Atlanto-occipital traumatic dislocation

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7. Lichtenstein D, Meziere G, Biderman P, et al: The comet tail artifact. An ultrasound sign of alveolar-interstitial syndrome. Am J Respir Crit Care Med 1997;156:1640-1646 8. Kearon C, Ginsberg JS, Hirsh J: The role of venous ultrasonography in the diagnosis of suspected deep venous thrombosis and pulmonary embolism. Ann Intern Med 1998;129:1044

HEMORRHAGIC CORPUS LUTEUM PRESENTING AS ACUTE GASTROENTERITIS To the Editor:—Some abdominal emergencies can mimic acute gastroenteritis. Acute appendicitis and bowel ischemia are some examples.1 Textbooks of gynecology remind us that acute gastroenteritis should be included in the differential diagnosis of acute pelvic pain. However the prevalence of gastrointestinal symptoms in acute gynecological emergencies is uncertain. During the last 3 years we have seen 2 patients with hemorrhagic corpus luteum who presented to the emergency department (ED) with a clinical picture of acute gastroenteritis. A 34-year-old woman presented to the ED because of lower abdominal pain, nausea, and watery diarrhea of 2 days duration. The day of admission to the ED the patient felt dizzy and fainted, but she said that such episodes had occurred in the past. Past medical history revealed hypothyroidism treated with L-Thyroxine. Her gynecologic medical history was unremarkable. On examination, the patient was in no distress, heart rate was 72 beats/min, regular, blood pressure 123/80 mm Hg without orthostatic hypotension, temperature 36°C. Heart and lungs were normal. The abdomen was soft, the lower abdomen was tender without signs of peritoneal irritation. Laboratory examinations were normal except for a white blood cell count of 13,200/␮L. Owing to the syncope and abdominal complains a test for ␤-HCG in the urine was ordered and it was found positive. The patient underwent a pelvic ultrasound examination which showed an hypoechogenic finding in the right ovary compatible with a vitelline sack, an a large amount of fluid in the Douglas space. The patient was taken to the operation room with the presumptive diagnosis of ectopic pregnancy. Laparoscopy was performed which revealed a ruptured hemorrhagic corpus luteum in the right ovary, the left ovary and the uterus were normal. Around 500 mL of blood was collected from the pelvis. The postoperative course was normal and later on the patient had an uneventful delivery. A 40-year-old woman presented to the ED because of lower abdominal pain and small volume diarrhea of 1 day duration, which were followed by an episode of syncope. Past gynecologic history revealed ruptured ovarian cyst and a number of uterine myomectomies. On physical examination, the patient was in no distress, heart rate was 74 beats/min, regular, blood pressure 100/65 mm Hg, temperature 37.1°C. Heart and lungs were normal. The abdomen was swollen, soft, and marked tenderness without peritoneal signs of irritation were found in the lower abdomen. Laboratory examinations were normal except for a mild leucocytosis of 11.300/␮L. ␤-HCG was negative. A pelvic ultrasound showed a cystic finding measuring 65⫻39 mm close to the left ovary and surrounded by turbid fluid. A moderate amount of fluid was seen in the Douglas space. These findings were compatible with rupture of hemorrhagic corpus luteum. The patient was admitted to the hospital for observation, and after a few days the pain and the ultrasonographic findings resolved completely. The main causes of acute pelvic pain are complications of pregnancy (ruptured ectopic pregnancy, abortion), acute infections Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2002-0021$35.00/0 doi:10.1053/ajem.2002.31137

