom results in neurological deficit or death if there is a normal contralateral vertebral artery. Complications of unilateral vertebral ligation, however, including fatal midbrain and cerebellar necrosis have been reported.22 One author predicted that if the right vertebral artery is sacrificed, 1.8% of patients will develop an acute midbrain syndrome; if the left vertebral artery is sacrificed, 3.1% of patients will suffer an acute insult.23 There was a significant variation in size of the two vertebral arteries: the right was hypoplastic in 9.7% of cases and the left was hypoplastic in 5.7% of cases. The signs and symptoms of vertebral artery injury with midbrain ischaemia vary from a ‘locked in’ syndrome with respiratory failure and high quadriplegia to Wallenburg’s syndrome with cranial nerve deficits, Horner’s syndrome, ataxia, contralateral loss of sensation and pain or simple cranial nerve deficits. Hence it has been suggested that even without neurological deficits or overt signs of arterial injury, all patients who have sustained a penetrating neck injury close to the vertebral artery should undergo four-vessel angiography, and particular attention should be paid to the contralateral vertebral artery and the dominant blood supply to the basilar artery and the posterior inferior cerebellar arteries.21 Fistulas between the vertebral artery and jugular vein as a result of penetrating neck trauma are extremely rare: there are only 10 documented cases in the literature.22 Fistulas between the vertebral veins and the vertebral artery are much more common and account for 3% of all traumatic arteriovenous (AV) fistulas in a civilian population.24 These lesions are clinically insidious and diagnosis may be delayed if angiography is not used liberally to exclude them. Vertebral AV fistulas should be treated to prevent their enlargement, which may precipitate neurological symptoms of posterior circulation insufficiency attributable to steal phenomenon or spinal cord compression. Unilateral exopthalmos and heart failure has also been reported.25 The goal of treatment is occlusion of the fistula site and preservation of the patency of the vertebral artery, if possible.22 Surgical exposure of this region is difficult. Currently, percutaneous transcatheter embolization is the treatment of choice for traumatic vertebral AV fistulas, as was performed in the present case. In summary, the present case demonstrates the difficulties that exist in the diagnosis and management of penetrating neck trauma. Although management has tended towards a more selective approach in recent years in major trauma centres, the best practice for institutions managing very occasional penetrating neck trauma is unclear. Mandatory exploration has been highly recommended for use in such hospitals, especially in regard to zone 2 injuries. The predilection of low-velocity trauma may

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allow the Australasian surgeon to consider selective management in penetrating neck trauma to zone 1 and 3 in which, as illustrated in the present case, angiography remains the most useful diagnostic tool. This will allow a significant number of injuries to be managed non-operatively.

REFERENCES 1. Apffelstadt JP, Muller R. Results of mandatory exploration for penetrating neck trauma. World J. Surg. 1994; 18: 917–20. 2. Biffl WL, Moore EE, Rehse DH et al. Selective management of penetrating neck trauma based on cervical level of injury. Am. J. Surg. 1997; 174: 678–82. 3. Demetriades D, Charalmbides D, Lakhoo M. Physical examination and selective conservative management in patients with penetrating injuries of the neck. Br. J. Surg. 1993; 80: 1534–6. 4. Demetriades D, Theodorou D, Cornwell E et al. Penetrating injuries of the neck in patients in stable condition. Arch. Surg. 1995; 130: 971–5. 5. Demetriades D, Theodorou D, Cornwell E et al. Evaluation of penetrating injuries of the neck: Prospective study of 223 patients. World J. Surg. 1997; 21: 41–8. 6. Irish JC, Hekkenberg R, Gullane PJ et al. Penetrating and blunt neck trauma: 10 year review of a Canadian experience. Can. J. Surg. 1997; 40: 33–8. 7. Levy D, Hooker E. Neck trauma. Emedicine http://emedicine.com/emerg/topic331.htm. 8. Ordog GJ. Penetrating neck trauma. J. Trauma 1987; 27: 543–54. 9. Roon AJ, Christianson N. Evaluation and treatment of penetrating cervical injuries. J. Trauma 1979; 19: 391–7. 10. Atta HM, Walker ML. Penetrating neck trauma: Lack of universal reporting guidelines. Am. Surg. 1998; 64: 222–5. 11. Hartling RP, McGahan JP, Lindfors KK et al. Stab wounds to the neck: Role of angiography. Radiology 1989; 172: 79–81. 12. Swor RA. Penetrating and blunt neck trauma. In: Tintinalli JE, Ruiz E, Krome RL (eds) Emergency Medicine: A Comprehensive Study Guide, 4th edn. Chapel Hill, NC: McGraw-Hill, 1996; 1153–6. 13. Adame N, Bayless P. Carotid arteriovenous fistula in the neck as a result of a facial laceration. J. Emerg. Med. 1998; 16: 575–8. 14. Munera F, Soto JA, Palacio D et al. Diagnosis of arterial injuries caused by penetrating trauma to the neck: Comparison of helical CT angiography and conventional angiography. Radiology 2000; 216: 356–62. 15. Eddy VA. Is routine arteriography mandatory for penetrating injuries to zone 1 of the neck? J. Trauma 2000; 48: 208–14. 16. Asenio JA, Chahwan S, Forno W et al. Penetrating esophageal injuries: Multicenter study of the American Association for the Surgery of Trauma. J. Trauma 2001; 50: 289–96. 17. Asenio JA, Berne J, Demetriades D et al. Penetrating esophageal injuries: Time interval of safety for preoperative evaluation: How long is safe? J. Trauma 1997; 43: 319–24. 18. Stanley RB, Armstrong WB, Fetterman BL et al. Management of external penetrating injuries into the hypopharyngeal-cervical esophageal funnel. J. Trauma 1997; 42: 675–9. 19. Flowers JL, Graham SM, Ugarte MA et al. Flexible endoscopy for the diagnosis of esophageal trauma. J. Trauma 1996; 40: 261–6. 20. Davis JM, Zimmerman RA. Injury of the carotid and vertebral arteries. Neuroradiology 1983; 25: 55–69. 21. Pearce WH, Whitehill TA. Carotid and vertebral arterial injuries. Surg. Clin. North Am. 1988; 68: 705–23. 22. Kypson AP, Wentzenson N, Georgiade GS et al. Traumatic vertebrojugular arteriovenous fistula: Case report. J. Trauma 2000; 49: 1141–3. 23. Mittendorf E, Marks JM, Berk T et al. Anomalous vertebral artery anatomy and the consequences of penetrating vascular injuries. J. Trauma 1998; 44: 548–51.

