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Carotid blow out syndrome

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discuss a patient presenting with impending carotid blow out with emphasize on management implications
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Carotid blow out syndrome Mawaddah Azman
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  • 1. Mawaddah Azman

2. Summary of history 74/Chinese gentleman Radical Neck Dissection 8thJune 2011 Now presents with persistentbloody discharge fromoperative wound He underwent Totalthyroidectomy andfunctional neck dissection inFeb 02 for Papillary ThyroidCarcinoma Subsequently presented withrecurrent neck swelling in2009, Selective NeckDissection performed Oct 09 3. Examination Wounddehiscenceoververticallimb ofincisionmeasuring2x1.5cmwith slowooze fromanterioraspect ofthe wound Noexposedcarotid 4. Preoperative radiological findings Matted, necrotic nodes at right side, encasing thecarotid artery and medially invading mucosa of theoropharynx Laterally the SCM is displaced and infiltrated Posteriorly prevertebral muscles are involved 5. Patient progress 6. Introduction An emergency, pose risk of Exsanguinatinghaemorrhage andpotential bleedingdiathesisThreatenedImpendingAcute CBS Compression toCBS CBSairway Neurologicalcomplications ClinicalCM, Citardi MJ, Ross DA, Sasaki CT. Endovascular therapy of the carotid blowout syndrome inChaloupka JC, Putman spectrumhead and neck surgical patients: diagnostic and managerial considerations. AJNR Am J Neuroradiol 1996;17:843852 7. Incidence First recognized in 1962; with a high mortality rate 40%; neurologic morbidity - 60% occur in 3-4% of all patients who have underwent Head and Neck Surgery 1,2. In advanced disease this can account for 11.6% of head and neck cancer deaths 3,4.1. Morrissey, D.D., Andersen, P.E. Nesbit, G.M. Barnwell, S.L. Events, E.C. Cohen, J.I. (1997) Endovascular management of haemorrhage in patients with head and neck cancer. Archives of otolaryngology, head and neck surgery; 123:15-192. Koch, W.M. (1993) Complications of surgery to the neck. In complications of head and neck surgery. Edited by Eisele D. St Louis: Mosby; 393-4133. Shedd, D.P. Shedd, C. (1980) Problems of terminal head and neck cancer patients, Head and Neck Surgery, 2:476-4824. Smith, A. M. (1992) Emergencies in Palliative Care, Annals Academy of Medicine, vol 23, no2, 186-190 8. Type 1: Threatened CBS Visibly exposed carotid artery segment thatwill inevitably rupture if not covered witha viable tissue or Evidence on diagnostic angiograms ofneoplastic invasion of the carotid artery ornonhemorrhagic pseudoaneurysm Grading system: Grade 0: No evidence of vascular disruption asseen in imaging Grade 1: There is focal weakening /irregularity of the vascular wall1. Citardi MJ, Chaloupka JC, Son YH, Sasaki CT. Management of carotid artery rupture by monitored endovascular therapeutic occlusion (19881994). Laryngoscope 1995;1086-1092 Grade 2: There is pseudoaneurysm2. Chaloupka JC, Roth TC, Putman CM, et al. Recurrent carotid blowout syndrome: diagnostic and therapeutic challenges in a newly recognized subgroup of patients. AJNR Am J Neuroradiol 1999;20:10691077 Grade 3: There is evidence of extravasationFrom The Interventional Neuroradiology Service Yale University School of Medicine 1995 9. Type 2: Impending CBS Presents as sentinel bleeding from the neckwhich may precede ultimate blow out. Typically resolves spontaneously or withsurgical packing The period is highly variable and can rangefrom moments to months.1. Citardi MJ, Chaloupka JC, Son YH, Sasaki CT. Management of carotid artery rupture by monitored endovascular therapeutic occlusion (19881994). Laryngoscope 1995;1086-10922. Chaloupka JC, Roth TC, Putman CM, et al. Recurrent carotid blowout syndrome: diagnostic and therapeutic challenges in a newly recognized subgroup of patients. AJNR Am J Neuroradiol 1999;20:10691077From The Interventional Neuroradiology Service Yale University School of Medicine 1995 10. Type 3: Acute CBS Acute, profuse hemorrhage that is not self-limiting and is not well-controlled withsurgical packing, invariably owing tocomplete rupture of the affected artery. Torrential bleeding due to rupture ofcarotid artery. This type carries