Phrenic Nerve Injury Following Blunt Trauma

J Accid Emerg Med 2000;17:419–428 419 J Accid Emerg Med: first published as 10.1136/emj.17.6.426 on 1 November 2000. Downloaded from

CASE REPORTS

Phrenic nerve injury following blunt trauma

David Bell, Ajith Siriwardena

Abstract Phrenic nerve trauma in the absence of direct injury is unusual and may present diagnostic diYculty. Diaphragmatic paralysis resulting from phrenic nerve injury may closely mimic diaphragmatic rupture. This case highlights the value of magnetic resonance imaging in establishing diaphragmatic integrity and of ultrasono- graphic assessment during respiratory excursion in conﬁrming diaphragmatic paralysis. In cases of non-contact injury involving torsional injury to the neck, an index of clinical awareness may help to establish the diagnosis of phrenic nerve trauma. Figure 1 Posteroanterior chest radiograph taken after (J Accid Emerg Med 2000;17:419–420) injury showing elevated right hemi-diaphragm.

Keywords: phrenic nerve injury; blunt trauma diaphragmatic rupture was made. Computed tomography demonstrated mild rotation of the axis of the liver (anti-clockwise rotation Case report through the plane of the middle hepatic vein) A 36 year old man was admitted to the compatible with diaphragmatic rupture. How- accident and emergency department two hours ever, a magnetic resonance scan conﬁrmed Y after a road tra c accident. The patient was that the diaphragm was intact but elevated. driving a car that had been struck on the near- Ultrasound scan with respiratory excursion http://emj.bmj.com/ side by another vehicle. The patient’s vehicle demonstrated paralysis of the right hemi- had been stationary at the time of impact. The diaphragm. patient was wearing a seatbelt and reported A diagnosis of right hemi-diaphragmatic that he had not struck his head. There was no paralysis secondary to phrenic nerve damage history of loss of consciousness. He com- plained of pain in the head, neck and back. He had also brieﬂy experienced paraesthesiae in

the right hand but this had resolved by the time on September 30, 2021 by guest. Protected copyright. of arrival in the department. At primary survey his neck was immobilised in a hard collar. He was maintaining his airway, self ventilating with a respiratory rate of 20/minute and there was decreased air entry to the right lower zone. The trachea was central. Cardiovascular examination was normal. Oxy- gen saturation was 97% on air and an electrocardiograph was normal. Secondary survey demonstrated severe lumbar spine tenderness over T12 and L1 vertebrae but no obvious University Department of neurological deficit. Physical examination was Surgery, Royal otherwise normal. His past medical history was Infirmary of significant for a myocardial infarction one year Edinburgh, Edinburgh previously. Radiographs of the cervical spine were nor- Correspondence to: Mr Siriwardena, Department mal. Lumbar spine films demonstrated a of Surgery, Manchester stable anterior wedge compression fracture of Royal Infirmary, Manchester T12. Chest radiograph showed an elevated M13 9WL right hemi-diaphragm (fig 1). This was not ([email protected]) Figure 2 Posteroanterior chest radiograph taken 12 evident on a chest film taken 12 months previ- months before injury showing normal position of right Accepted 29 February 2000 ously (fig 2). A provisional diagnosis of hemi-diaphragm.

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was made. The injury was treated conserva- and confirmed by fluoroscopy or ultrasonogra- tively with non-opioid analgesia for the phy with respiratory excursion. An important lumbar spine injury. The patient remains well practical consideration is that the clinical find- six months after injury with no clinical ings and radiological appearances on plain evidence of respiratory compromise. He has radiographs and computed tomography may declined further assessment of diaphragmatic mimic diaphragmatic rupture. function. In summary, this case highlights a rare cause of phrenic nerve injury in the absence of direct Discussion trauma. The clinical presentation may closely Traumatic phrenic nerve injury is well recog- resemble diaphragmatic rupture. nised after both penetrating and blunt trauma 12 Contributors to the neck. In contrast, injury as a result of David Bell initiated the writing of the report and the distraction or stretching of the nerve is rare.3 MEDLINE search. Ajith Siriwardena supervised the writing of the report and the phrasing of the final draft and reviewed the In several of these previous reports, a compo- adequacy of the literature search and review of relevant publica- nent of nerve damage may have been as a tions. result of blunt trauma. There was no evidence Funding: none. of blunt trauma in this case with the Conflicts of interest: none. mechanism of injury thought to be lateral hyperextension of the neck. There are no pre- 1 Iverson LI, Mittal A, Dugan DJ, et al. Injuries to the phrenic nerve resulting in diaphragmatic paralysis with special ref- vious reports of phrenic nerve palsy by this erence to stretch trauma. Am J Surg 1976;132:263–9. mechanism. 2 Dalshaug GB, Rothwell BC. Diaphragmatic paralysis following minor blunt trauma. Journal of Trauma, Injury, Clinical manifestations of this injury include Infection and Critical Care 1999;47:413–15. breathlessness, orthopnoea and respiratory 3 Snyder RW, Kukora SJ, Bothwell WN, et al. Phrenic nerve 4 injury following stretch trauma. J Trauma 1994.36:734–6. distress. The diagnosis may be suspected on 4 Carter RE. Unilateral diaphragmatic paralysis in spinal cord chest radiography and computed tomography injury. Paraplegia 1980;18:267–74. http://emj.bmj.com/ on September 30, 2021 by guest. Protected copyright.