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24. Kollmeyer KR, Hunt JL, Ellman BA et al. Acute and chronic traumatic arteriovenous fistulae in civilians. Arch. Surg. 1981; 116: 697–702.

25. Amirjamshidi A, Zafarghandy MR, Edraki K et al. Unilateral exopthalmos caused by traumatic vertebral artery to vertebral and jugular vein fistula: Problems in diagnosis and management. Br. J. Neurosurg. 1999; 13: 201–5.

ANZ J. Surg. (2001) 71, 692–693

CASE REPORT CASE REPORT

HYDATID DISEASE OF THE LIVER IN PREGNANCY HODO Z. HAXHIMOLLA AND PHILIP CROWE Department of Surgery, University of New South Wales, Prince of Wales Hospital, Sydney, New South Wales, Australia Key words: hydatid disease of the liver, investigations, management, pregnancy.

INTRODUCTION Unilocular hydatid cysts in the liver in humans most commonly arise from infection by Echinococcus granulosus. Infection by this organism leading to hydatid disease is more common in sheep-raising areas of western USA, Australia, New Zealand, Argentina and Mediterranean basin and is seen more rarely in non-sheep-raising industrialized Western countries. Hydatid disease has been anecdotally known to be more symptomatic during pregnancy. It has also been noted that during pregnancy the recurrence of hydatid disease is more common.1 In pregnancy it is not possible to treat the patient medically due to the teratogenic effects of the drugs on the fetus. The present case exemplifies the relative safety of surgical treatment, even in the first trimester of pregnancy.

CASE REPORT A 29-year-old, 6-week pregnant, Lebanese woman who had recently immigrated to Australia presented to the Prince of Wales Hospital Randwick Accident and Emergency Department with acute epigastric and right upper quadrant pain of 3 days’ duration. The pain became colicky and was complicated by bilateral shoulder tip pain. She had a similar presentation 1 week prior to this. The patient denied having lived in a rural area. On examination the patient was haemodynamically stable, afebrile and non-icteric. She had upper abdominal distension with voluntary guarding of the right upper quadrant and epigastric region with a non-pulsatile tender epigastric mass. The remainder of the examination was normal. Investigations revealed normal haematological and biochemical results. Ultrasound of the upper abdomen showed a large cystic mass arising from the liver measuring 15.6 × 10.6 × 7.0 cm with no internal echoes. The rest of the ultrasound examination was normal. A gestational sac of 1 centimetre in diameter was noted in the uterus. Indirect haemagglutination test and complement fixation test both confirmed the diagnosis of a hydatid disease. The patient settled with conservative management. The decision was made to proceed with laparotomy and removal of the cyst due to the potential of free rupture of the cyst during pregnancy. The patient was readmitted to hospital 1 week after discharge for elective surgery.