themaximum mortality since the death isnearly instantaneous.1. Citardi MJ, Chaloupka JC, Son YH, Sasaki CT. Management of carotid artery rupture by monitored endovascular therapeutic occlusion (19881994). Laryngoscope 1995;1086-10922. Chaloupka JC, Roth TC, Putman CM, et al. Recurrent carotid blowout syndrome: diagnostic and therapeutic challenges in a newly recognized subgroup of patients. AJNR Am J Neuroradiol 1999;20:10691077From The Interventional Neuroradiology Service Yale University School of Medicine 1995 11. Risk factors Surgery to sites local to the carotid artery Radical Neck Dissection Generally 4% Mainly due to 3 Removal of soft tissues protecting the carotid Iatrogenic or machanical injury to adventitia of the carotids Decreased healing d2 removal of lymphatics and increased venous stasis Risk increases Salvage surgery Flap necrosis Wound infection 21. Cohen, J. Rad, Previous irradiation 1 I. (2004) Contemporary management of carotid blowout, Current opinion in otolaryngology & Head and Neck Surgery, 12: 110-1152. Nieto, C.S. Solano, J.M.E, Martinez, C.B. Martin, E.F. Colunga, J.C.M. Garcia, A.A. (1980) The carotid artery in head and neck oncology, Clinical Recurrent tumour involving the carotid artery Otolaryngology, 5, 403-4173. Rodriguez, F. Carmeci, C. Dalman, R.L. Lee, A. (2001) Spontaneous Late Carotid-Cutaneous Fistula following radical neck dissection- a case report. Vascular surgery, vol 35, (5) 12. Risk factors Radiotherapy Most common factor leading to CBS 2,3,4,5 Almost 100% of CBS occurs within an irradiated field Moreso if delivered within 2 months of surgery2 Associated with a 7.6fold increase in the risk of CBS in patients with head and neck cancer 1. Aetiology Reduced flow in the vaso vasorum blood flow to the carotid wall is reduced by 50 % after acourse of 30 Gy radiotherapy course6. Adventitial fibrosis Premature atherosclerosis Weakening of the arterial wall, sub endothelial vacuolization and1. Cohen, J. Rad, I. (2004) Contemporary management of carotid blowout, Current opinion in otolaryngology & Head and Neck Surgery, 12:fibres .oedema, and fragmentation of the tunica media elastic 110-115 72. Nieto, C.S. Solano, J.M.E, Martinez, C.B. Martin, E.F. Colunga, J.C.M. Garcia, A.A. (1980) The carotid artery in head and neck oncology, Clinical Otolaryngology, 5, 403- 4173. Rodriguez, F. Carmeci, C. Dalman, R.L. Lee, A. (2001) Spontaneous Late Carotid-Cutaneous Fistula following radical neck dissection- a case report. Vascular surgery, vol 35, (5)4. Shumrick, D.A. (1973) Carotid artery rupture, Laryngoscope, 83(7): 1051-615. Swain, R. E. et al (1974) An experimental Analysis of causative factors and protective methods in Carotid Artery Rupture. Arch Otolaryngology vol 99, April, 235-2416. Smith, A. M. (1992) Emergencies in Palliative Care, Annals Academy of Medicine, vol 23, no2, 186-1907. Huvos, A.G. Leaming, R.H. Moore, O.S. (1973) Clinicopathologic study of resected carotid artery: analysis of 64 cases. American journal of surgery, 126:570-574 Lesarge, C. (1986) 13. Risk factors Postoperative impaired healing due to previous radiotherapy, infection and excision of the lymphatic chains The carotid artery can be exposed, flap necrosis can occur, which allows the invasion of bacteria and further desiccation of the adventitia 1-5. Improper incision: vertical limb or three1. Cohen, J. Rad, I. (2004) Contemporary management of carotid blowout, Current opinion in otolaryngology & Head and Neck point junction6 Surgery, 12: 110-1152. Lesarge, C. (1986) Carotid artery rupture. Prediction, prevention and preparation. Cancer Nursing, 9 (1) 1-73. Nieto, C.S. Solano, J.M.E, Martinez, C.B. Martin, E.F. Colunga, J.C.M. Garcia, A.A. (1980) The carotid artery in head and neck oncology, Clinical Otolaryngology, 5, 403-4174. Shumrick, D.A. (1973) Carotid artery rupture, Laryngoscope, 83(7): 1051-615. Swain, R. E. et al (1974) An experimental Analysis of causative factors and protective methods in Carotid Artery Rupture. Arch Otolaryngology vol 99, April, 235-2416. Maran, A.G.D. Amin M.A. Wilson, J.A. (1989) Radical neck dissection: a 19 year experience. The Journal of Laryngology and Otology, August, vol.103 pp 760-764 14. Risk factors Pharyngocutaneous fistula important causative factor in CBS. adventitia