www.jnlaem.com Non-penetrating chest blows and sudden death in the young 421 J Accid Emerg Med: first published as 10.1136/emj.17.6.426 on 1 November 2000. Downloaded from Non-penetrating chest blows and sudden death in the young

S Thakore, M Johnston, E Rogena, Z Peng, D Sadler

Abstract right and left lower lung lobes. There was a 15 Sudden death in the young after low mm long and 8 mm deep laceration within the energy anterior chest wall impact is an left ventricular myocardium at the apex. There under-recognised phenomenon in this was no natural disease and toxicological analy- country. Review of the literature yields ses were negative. Death was attributed to several American references to commotio blunt force chest trauma. cordis, mainly in the context of sporting events. Two cases are reported of sudden Case report 2 death in young men as a result of blunt A 19 year old man was playing in goal in a five a impact anterior chest wall trauma. It is side football game when he was struck in the suggested that these cases draw attention central chest by a leather football, kicked with to a lethal condition of which many considerable force from a range of only a few practitioners are unaware. yards. Although initially in obvious discomfort (J Accid Emerg Med 2000;17:421–422) and “winded”, he continued to stand in goal for Keywords: chest blows; sudden death an estimated 5–10 minutes before crying out and collapsing. Bystander cardiopulmonary re- Case report 1 suscitation was started promptly by a doctor The deceased was a 15 year old boy who participating in a neighbouring game. Ambu- collapsed to the ground immediately after lance paramedics performed advanced life being struck centrally in the chest with a 500 g support, including repeated administration of stone, thrown from a distance of 8 to 10 feet epinephrine and attempts at electrical cardiover- during a gang fight. Upon collapse he was said sion. On arrival in the A&E department to have suVered a fit and was carried bodily a approximately 70 minutes after the collapse he short distance by friends and laid on the was in asystole. Further attempts at resuscita- ground. There was no basic life support until tion, including pericardiocentesis and external ambulance paramedics arrived, five minutes pacing, were performed but unfortunately failed after receiving the emergency call. to achieve return of spontaneous circulation. The cardiac rhythm at the scene was pulseless electrical activity, which degenerated NECROPSY FINDINGS to ventricular fibrillation resistant to electrical There were signs of medical intervention in the cardioversion. Appropriate advanced life sup- form of electode pads, endotracheal intubation http://emj.bmj.com/ port continued and he arrived at the accident and a needle puncture mark in the left cubital and emergency (A&E) department 27 minutes fossa. Marked upper anterior mediastinal after the emergency call. His pupils were fixed bruising was present in relation to right subcla- and dilated and he had an agonal rhythm, inter- vian cannulation. There was 350 ml of blood rupted by runs of ventricular tachycardia and within the pericardial sac and a small puncture episodes of ventricular fibrillation. Right needle mark over the lower sternum entering the right ventricular apex, representing the attempt at

thoracocentesis was performed because of on September 30, 2021 by guest. Protected copyright. reduced air entry on auscultation but no air was pericardiocentesis. There was no other myo- aspirated. Internal jugular and femoral venous cardial abnormality and no injury to the chest lines were inserted and a crystalloid bolus was wall. There was no natural disease but infused. Ventricular fibrillation developed, but toxicological analyses were not performed. electrical cardioversion proved unsuccessful. Death was attributed to blunt force chest Accident and His rhythm degenerated into asystole and trauma resulting from being struck on the Emergency resuscitation attempts were stopped. chest by the football. Department, Ninewells Hospital, Dundee, DD1 9SY, Scotland NECROPSY FINDINGS Discussion S Thakore There were signs of medical intervention in the We suggest that the above cases illustrate death M Johnston form of needle puncture marks in the cubital attributable to primary arrhythmia occurring fossae, right lower neck, right groin and right after blunt chest trauma. This is often described Department of upper anterior chest, and defibrillator paddle as commotio cordis, which typically occurs in Forensic Medicine, marks on the anterior chest wall. There were the absence of structural cardiac damage. University of Dundee, Dundee minor abrasions to both anterior knees, the fin- Collapse is usually near instantaneous, but there E Rogena gers of the right hand and the left eyebrow, can be a period of activity following impact, 1–3 Z Peng cheek, and chin. There was no significant usually only of a few seconds duration. D Sadler externally apparent injury to the anterior chest Most previous reports are concentrated in wall. There was minor bruising over the left American literature and occur mainly in base- Correspondence to: pectoralis major muscle. Internal examination ball and ice hockey, where projectile impacts to Mr Johnston revealed moderate bruising of the lingula and the precordium are frequent.1–3 Such projec- Accepted 8 December 1999 patchy subpleural bruising on the posterior tiles cause a focused impact of short duration