A large hydatid cyst, involving almost the entire left lobe of the liver, was found. The omentum was adhered to the liver suggesting recent perforation which had now sealed. No evidence of peritoneal hydatid disease was noted. Sponges soaked in 3% hypertonic saline were used to pack off and protect the peritoneal cavity. A large sheet of plastic with a hole in the centre was sewn over the top of the hydatid cyst through the adventitial layer to provide further protection of the peritoneal cavity. A large bore needle was inserted into the cyst and 20 mL of clear fluid was drained. One per cent Cetrimide solution (ICI, Australia) was then injected into the cyst to kill the protoscolices. The cyst contents were aspirated and several daughter cysts were removed. The laminated membrane and germinal epithelium were removed and the adventitial layer checked for biliary communication. No bile leaks were found. The cyst cavity was irrigated with 3% saline solution. The cyst was than packed with omentum and the adventitial layer was closed. The abdomen was irrigated with 3% saline solution. Histopathology confirmed hydatid disease. The patient was discharged on the fifth postoperative day. She proceeded to have a normal pregnancy and normal term delivery of a healthy male infant. At 7 years follow up she had no clinical or radiological evidence of recurrence and has delivered a second full-term normal infant. The arc 5 serological test is presently negative.

DISCUSSION The most common cause of hydatid disease of the liver in humans is Echinococcus granulosus causing cystic hydatid disease. The ova are ingested by the human via a faeco-oral route from the infected dog. The ova hatch in the stomach and the cyst capsules are dissolved in the alkaline environment of the duodenum; the larvae penetrate the wall of the intestine and enter the portal venous system to reach the liver. Hydatid cysts develop most commonly in the liver where they are seen in 60–70% of patients. There is little in the literature about natural history, progression and management of hydatid disease in pregnancy. In endemic areas the incidence is 1/20 000 births.2 Kain and Keystone suggested that decreased cell-mediated immunity in pregnancy may explain their patient’s rapid progression of the disease and may have contributed to the acute symptomatic presentation in the present patient.1 Other reports, dealing with immune responses

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during pregnancy, seem to support the view that selective suppression of cellular immunity may occur in response to soluble immunosuppressive factors, specific antigens and subtle local shifts in T cell subset populations.3–5 But it is difficult to know how much of this applies to Echinococcus granulosus infection. Diagnosis of hydatid disease is made by radiology and serological testing which confirms the diagnosis. We used ultrasound examination to avoid the radiation exposure during the embryonic phase. The most commonly used serological tests for diagnosing hydatid disease are indirect haemagglutination test (IHA) and complement fixation test (CF). The CF test returns to negative and is important in postoperative follow up. The most accurate serological test is immunoelectrophoresis (commonly known as ‘arc 5’), which is produced by the interaction of the serum from the hydatid-infected patient with the antigen compared to a control. The test turns positive only with Echinococcus granulosus and Echinococcus alveolaris, making it most valuable in the diagnosis of human hydatid disease.6 The ‘arc 5’ test reverts to negative after successful surgical treatment. Surgery remains the mainstay treatment of cystic hydatid disease of the liver.7 There is still ongoing debate as to the aggressiveness of surgical treatment: surgeons from endemic areas tend to favour conservative management whereas those outside the endemic areas tend to favour radical surgery.8 There have been very few reports dealing with surgical treatment of hydatid liver cysts in pregnancy. Crow et al. alluded to the importance of operation for pregnant patients to prevent possible rupture of the large cyst during parturition.9 The preferred operative option used was cyst capsulorrhaphy and insertion of hyertonic saline as described by Cohen et al.7 Saidi and Nazarian used 0.5% silver nitrate as a scolicidal agent as well as using cryogenic cone to freeze the cyst to prevent spillage.10 Kune and Sali have designed a suction cone with a variable angle of attitude to prevent spillage, and 1% Citramide has been used as an alternative scolicidal agent.11 The optimal timing of operation in a pregnant patient is the second trimester because there is a lower risk of spontaneous abortion and the uterus is not in the way of the operative field. In all the reported cases of hydatid disease in pregnancy the operations took place in the second trimester. We could not find any reported cases in which the management of this important problem took place in the first trimester of pregnancy. We chose to operate in the first trimester of pregnancy because the patient had two acute presentations to hospital in a period of 2 weeks with a possible contained leak of the cyst. In view of the large size of the cyst it was felt that, as pregnancy progressed, the chance of free intraperitoneal rupture was unexceptably high. Another treatment option would have been percutaneous drainage of the hepatic cyst, which has not been reported in a pregnant patient. Removal of all the viable cyst elements, however, can be very difficult and potential disease could be left behind in the cyst cavity which could become infected.12 Good results have been reported in the literature with regard to percutaneous treatment, which often also requires albendazole (a benzimidazole carbamate) coverage to counteract possible intra-abdominal spillage.13 Use of albendazole in the first trimester of pregnancy is contraindicated due to its teratogenic and embryotoxic effects.14 Albendazole treatment has been reported to have been given in the preoperative and postoperative period in one case of hydatid disease during the second trimester.15 The role of albendazole in fetal surfactant suppression, however, cannot be excluded15 nor, for that matter, its role in premature labour. Further studies are