being bathed in saliva, which isbacteria laden and damaging to the outerlining of the arterial wall 1,3 Fungating tumour invading the carotid artery Direct infiltration destructing the arterial wall1. Nieto, C.S. Solano, J.M.E, Martinez, C.B. Martin, E.F. Colunga, J.C.M. Garcia, A.A. (1980) The carotid artery in head and neck oncology, Tumour necrosis increasing vulnerability of Clinical Otolaryngology, 5, 403-4172. Shumrick, D.A. (1973) Carotid artery rupture, Laryngoscope, 83(7): 1051-613. Swain, R. the arterial Analysis of causative factors and protective methods in Carotid Artery Rupture. Arch E. et al (1974) An experimental wall Otolaryngology vol 99, April, 235-241 15. Risk factors General systemic Over 50 years of age 10-15% loss of body weight Diabetes mellitus and immune deficiencies Generalised atherosclerosis Malnourishment1. Nieto, C.S. Solano, J.M.E, Martinez, C.B. Martin, E.F. Colunga, J.C.M. Garcia, A.A. (1980) The carotid artery in head and neck oncology, Clinical Otolaryngology, 5, 403-4172. Lesarge, C. (1986) Carotid artery rupture. Prediction, prevention and preparation. Cancer Nursing, 9 (1) 1-73. Schiech, L. (2000) Carotid artery rupture. Clinical Journal of Oncology Nursing, vol 4, pp93-944. Shumrick, D.A. (1973) Carotid artery rupture, Laryngoscope, 83(7): 1051-615. Swain, R. E. et al (1974) An experimental Analysis of causative factors and protective methods in Carotid Artery Rupture. Arch Otolaryngology vol 99, April, 235-241 16. Clinical feature Attempt to predict patients most likely to be at risk as sometimes there may be no warning at all Sentinel bleeds or herald bleeds minor bleeding from wound, flap site,tracheostomy or mouth 2,3 process of erosion is gradual 4 this is caused by a small rupture of the intima oncology, at the site 5, 403-417Clinical Otolaryngology, of the defect of the tunica which1. Nieto, C.S. Solano, J.M.E, Martinez, C.B. Martin, E.F. Colunga, J.C.M. Garcia, A.A. (1980) The carotid artery in head and neckseals temporarily. 12. Lovel, T. (2000) Palliative care and head and neck cancer. Editorial, British Journal of Oral and Maxillofaxillofacial Surgery, 38, 253-254 Schiech, L. (2000)3. Forbes, K. (1997) Palliative care in head and neck cancer. Clinical Otolaryngology 22:117-224. Macmillan, K. Stuthers, C. (1987) Algorithm for the Emergency Nursing Management of spontaneous Carotid Artery Rupture. Canadian Critical Care Nursing Journal- March/April, 20-21 17. Clinical feature Pulsations from artery or tracheostomy or flapsite 1,2. Ballooning of an artery 2,4,5. Haemorrhage externally from the neck internally from within the oropharynx, directly into the airway or tracheostomy Death due to: Hypovolaemic shock is often the cause of death. Asphyxiation of blood may also be a contributoryfactor. 14-18 Cerebral hypoxia1. Kane, K. K. (1983) Carotid artery rupture on Advanced Head and Neck Cancer Patients, Oncology Nursing Forum Vol 10, No.1,2. Casey, D. (1988) Carotid Blow-out. Nursing Standard 2 (47): 303. Parsons, R. (1995) Practice Guidelines, carotid Artery rupture, Fall, vol 13, no.4, 30-314. Luo, C.B. Chang, F.C. Mu-Huo Teng, M. Chi-Chang Chen, C. Feng Lirng, J. Cheng, Y. (2003) Endovascular treatment of the carotid artery rupture with massive haemorrhage, Journal of Chinese medical Association, 66, 140-1475. Schiech, L. (2000) Carotid artery rupture. Clinical Journal of Oncology Nursing, vol 4, pp93-94 18. Patophysiology Adventitial layer protects the artery,nourished by vasovasorum. Interrupted blood supply due to variousreasons causes destruction of arterial walloccuring over 6-10 days 1,2 Damage and loss of adventitia formingeschar and slough Exposure of tunica media Sloughing of tunica media1. Exposureartery rupture. Prediction,intimapreparation. Cancer Nursing, 9 (1) 1 Lesarge, C. (1986) Carotid of tunica prevention and with subsequent2. Kane, K. K. (1983) Carotid artery rupture on Advanced Head and Neck Cancer Patients, Oncology Nursing Forum Vol 10,thinning No.1, 14-18 19. First case in late 18th century Dr John Abernathy Traumatic laceration of the ICA after being gored in the neck by bulls horn Treated with ligation of the vessel, well tolerated by the patient 20. Management What has changed? Historically CBS was associated with 60% neurologic morbidity