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with virtually no rebound, allowing almost responsible for death. The attempt at pericar- complete transfer of kinetic energy to the chest diocentesis produced no blood, suggesting that wall.3 Commotio cordis has not been reported there was no sizeable collection of blood at the in the game of cricket, Britain’s nearest time of resuscitation. This reflects the diYculty sporting equivalent. Maron et al4 have de- in determining whether the pericardial haemor- scribed four cases of commotio cordis occur- rhage resulted from an injury at the time of ring in relation to criminal activity. trauma or by attempts at pericardiocentesis. We An experimental model for commotio cordis considered it possible that chest impact, pre- suggests that the impact of projectiles on the sumably during the QRS complex, produced chest wall of pigs during the period of cardiac one of the above electrical abnormalities that repolarisation, prior to the peak of the T wave, then degenerated into a malignant arrhythmia typically induced ventricular fibrillation.5 This with cardiac arrest after some minutes. situation probably corresponds to the typical The severity of impact required to cause death presentation reported in most fatalities, caus- after a blow to the chest is often unremarkable ing immediate collapse and cardiac arrest. In and careful enquiry should be made for a history contrast, impact during the QRS complex is of chest wall impact after cardiac arrest or more likely to induce complete heart block, ST sudden death in the young. We further suggest segment elevation or left bundle branch block.5 that the classic impression of instantaneous Other reported ECG abnormalities include collapse may not be true in every case. sinoatrial nodal dysfunction, atrial fibrillation, Contributors right bundle branch block and ventricular Shobhan Thakore, Emily Rogena, Zhang Peng, David Sadler extrasystoles.67 and Michael Johnston collected the clinical data on the two cases and wrote the paper. David Sadler and Michael Johnston In the first case, the sequence of events after act as guarantors of the paper. impact were typical of commotio cordis. How- ever, it is unusual in that it occurred in a homi- 1 Abrunzo TJ. Commotio cordis—the single, most common cause of traumatic death in youth baseball. American Jour- cidal manner, with an object that is heavier than nal of Diseases of Children 1991;145:1279–82. usual, thrown over a shorter distance and at 2 Maron BJ, Strasburger JF, Kugler JD, et al. Survival following blunt chest impact-induced cardiac arrest during sports lower velocity. In this case there was evidence of activities in young athletes. Am J Cardiol 1997;79:840–1. structural cardiac damage. The apical endocar- 3 Maron BJ, Poliac LC, Kaplan JA, et al. Blunt impact to the chest leading to sudden-death from cardiac-arrest during dial laceration may be attributable to the sports activities. N Engl J Med 1995;333:337–42 hydraulic ram eVect of ventricular compression, 4 Maron BJ, Link MS, Wang PJ, et al. Clinical profile of commotio cordis: an under appreciated cause of sudden death causing blood to be forced into the blind-ending in the young during sports and other activities. J Cardiovasc apex of the left ventricle. This could have been Electrophysiol 1999;10:114–20 5 Link MS, Wang PJ, Pandian NG, et al. An experimental attributable either to impact by the stone itself model of sudden death due to low-energy chest-wall impact or may represent resuscitation artefact.8 (commotio cordis). N Engl J Med 1998;338:1805–11. 6 Crown LA, Hawkins W. Commotio cordis: clinical implica- Our second reported case diVered signifi- tions of blunt cardiac trauma. Am Fam Physician 1997;55: cantly from the usual presentation of commotio 2467–70. 7 Kumpuris AG, Casale TB, MokotoV DM, et al. Right bun- cordis in that collapse occurred several minutes dle branch block; occurrence following nonpenetrating after chest impact. Blood was found in the peri- chest trauma without evidence of cardiac contusion. JAMA cardial sac at necropsy suggesting a slowly 1979;242:172–3. 8 Leadbeatter S, Knight B. Resuscitation artefact. Med, Sci http://emj.bmj.com/ developing cardiac tamponade may have been Law 1988;23:200–4.