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needed to clarify the effect of this drug on the fetus before it is recommended for use in pregnancy. Surgical management has been associated with a recurrence rate of approximately 10%.16 Albendazole has been used in treatment of liver hydatid cyst to prevent this relatively high recurrence rate. Its use has been recommended preoperatively and also in the postoperative period for up to 1 month depending on the viability of the protoscoleces. There was no recurrence of disease in 67 patients in an average follow-up period of 41 months.17 Richards and Morris have shown that, on ultrastructural examination of hepatic hydatid cyst after 1 month of treatment with albendazole, pieces of daughter cyst germinal layer appeared normal and had unaffected protoscoleces. This prompted them to advocate treatment for longer than 1 month in liver hydatid cysts, and the longer period of treatment was particularly recommended if daughter cysts are present.18

REFERENCES 1. Kain KC, Keystone JS. Recurrent hydatid disease during pregnancy. Am. J. Obstet. Gynecol. 1988; 159: 1216–17. 2. Rahman MS, Rahman S, Lysikiewicz A. Obstetric and gynaecological presentations of hydatid disease. Br. J. Obstet. Gynaecol. 1982; 89: 665–70. 3. Gehrz RC, Christianson WR, Linner KM, Conory MM, McCue SA, Balfour HH. A longitudinal analysis of lymphocyte proliferative responses to mitogens and antigens during human pregnancy. Am. J. Obstet. Gynecol. 1981; 140: 665–70. 4. Weinberg ED. Pregnancy associated depression of cell mediated immunity. Rev. Infect. Dis. 1984; 6: 814–31. 5. Fienberg B, Gonik B. General precepts of the immunology of pregnancy. Clin. Obstet. Gynecol. 1991; 34: 3–16. 6. Kune GA, Morris DL. Hydatid disease. In: Schwartz S, Ellis H (eds) Maingot’s Abdominal Operations, 9th edn. Stamford, CT: Appleton and Lange, 1989. 7. Cohen Z, Stone RM, Langer B. Surgical treatment of hydatid disease of the liver. Can. J. Surg. 1976; 19: 416–20. 8. Aeberhard P, Fuhrimann R, Straham P, Thommen A. Surgical treatment of hydatid disease of the liver: An experience from outside the endemic area. Hepatogastroenterology 1996; 43: 627–36. 9. Crow JP, Larry M, Vento EG, Prinz RA. Echinococcal disease of the liver in pregnancy. HPB Surg. 1990; 2: 115–19. 10. Saidi F, Nazarian I. Surgical treatment of hydatid cysts by freezing of cyst wall and installation of 0.5% silver nitrate solution. N. Engl. J. Med. 1971; 284: 1346–50. 11. Kune GA, Sali A. Hydatid disease. In: Fitzpatrick S, Aarons BJ (eds) The Practice of Biliary Surgery, 2nd edn. Oxford: Blackwell Science, 1980; 399–416. 12. Alper A, Emre A, Hazar H et al. Laparoscopic surgery of hepatic hydatid disease: Initial results and early follow-up of 16 patients. World J. Surg. 1995; 19: 725–8. 13. Akhan O, Ozman MN, Dincer A, Sayek I, Gocmen A. Liver hydatid disease. Long-term results of percutaneous treatment. Radiology 1996; 198: 259–64. 14. Morris DL. Echinococcus of the liver. Gut 1994; 35: 1517–18. 15. Golaszewski T, Susani M, Golaszewski S et al. A large hydatid cyst of the liver in pregnancy. Arch. Gynecol. Obstet. 1995; 256: 43–7. 16. Demirici S, Eraslan S, Anadol E, Bazotli L. Comparison of the results of different surgical techniques in the management of the hydatid cyst of the liver. World J. Surg. 1989; 13: 88–91. 17. Tsimoyiannis EC, Siakas P, Moutesidou K, Karayianni M, Kontoyiannis D, Gossios K. Perioperative Benzimidazole therapy in human hydatid liver disease. Int. Surg. 1995; 80: 131–3. 18. Richards KS, Morris DL. Effect of albendazole on human hydatid cysts: An ultrastructural study. HPB Surg. 1990; 2: 105–13.

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