and 40% mortality Open surgical ligation Outcomes substantially improved with theadvent of various endovascular surgicaltechniques Permanent balloon occlusion (15-20% neurologicmorbidity) in a newly Endovascular Reconstruction of Carotid Artery1. Chaloupka JC, Roth TC, Putman CM, et al. Recurrent carotid blowout syndrome: diagnostic and therapeutic challenges recognized subgroup of patients. AJNR Am J Neuroradiol 1999;20:106910772. Chaloupka JC, Putmanneurologic morbidity)(8% CM, Citardi MJ, Ross DA, Sasaki CT. Endovascular therapy of the carotid blowout syndrome in head and neck surgical patients: diagnostic and managerial considerations. AJNR Am J Neuroradiol 1996;17:8438523. Debate over indication and selection of patients Citardi MJ, Chaloupka JC, Son YH, Ariyan S, Sasaki CT. Management of carotid artery rupture by monitored endovascular therapeutic occlusion (1988 1994). Laryngoscope 1995;105:10861092 21. Yale1995:simple clinicalclassificationscheme withinterdisciplinarytreatmentalgorithm 22. Imaging modalities CT/MR Gold standard DSA Selective catheterization of each common carotid, external carotid and or internal carotid artery Active extravasation Pseudoaneurysm Tumour bleeding (nodal or primary) Assess intracranial circulation prior tointervention (surgery or endovascular) Selective carotid and vertebral injection Incomplete circle of Willis 23. ManagementPatient andfamilyIntentof careSeverity of bleeding 24. Management of non terminalbleeding Resuscitation Airway Breathing Circulation Large bore branullas Volume replacement, preferably with blood Measurement of volume status Specific measures Compression Packing Hemostatic material Endovascular techniques Operative ligation 25. Endovascular treatment of CBS Evolved since 1980s Divided into Deconstructive techniques: permanently occluding Reconstructive techniques: preserving flow Percutaneous Balloon Occlusion Using a detachable balloon (latex or silicone) Rapid occlusion of a large vessel can be achieved, hence more suitable for emergent conditions Multiple balloons can be used in the same setting Achieve success rate of 95% in Type 2 &3 CBS Embolization with coils (platinum based), polyvinyl alcohol or cyanoacrylate. 26. Reconstructive techniques Using overlapping or covered stents to diminish porosity between the stent struts. Promote sluggish flow and subsequent thrombosis around the stent Allows blood flow through stent and strengthen integrity of vessel Confirmed by second look angiography Technically more demanding and time consuming Indicated in patients at high risk for carotid occlusion: Angiographic documentation of incomplete circle of willisAmerican Contralateral carotid artery occlusionChaloupka, J.C. Lesley W.S.Weigele J.B. (2003) Endovascular reconstruction for the management of carotid blow-out syndrome.journal of neuroradiology; 24: 975-981 27. Long term outcomes Although deployment of stent-grafts canachieve immediate and initial hemostasis inpatients with head-and-neck cancer and CBS,the long-term safety, stent patency, andpermanency of hemostasis appearunfavorable. Complications: Rebleeding : periprocedure patients need tobe on antiplatelet therapy Thrombosis Persistent infection : reported brain abscess 28. Emergent endovascular techniques Direct carotid puncture Technically feasible for rapid arrest of haemorrhage in unstable patients 29. Open technique Principles: Often done in emergency setting hence less time for planning Ligate more proximally Ligation is preferable if there is multi level rupture or multiple pseudoaneurysm Site of ligature must always be covered with a thick viable muscle flap and is not infected Preferable in clinically unstable patients Provides rapid securing of bleeding Technically less demanding compared to endovascular technique 30. Ligation of Common Carotid Artery Carries significant neurologic morbidity andmortality due to variable intracranial crosscirculation Ideally preceded with balloon occlusion testor angiography of collateral circulation Above the omohyoid Transverse incision middle portion of SCM Fascia at anterior border of SCM longitudinallyincised SCM retracted posteriorly Omohyoid tendon retracted downwards Carotid sheath opened IJV retracted laterally Mobilize the CCA, free from the