Extracorporeal rewarming in a severely hypothermic patient using venovenous haemoﬁltration in the on September 30, 2021 by guest. Protected copyright. accident and emergency department

K Spooner, A Hassani

Abstract general hospital. Venovenous haemofiltra- Severe hypothermia is a medical emer- tion is now commonly found in district gency and requires active and occasion- general hospitals around the country and ally rapid core rewarming to prevent can be used safely for core rewarming. A Anaesthetic cardiac arrhythmias and death. In the case is reported of a severely hypothermic Department, accident and emergency department re- elderly patient successfully rewarmed Broomfield Hospital, warming is often limited to warmed intra- using venovenous haemofiltration, in an Chelmsford, Essex CM1 7ET, UK venous fluids, heated blankets, gastric and accident and emergency department, bladder lavage. Extracorporeal methods, when other conventional methods had Correspondence to: which rewarm core blood directly, for failed. Dr Hassani, Consultant example haemodialysis and cardiopul- (J Accid Emerg Med 2000;17:422–424) Anaesthetist monary bypass, require expertise and Accepted 26 April 2000 equipment not always found in a district Keywords: hypothermia; venovenous haemofiltration

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Hypothermia is defined as a core body Because of the previous large warmed fluid temperature below 35°C.1 Patients presenting transfusions, the machine was set to take oV with severe hypothermia (<28°C)2 are at high one litre of fluid to prevent overload. Haemofil- risk of serious arrhythmias and asystole.1 tration was stopped after one hour having Rewarming severely hypothermic patients in reached the desired temperature of 34°C. the accident and emergency (A&E) department initially requires non-invasive methods, which are usually successful. However, if these Discussion methods fail, or the patient is in circulatory This case shows a practical and safe method of arrest, then invasive methods are needed. warming severely hypothermic patients using Extracorporeal rewarming is an invasive venovenous haemofiltration in the A&E de- method, which can rapidly and safely rewarm partment. core blood.3–5 Venovenous haemofiltration is one form of Venovenous haemofiltration is readily avail- extracorporeal rewarming. Successful out- able now in most district general hospitals comes with rewarming hypothermic patients where it can be used as an alternative to have been reported with cardiopulmonary arteriovenous haemofiltration in treating pa- bypass,34 haemodialysis6 and peritoneal dialy- tients with acute renal failure. It is an extracor- sis .7 poreal circulation that is an eYcient rewarmer For severe hypothermia with circulatory of core blood and thus, can be used to rewarm arrest, rewarming with cardiopulmonary by- severely hypothermic patients who need more pass is the most eYcient by being rapid and invasive measures. providing adequate and immediate circulatory support.458 However, it requires considerable Case history time to set up (sometimes, exceeding one A 77 year old woman found collapsed at home hour) and technical support. Its use is there- was admitted to hospital with a Glasgow Coma fore often limited to operating theatres. Scale (GCS) of 8 and rectal temperature of Continuous arteriovenous haemofiltration 26°C. Blood pressure was 93/55 and heart rate has also been successfully used to rewarm 89 in sinus rhythm. While rewarming with a hypothermic patients.9 However, at our dis- heated blanket and warmed intravenous fluids trict general hospital, venovenous haemofiltra- she had a prolonged ventricular fibrillation tion, involving insertion of a single large dou- (VF) arrest with episodes of other serious ble lumen central venous catheter has been arrhythmias. Defibrillation was used while found to be more practical. A roller pump is conventional rewarming methods continued, used instead of the patient’s blood pressure, to together with gastric lavage and bladder circulate the blood through the filtration unit catheter irrigation, but with no success. before it is warmed and returned to the Even after five hours the core temperature patient. Continuous venovenous rewarming was still only 30°C and she was continuing to has been successfully used in both a juvenile have episodes of VF arrest that responded to animal model,10 and in adult intensive care defibrillation. As the cause of her obtunded patients.5 conscious was not clear (GCS remained 7/15), Extracorporeal venovenous rewarming http://emj.bmj.com/ and adrenaline (epinephrine) was maintaining warms core blood directly and thus is more her blood pressure, we intended to warm her eYcient than standard rewarming techniques eYciently to normothermia using venovenous (for example, warming blankets, warmed haemofiltration in the A&E department. A intravenous fluids, gastric, bladder and perito- temperature of 34°C was reached after one neal lavage).5 hour, her blood pressure was now 120/73 with Haemofiltration is now commonly used