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and adnexal disorders (hemorrhagic corpus luteum, torsion of adnexa, rupture of functional or neoplastic ovarian cyst). The differential diagnosis of acute pelvic pain is with gastrointestinal disorders such as inflammatory bowel disease and acute appendicitis, genitourinary disorders such as urolithiasis and other disorders such as pelvic thrombophlebitis or acute porphiria.1 Irritation of the cul de sac by blood, such as in rupture of hemorrhagic corpus luteum or ruptured ectopic pregnancy could lead to altered bowel movements.2 An inflammatory process such as that seen in pelvic inflammatory disease could cause the same symptoms. Hallatt et al reported the clinical features of 173 patients suffering from ruptured corpus luteum and hemoperitoneum. In this study, the main complain in all the patients was sudden severe pain of hemoperitoneum and was present for less than 24 hours in over one half of the patients. About one-third of the patients complained of a crampy intermittent type of pain for 1 to 2 weeks before the severe acute pain of hemoperitoneum caused them to be hospitalized. In this series nausea or vomiting or diarrhea occurred in about one-third of the cases.2 Speroff reported nausea and vomiting in 45% and 20% respectively of 40 cases of bleeding corpus luteum. None of the patients suffered from diarrhea.3 Acute gastrointestinal symptoms as the main presentation of acute pelvic emergencies are probably rare. Among 50 women admitted to the ED with the diagnosis of ruptured corpus luteum between 1997 and 2000, only in 2 of them (4%) the main complain was acute diarrhea. However, if diarrhea is accompanied by severe abdominal pain or hemodynamic instability especially in a premenopausal woman other diagnostic possibilities should be considered. RUTH STALNIKOWICZ, MD Department of Emergency Medicine Hadassah University Hospital Mount Scopus Jerusalem, Israel

References 1. Rapkin AJ: Pelvic pain and dysmenorrhea, in Berek JS, Adashi EY, Hillard PA (eds): Novak’s Gynecology (ed 12). Baltimore, MD, Williams & Wilkins, 1988, pp 399-408 2. Hallatt JG, Steele CH, Snyder M: Ruptured corpus luteum with hemoperitoneum: A study of 173 surgical cases. Am J Obstet Gynecol 1984; 149: 5-9 3. Speroff L: The bleeding corpus luteum. Analysis of 40 confirmed cases. Obstet Gynecol 1966; 28: 416-420

ATLANTO-OCCIPITAL TRAUMATIC DISLOCATION To the Editor:—Spinal injuries are relatively common among head trauma patients and their occurrence should be considered in every comatose patient. The cervical spine is mostly involved, and the C5 and C6 metameres appear particularly vulnerable.1 Conversely, traumatic atlanto-occipital dislocation (AOD) is a rare and often immediately fatal injury. In survivors, the AOD is usually associated with severe neurologic symptoms, albeit very few symptom-free patients have been described. We report on a patient who was admitted comatose to the hospital after a traffic accident and in whom the diagnostic investigations showed an AOD causing the complete separation between the spine and the skull. A 28-year-old man was projected away from a motorbike which collided with a car. At the arrival of the emergency team, the patient was deeply comatose (Glasgow Coma Scale ⫽ 3), hypotensive, and apnoeic; after the immobilization of the cervical spine he was orotracheally intubated and brought to the hospital, where

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a diagnostic work-up was implemented. The lateral radiograph of the cervical spine showed the complete detachment of the cervical spine from the skull base (Fig 1); a prevertebral hematoma with the forward displacement of the trachea was also present. The computed tomography (CT) scan of the same tract confirmed this finding and showed also the fracture and the detachment of the left occipital condyle associated with the fracture of the atlas (Fig 2). The CT of the brain showed a diffuse and intense edema affecting both the white and the gray matter associated with a subarachnoid hemorrhage; the brainstem was compressed by a hematoma probably originating from the above-described fractures. An incremental skull traction up to 6 kg was applied. No other injuries were present. The patient remained comatose despite the restoration of the arterial pressure; the pupils were fixed and the brainstem reflexes were absent. As the electroencephalograms (EEGs) were repeatedly isoelectric, on the following day the patient was decleared brain dead and an organharvesting procedure was performed. Spinal cord injuries are relatively common in politrauma patients, and their real incidence is probably even higher than reported as many patients die immediately or soon after the trauma.2 Almost 50% of the lesions involve the cervical spinal cord, particularly at the C5 and C6 level.2,3 Actually, these tracts are most vulnerable to injury caused either by their mobility and to the relatively limited mechanical support for the vertebrae.2,3 The cervical spine can be divided in 2 parts with different biomechani-

FIGURE 1. Lateral plain film showing the detachement of the skull base from the cervical spine.