adrenaline and her heart rate 111 in sinus across the country in treating acute renal on September 30, 2021 by guest. Protected copyright. rhythm. failure patients and in intensive care units. The As her GCS remained the same with mild haemofiltration machine is mains driven, easy hypothermia, she was referred to the medical to operate and very portable. It can be set up team for further investigations towards a work- and ready to use in 20 minutes. ing diagnosis of a cerebral vascular accident, The experienced operator (intensivist/ which caused her to collapse two days before nephrologist/haemofiltration nurse) needs to admission. She died a day later. set the fluid volume to be exchanged, the required fluid loss and the filtration rate Haemofiltration (ml/min). The machine will then automatically Haemofiltration was performed using the carry out the treatment when activated, with Gambro AK-10 “Low flow” haemofiltration the nurse supervising all data and checking the machine with BMM 10–1 Blood Monitor and results. In our case, minimal filtration was HFM 10–1 Fluid Monitor. A vascath was required as the primary use was for rewarming. inserted into the right femoral vein. The Treatment was terminated early as the desired haemofiltration fluid was Normosol with 60 temperature was reached. mmol of potassium added and the exchange Complications of haemofiltration are rare. volume was set to 27 litres with a filtration rate For example air embolism, hypotension, infec- of 84 ml/min. Heparin was used as the antico- tions, leaks in the filter or anticoagulation agulant (10 000 units in 40 ml normal saline problems. run at 4 ml per hour). The Haemofilter was a This case report shows the eVectivess and polysulfone filter made by Link Medical/ simplicity of using venovenous haemofiltration Bellco. in the A&E setting.

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1 Gentilello LM. Advances in the management of hypother- 6 Hernandez E, Praga M, Alcazar JM, et al. Haemodialysis for mia. Surg Clin North Am 1995;75:243–56 treatment of accidental hypothermia. Nephron 1993;63: 2 Danzl DF, Pozos RS. Accidental hypothermia. N Engl J Med 214–16. 1994; 331:1756–60. 7 Vella J, Farrell J, Leavey S, et al. The rapid reversal of 3 Dobson JAR, Burgess JJ. Resuscitation of severe hypother- profound hypothermia using peritoneal dialysis. IrJMed mia by extracorporeal rewarming in a child. J Trauma Sci 1996;165):113–14. 1996;40:483–5. 8 Althanus U, Aeberhard P, Schupbach P, et al. Management 4 Walpoth BH, Walpoth-Aslan BN, Mattle HP, et al. Outcome of profound accidental hypothermia with cardiorespiratory of survivors of accidental deep hypothermia and circulatory arrest. Ann Surg 1982;195:492–5. arrest treated with extracorporeal blood warming. N Engl J 9 Broderson HP, Meurer T, Bolzenius K, et al. Haemoﬁltra- Med 1997;337:1500–5. tion in very severe hypothermia with favourable outcome. 5 Gregory JS, Bergstein JM, Aprahamian C, et al. Comparison Clin Nephr 1996;45:413–15. of three methods of rewarming from hypothermia: Advan- 10 Seigler RS, Golding E, Blackhurst DW. Continuous tages of extracorporeal blood warming. J Trauma 1991;31: venovenous rewarming: results from a juvenile animal 1247–52. model. Crit Care Med 1998;26:2016–20. http://emj.bmj.com/ on September 30, 2021 by guest. Protected copyright.

www.jnlaem.com Penile fracture 425 J Accid Emerg Med: first published as 10.1136/emj.17.6.426 on 1 November 2000. Downloaded from Snap without crackle or pop: a rude awakening. A case history of penile fracture

P Gilligan, M Smith, F Todd, P Bradley, A Shenton

Abstract with a sudden snap, pain, detumescence and a Penile fracture is a rare but worrying con- haematoma of the penis with deformity. The dition. The presentation to accident and “snap” heard when the tunica albuginea tears emergency or primary care should not has been well described, as has the fact that it is present diYculty in diagnosis but may also often heard by the sexual partner if the cause concern with regard to initial treat- fracture occurs during coitus. To our knowl- ment and definitive management. Emer- edge this is the first time that the snap has been gency admission to a urologist is reported as having been heard by a partner not mandatory. in the same room at the time of fracture. Clini- (J Accid Emerg Med 2000;17:425–426) cal examination consistently reveals a smooth, fixed, tender, palpable lump at the fracture site. Keywords: penile fracture; urology This lump apparently is formed by a clot in the torn corpus cavernosum, trapped in its well Case report localised position by Buck’s fascia.3 Investiga- A 32 year old white man presented to the acci- tions suggested for the condition include ultra- dent and emergency (A&E) department of sonography, cavernosography, magnetic reso- Bradford Royal Infirmary complaining of nance imaging, urethrography and surgical discomfort and bruising of his penis over a four exploration. Dissection in this condition tends hour period. That morning he had awoken to reveal a tear in the proximal third of the cor- with an erection, he wanted to pass urine and pus cavernosum.1 as a result had forcefully bent his penis. On Complications of the disorder include con- bending the shaft of his penis he heard a “ loud comitant urethral injuries (20%), penile curva- snap” and he experienced pain, loss of penile ture, abscess formation, penile pain, pulsatile tumescence and swelling and bruising of his diverticulum, urine extravasation, psycho- penis. His partner who was in the next room physical problems, and impotence.34 Urethral also heard the “snap” and insisted that they go injury should be suspected if there is blood at to an A&E department. The swelling of the the meatus or failure to pass urine. penis increased up until the time of assess- Treatment may be conservative or operative. ment. Conservative regimens include catheterisation Examination in the A&E department re-

once a urethral injury has been ruled out, pres- http://emj.bmj.com/ vealed a flaccid penis with a large fluctuant sure dressings, penile splinting, diazepam, haematoma on the dorsal aspect of his penis non-steroidal anti-inflamatory drugs and even stretching from the base of the shaft to the oestrogen therapy.5 The rationale for the use of glans. There was some tenderness on palpa- diazepam is that it reduces the frequency and tion. The patient had micturated successfully intensity of erections and so lessens discom- since sustaining the injury without any frank fort. haematuria. The more recent literature seems to favour

Investigations performed included a full operative management to lessen the likelihood on September 30, 2021 by guest. Protected copyright. blood count, coagulation profile and urea and of complications that are more common in the electrolytes, all of which were normal. conservatively treated group, up to 53% in the The patient was referred urgently to the study by Kalash et al.6 The operative manage- urology service. ment of the condition ideally is as soon as possible.7 The surgical approach may include a Discussion procedure under local anaesthesia or the more Fracture of the penis has attracted interest in extensive circumferential or longitudinal inci- the medical literature from many countries sion and degloving of the penis to evacuate the including Zimbabwe, Taiwan, Scandinavia, haematoma and locate and repair the tear.34 India, Iran, Hungary, the United States and England.1 Penile fracture is caused by a traumatic rupture of the tunica albuginea of one or both corpora cavernosa. The fracture is Conclusion most frequently reported as happening to the Penile fracture is a rare condition but it merits Bradford Royal erect penis during sexual intercourse, but it has sensitive handling and urgent referral to a Infirmary, Bradford been reported after manipulation and falling urologist for further management. onto the erect penis. Correspondence to: Funding: none. Dr Gilligan, 1 Far Moss, In St George’s Hospital in London 0.25% of Alwoodley, Leeds LS17 all emergency urology admissions are attribut- Conflicts of interest: none. 7NU, UK able to penile fracture.2 The diVerential ([email protected]) 1 Asgari MA, Hosseini SY, Safarinejad MR, et al. Penile frac- diagnosis includes a tear of the deep dorsal vein tures: evaluation, therapeutic approaches and long-term Accepted 26 April 2000 of the penis. Classically the condition presents results. J Urol 1996;155:148–9.

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2 Morris SB, Miller M, Anson K. Management of penile frac- 5 Abulata KA, Awad RA. Fracture shaft of penis: Non surgi- ture. JRSocMed1998;91:427–8. cal treatment of three cases. J R Coll Surg Edinb 3 Naraysingh V, Maharaj D, Kuruvilla T, et al. Urology. Sim- 1983;28:266–7. ple repair of fractured penis. J R Coll Surg Edinb 6 Kalash SS, Young TD. Fracture of the penis: controversy of 1998;43:97–8. surgical versus conservative treatment. Urology.1984;24: 4 Nicoliasen GS, Melamud A, McAnnich JW. Rupture of the 21–4. corpus cavernosum: surgical management. J Urol 1983; 7 Cummings JM, Parra RO, Boulier JA. Delayed Repair of 130:917–19. penile fracture. J Trauma 1998,45:153–4.

Brugada syndrome—the missed epidemic

J M Butler

Abstract fully defibrillated. During transfer to the A&E About 10–20% of patients dying suddenly department he required defibrillation for a fur- or resuscitated from ventricular fibrilla- ther episode of ventricular fibrillation. tion do not have demonstrable heart On arrival in hospital he was agitated, with a disease. These people are often young and Glasgow Coma Score of 8/15 but was breath- tragically in some cases sudden death is ing spontaneously with a partially obstructed the first and only clinical event. One of the airway. The monitor showed normal sinus three main electrophysiological diagnoses rhythm with an initial blood pressure of to be considered in these situations is the 130/80. He was given a rapid sequence induc- Brugada syndrome. A case of Brugada tion of anaesthesia to maintain and protect his syndrome is described, together with an airway. Initial primary and secondary trauma example of the classic electrocardio- surveys revealed no obvious injury and initial graphic manifestations and a discussion of chest, pelvis, and c-spine radiographs were the possible aetiology, diagnosis and man- unremarkable. Initial speculative diagnoses agement of this condition. (J Accid Emerg Med 2000;17:426–428) included spontaneous intracerebral haemor- rhage, cardiac arrhythmias and convulsion. Keywords: Brugada syndrome The patient had urgent computed tomography of the head, which was normal. Further history Case report from the family revealed no previous medical At approximately 6 pm one evening, a 29 year problems and no relevant drug history. The initial 12 lead electrocardiograph