FIGURE 2. CT scan showing the fracture and detachment of the left occipital condyle (arrow); the skull appears separated from the spine. cal properties that ultimately account for their susceptibility to trauma and patterns of fracture: the upper includes the C1 and C2 vertebrae and atlanto-occipital joint while the lower extends from the level of C3 downward.4 In particular, the C2 is flat and larger than the other vertebrae and supports the odontoid process, around which the atlas turns. Therefore, the primary movement of the C1-C2 joint is rotation rather than flexion or extension, which are more pronounced in the lower cervical spine.5 This unique arrangement is responsible for the occurrence of the AOD, which is usually the consequence of a direct trauma and/or a combination of hyperextension, distraction and rotation of the head.5 Alternatively, an anteroposterior force directed against the head can disrupt the transverse ligament or the odontoid process which are essential for the stability of the articulation.6 The AOD is frequently a fatal injury and probably is more common than reported in the literature. The elevated mortality is related to the frequent transection of the spinomedullary junction and the compression of the adjacent vertebral arteries.6,7 Among survivors, severe and persistent neurologic deficit are common findings and the recovery of neurologic function has been described only occasionally.8 Our patient presented the complete separation of the cervical spine from the skull with the downward displacement of the first vertebra. The AOD was initially shown by a plain lateral film of the cervical spine. The radiograph showed also an increased thickness of the prevertebral tissue associated with the forward displacement of the trachea. Other investigators9 described these latter findings associated with the concomitant occipital condyle fracture. As this injury is generally not visible on plain films, the use of the CT scan possibly associated with a 3-dimensional reconstruction has been recently advocated in the presence of such indirect signs.4 In our patient too, the plain lateral film of the cervical column failed to reveal the fractures either of the left occipital condyle and of the atlas, which were shown only by the CT; these injuries caused the complete detachement of the spine from the skull. In our patient, the extremely critical conditions prevented us from obtaining a magnetic resonance image (MRI). Hovewer, in circumstances such ours, this investigation could be considered somewhat redundant. Actually, the American College of Radiology stated that the conventional tomography or CT scan are appropriate for injuries involving the craniovertebral junction and suggested that MRI could be reserved to patients whose neurologic symptoms cannot be explained by the radiologic findings.4,10

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The treatment of AOD is particularly challenging and is mainly based on the pattern of injury. Non-aligned AOD should be reduced with skeletal traction before definitive treatment. However, in aligned AOD the traction must be considered with caution to prevent a stretch injury to the neurovascular structures at the cervicomedullary junction.11 When AOD occurs after an injury to the ligamentous structures in the absence of significant bony fractures, the internal emergency fixation should be considered.6 The occurrence of AOD is an uncommon but potentialy devastating complication of injuries involving the head and the cervical spine. As bony injuries can be not always evident with a plain film, it should be considered in the presence of abnormally thickened prevertebral tissues and/or downward displacement of the trachea. In all cases, the CT scan is warranted to confirm its presence and to plan the subsequent treatment. ARIELLA TOMASINI, MD GIORGIO BERLOT, MD ANNA RANDINO, MD MARINO VIVIANI, MD Department of Anesthesia and Intensive Care University of Trieste Trieste, Italy