old man presented at the accident and http://emj.bmj.com/ emergency (A&E) department in a critical (ECG) (see ﬁg 1) showed a partial right bundle condition. The history obtained from both the branch block with ST segment elevation in paramedics and police was unusual. The chest leads V1 to V3. At this stage a primary policeman had been driving his car on the cardiac problem was thought to be more likely. motorway when the car in front, carrying a sin- Urgent echocardiography to look for structural gle occupant, suddenly veered oV the road, cardiac disease was performed. No abnormal- crashed through a barrier and came to a stop in ity was found. Throughout this time period the

a ﬁeld. The policeman found the driver to be in patient maintained a normal sinus cardiac on September 30, 2021 by guest. Protected copyright. cardiorespiratory arrest, and started resuscita- rhythm. He was transferred to an intensive care tion at the scene. On arrival, the paramedics bed and weaned uneventfully from ventilation discovered the driver’s initial cardiac rhythm to over a period of 24 hours. Toxicology screening be ventricular ﬁbrillation and he was success- was negative.

I aVR V1 V4

II aVL V5 V2 Hope Hospital, Stott Lane, Salford M6 8HD

Correspondence to: Mr Butler, SpR in III Emergency Medicine aVF V6 ([email protected]) V3 Accepted 29 February 2000 Figure 1 ECG showing classic ST segment elevation in chest leads V1–V3 with right conduction delay.

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After extubation he was neurologically intact interval and persistent ST elevation in the pre- and was transferred to the care of the cardiolo- cordial leads V1 to V2–V3 not explainable by gists for further investigation. Coronary angio- electrolyte disturbances, ischaemia or struc- graphy was carried out to exclude coronary tural heart disease. All these patients had right artery disease and congenital artery anomalies. bundle branch block. Repolarisation was ab- None were found. Right ventricular angio- normal, characterised by persistent ST eleva- graphy showed no impairment of function. tion (at least 0.1 mV) in leads V1 to V2–V3. The clinical and electrocardiographic features The PR and QT intervals were within normal confirmed the diagnosis of Brugada syndrome. limits. ECG features of right bundle branch An implantable defibrillator was inserted block with ST elevation in the right precordial within days of presentation and the patient was leads has subsequently been described as the discharged home. “Brugada sign”.4 Subsequent follow up has been unremark- ST segment elevation in the right chest leads able with no further episodes of arrhythmias. is observed in a variety of clinical and experimental settings and is not unique or Discussion highly specific for the Brugada syndrome. A About 10–20% of patients dying suddenly or clear distinction of this syndrome cannot be resuscitated from ventricular fibrillation do not 1 made on the basis of the ECG alone. The have demonstrable heart disease. Unexpected prevalence of idiopathic ST segment elevation arrhythmogenic death occurring in people with is reported to be 2.1% to 2.65%. An elevated minimal or no structural heart disease is ST segment limited to the right precordial estimated to represent 3% to 9% of out of hos- leads occurs in less than 1% of all cases of pital cases of ventricular fibrillation unrelated elevated ST segment.2 However, ST segment to myocardial infarction.2 These patients are elevation in the right precordial leads in the often young and tragically sudden death may absence of ischaemia, electrolyte or metabolic be the first and only clinical event. When acute ischaemia is not the cause of disorders, pulmonary or inflammatory disor- sudden cardiac arrest, there are three main ders or abnormalities of the central or periph- electrical cardiac disorders to be considered as eral nervous system is suggestive of the the possible cause of ventricular fibrillation: the Brugada syndrome. In many cases of Brugada Brugada syndrome, the long QT syndrome, syndrome, the ECG manifestations can nor- and the WolV-Parkinson White syndrome. If malise transiently, leading to underdiagnosis of 2 these three disorders are excluded, and the the syndrome. Strong sodium channel block- heart is structurally normal, then ventricular ing agents such as procainamide and flecainide fibrillation is considered idiopathic. can unmask the ST segment elevation in many In 1992 Pedro and Josep Brugada3 described patients thus aiding diagnosis. eight otherwise healthy patients with sudden Brugada reported that malignant arrhyth- and aborted cardiac death, in whom they mias eventually occur in 27% of initially found “right bundle branch block and persist- asymptomatic patients who have the Brugada sign. On the basis of reports published it has

ent ST segment elevation in leads V1 to V3”. http://emj.bmj.com/ Based on these observations they outlined a been speculated that 40% to 60% of patients new distinct clinical and electrocardiographic diagnosed as having idiopathic ventricular syndrome. This was subsequently called the ﬁbrillation may actually suVer from Brugada Brugada syndrome. In these patients the ECG syndrome.5 It is now thought to be the most showed right bundle branch block, normal QT frequent cause of sudden cardiac death in

V6 Figure 2 ECG of patient with Brugada syndrome showing classic precordial ST elevation followed by the development of ventricular ﬁbrillation.

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lar epicardium has been proposed as a KEY POINTS mechanism for Brugada syndrome. Three x Brugada syndrome is a cause of sudden diVerent mutations of the gene of the sodium cardiac death in previously healthy young channel SCN5A on chromosome three have people. been identified.8 The Brugada syndrome is x ECG characteristics include: ST eleva- autosomal dominantly inherited but has vari- tion in pre-cordial leads (V1–V3), right able expression. Testing of all family members ventricular conduction delay with a nor- is important because of the high incidence of mal QT interval. familial occurrence. x These patients require early cardiology Patients with Brugada syndrome have a high opinion and electrophysiological investi- incidence of sudden death, and prophylactic gation. defibrillators are indicated in those with induc- x Treatment consists of implantable defi- ible arrhythmias at electrophysiological study, brillators to prevent sudden death from irrespective of symptoms.9 In contrast, the ventricular fibrillation. incidence of sudden death in the long QT syndrome is very low, making prophylactic defibrillator implantation not cost eVective. Even patients without structural heart disease under with the best medical treatment, arrhythmia the age of 50 years. recurrence rates are still 45–50% at five years. The mean age of aVected people is mid to Pharmacological treatment does not protect late thirties. In the majority of cases tachyar- against recurrent events and implantation of an rythmias occur at rest and in many cases cardiac defibrillators is the only proven eVec- during the night. The recurrence rate of new tive treatment in preventing sudden death in arrhythmic events is as high as 40% in these patients with the Brugada syndrome.10 11 Emer- patients.5 gency physicians therefore have an important Current available data suggest that the Bru- role in referring suspected cases of Brugada gada syndrome is a primary electrical disease syndrome for urgent cardiology opinion for resulting in abnormal electrophysiological ac- consideration of an implantable defibrillator. tivity in the right ventricular epicardium. Elec- Funding: none. trical heterogeneity within the right ventricular epicardium leads to the development of Conflicts of interest: none. coupled premature ventricular contractions via 1 Zipes D, Wellens HJJ. Sudden cardiac death. Circulation a re-entrant mechanism that precipitates ven- 1998;98:2334–51. tricular tachycardia/fibrillation (see fig 2). The 2 Gussak 1, Antzelevitch C, Bjerregaard P, et al. The Brugada syndrome. clinical, electrophysiologic and genetic aspects. role of right bundle branch block in Brugada J Am Coll Cardiol 1999;33:5–15. syndrome has been a matter of controversy. 3 Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct Conduction delay in the right ventricle does clinical and electrocardiographic syndrome. J Am Coll Car- not seem to be an integral part of the diol 1992;20:1391–6. 4 Viskin S, Belhassen B. Polymorphic ventricular tachyar- syndrome. Furthermore, there seems to be no rhythmias in the absence of organic heart disease: Classifi- correlation between right bundle branch block cation, diVerential diagnosis, and implications for therapy. Prog Cardiovasc Dis 1998;41:17–34. http://emj.bmj.com/ and cardiac death, whereas a definite link exists 5 Alings M, Wilde A. “Brugada” syndrome. Clinical data and between the magnitude of ST elevation and the suggested pathophysiological mechanism. Circulation 1999; 99:666–73. incidence of the life threatening arrythmias 6 Brugada P, Brugada J. Right bundle branch block and ST seen in these patients.2 segment elevation in leads V1-V3. A marker for sudden death in patients with no demonstrable structural heart The aetiology of Brugada syndrome is disease. Circulation 1998;97:457–60. controversial. Brugada and Brugada suggested 7 Tada H, Aihara N, Ohe T, et al. Arrhythmogenic right ventricular cardiomyopathy underlies syndrome of right no structural abnormality of the heart, claim- bundle branch block, ST segment elevation and sudden

ing the syndrome was attributable to the pres- death. Am J Cardiol 1998;81:519–22. on September 30, 2021 by guest. Protected copyright. 6 8 Kirsch GE, Zhang D, Brugada R, et al. Genetic basis and ence of a functional electrical disease. Martini molecular mechanisms for idiopathic ventricular fibrilla- et al suggested the presence of concealed right tion. Nature 1997;392:293–6. 9 Brugada P, Brugada R, Brugada J, et al. Use of the prophy- ventricular myocardial disease. Corrado et al lactic implantable cardioverter defibrillator for patients report that a familial cardiomyopathy that with normal hearts. Am J Cardiol 1999;83:98–100D. 10 Causer J, Connelly D. Implantable defibrillators for life mainly involves the right ventricle and con- threatening ventricular arrhythmias. BMJ 1998;317:762–3. ducting syndrome is responsible.7 An ion 11 The AVID Investigators. A comparison of anti-arrhytmic drug therapy with implantable defibrillators in patients channel defect resulting in heterogeneous loss resuscitated from near-fatal ventricular arrhythmias. N of the action potential dome in right ventricu- Engl J Med 1997;337:1576–83.