References 1. Highland T, Salsiccioli G, Wilson R: Spinal cord injuries, in Wilson RF (ed): Handbook of Trauma; Pitfalls and Pearls. Philadelphia, Lippincott Williams & Wilkins, 1999, pp 142-159 2. Johnson GE: Spine injuries, in Hall JB, Schmidt GA, Wood LDH (eds): Principles of Critical Care (ed 2). New York, McGraw-Hill, 1998 pp 1375-1385 3. Belanger E: The acute and chronic management of spinal cord injury. J Am Coll Surg 2000;190:603-618 4. Kathol MH: Cervical spine trauma. Rad Clin North Am 1997; 35:507-531 5. Pathria MN, Petersilge CA: Spinal trauma. Rad Clin North Am 1991;29:847-865 6. McKee TR, Tinkoff G, Rhodes M: Asymptomatic occult cervical spine fracture: Case report and review of the literature. J Trauma 1990;30:623-626 7. Papadopoulos SM, Dickman CA, Sonntag VKH, et al: Traumatic atlantooccipital dislocation with survival. Neurosurgery 1991; 28:574-579 8. Bohlman HH: Acute fractures and dislocation of the cervical spine: An analysis of three hundred hospitalized patients and a review of the literature. J Bone Joint Surg Am 1979;61:1119-1142 9. Ahuja A, Glasauer FE, Alker GJ Jr: Radiology in survivors of traumatic atlantooccipital dislocation. Surg Neurol 1994;41:112 10. Raila FA, Aitken AT, Vickers GN: Computed tomography and three-dimensional reconstruction in the evaluation of occipital condyle fracture. Skeletal Radiol 1993;22:269 11. Traynelis VC, Marano GD, Dunker RO, et al: Traumatic atlanto-occipital dislocation. Case report. J Neurosurg 1986;65:863-870

FIGURE 1.

ADENOSINE-INDUCED VENTRICULAR FLUTTER IN AN ETHANOL-INTOXICATED PATIENT To the Editor:—A 45-year-old man presented to our ED with a 12-hour history of his heart “pounding in my chest.” The patient related no previous history of palpitations, and his associated symptom was a vague complaint of weakness. The patient admitted to a moderate amount of mixed alcohol consumption 12 hours previously, and he did not take any medicines on regular basis. His initial vital signs were blood pressure 120/85 mm Hg, heart rate 190 beats/min, respiratory rate 16 breaths/min and afebrile. Physical examination revealed a well-nourished man. No murmur, rubs, or gallops heard on cardiac auscultation. Results of the remaining examination were benign. Patient was placed on a continuous electrocardiograph (ECG) monitor, which showed a narrow complex tachycardia. A 12-lead ECG was obtained and the rhythm was interpreted as PSVT. The patient was treated first with carotid massage and then the Valsalva maneuver, no response was observed for either treatment. Next the patient received 6 mg of adenosine IV rapid bolus over 2 seconds. No change seen in cardiac rhythm. A second dose of 12 mg of adenosine was ordered 1 minute later. Right after administering the second dose of adenosine intravenously, patient’s cardiac rhythm converted from PSVT to ventricular flutter (Fig 1). This ventricular flutter lasted only 15 seconds and then converted spontaneously to atrial flutter that also lasted briefly before returned to normal sinus rhythm. The patient remained awake, alert, and verbally responsive, he denied shortness of breath, stated his heart was “pounding” really fast. Blood pressure was measurable at 101/70 mmHg during ventricular flutter run. The laboratory work-up included CBC and chemistry (BUN, Cr, Na, K, glucose), whose results were normal. The serum ethanol was 120 mg/dL; the local acceptable level is ⬍50 mg/dL. Radiograph of the chest was unremarkable. He stayed in our observation unit with continuous cardiac monitor for another 4 hours without any further arrhythmic episodes. The patient was discharged on AMA, but he did returned to our cardiac clinic for further cardiac work-up, which revealed no structural heart disease. Adenosine is an endogenous purine nucleoside, has a half-life of less than 5 seconds and a brief pharmacologic response as it is rapidly sequestered by red blood cells. Adenosine is effective terminating PSVT because it restores the normal sinus rhythm by blocking the reentry pathways involving the AV node. Adenosine also helps to clarify the diagnosis of arrhythmias other than PSVT.1 Administration of adenosine is not without any side effects. Flushing, dyspnea, and chest pain are common but brief.2 Adenosine may be proarrhythmic in some patients, bradyarrhythmias of short duration are the most

Copyright 2002, Elsevier Science (USA). All rights reserved. 0735-6757/02/2002-0023$35.00/0 doi:10.1053/ajem.2002.31134

The sine wave configuration at a rate of 300 beats/min is characteristic of ventricular flutter.