vagus and ligateCCA 31. Below the omohyoid Transverse incision at lower portion of SCM Anterior jugular vein ligated Fascia at anterior border of SCM longitudinally incised, omohyoid transected Inferiorly, carotid sheath is covered by omoclavicular fascia Omoclavicular fascia exposed Carotid sheath opened IJV retracted laterally Mobilize the CCA, free from the vagus and 32. The branches of theexternal carotidanastomose acrossthe median line. Superiorthyroid Facial The internalcarotidscommunicate bymeans of the circleof Willis. From thesubclavian thevertebral arterycommunicates bymeans of thebasilar with thecircle of Willis. The thyroid axis byits inferior thyroidbranchcommunicates withthe thyroidarteries of theopposite side. Finally thesuperiorintercostal, which,like the vertebral 33. Options: Ligation End-to-end anastomosis if the rupture is smalland one level Interpositional grafts for reconstruction: Autologous graft: Saphenous vein Synthetic grafts: PTFE (Polytetrafluoroethylene) Dacron Theoretical as usually ligation is life saving in emergency situations and rarely anastomosis or graft reconstruction is attempted 34. Muscular flaps Levator Scapulaeflap; is an optionduring radicalneck dissection Inferior borderof muscledivided, takingcare not todamage thebrachial plexus Posteriorborder of themuscle flipped 35. Preparation for the event The Consultant in charge of the patient,accompanied will break the news of the likelyoccurrence of a CBS and its implications. Theinformation should ensure thatpatients/relatives have a clear plan of care andare aware that NO resuscitation will takeplace; this must then be documented. In cases where herald bleeding occurs, patientsand their families will undoubtedly have beenextremely frightened and distressed by thisexperience. This may have been an event whichhad been unpredicted and which they were notprepared for, in which case it may be possibleto explain how the experience may be helped inthe future with better preparation. They may becomforted by the knowledge that sedation will 36. Open and honest approach 1,2,4. Contemplating the truth, knowing what to expect, what to do, and how distress can be relieved can be helpful to the patient and family 4. It may also help the patient and family to know that, in the event of a massive carotid rupture there should be little pain and that death is usually very quick 3,5.1. Feber, T. (2000) Head and Neck Oncology Nursing. Whurr Publishers Ltd, London Chapter 2.8, 245 2522. Forbes, K. (1997) Palliative care in head and neck cancer. Clinical Otolaryngology 22:117-22 When?3.Cohen, J. Rad, I. (2004) Contemporary management of carotid blowout, Current opinion in otolaryngology & Head and Neck Surgery, 12: 110-1154. Kane, K. K. (1983) Carotid artery rupture on Advanced Head and Neck Cancer Patients, Oncology Nursing Forum Vol 10, No.1, 14-185. Smith, A. M. (1992) Emergencies in Palliative Care, Annals Academy of Medicine, vol 23, no2, 186-190 37. The Event Equipments to be made available: Call bell Suction Syringes (10ml) for cuff inflation on a tracheostomy tube (if appropriate) Bowl Gloves, Plastic apron, eye protector/face shield Dark coloured towels Bedside locker with attached individual drug cabinet Midazolam ampoules, syringes, needles and alcohol wipes Patent IV access Patients should be nursed in a side ward to avoid shock and distress to other patients and 38. The Event Stay with the patient, hold their hand and callfor assistance calmly 1. Be aware of family presence and needs. Decidebeforehand with the family if they wish to staywith the patient. Draw curtains and maintain theprivacy of the patient as much as possible 1. Apply towels around the bleeding site toabsorb the blood loss. If a cuffedtracheostomy tube is insitu, inflate the cuff 2. Apply gentle suctioning to mouth andtracheostomy site as necessary 2. Administer Midazolam intravenously 2. In the event of a massive, terminal bleed thepatient may be unconscious within minutes and1. Kane, K. K. (1983) Carotid artery rupture on Advanced Head and Neck Cancer Patients, Oncology Nursing Forum Vol 10,2. Smith, A. M. (1992) Emergencies in Palliative Care, Annals Academybefore 23, no2, 186-190may die very quickly, even of Medicine, vol the sedation No.1, 14-18 39. Use of Benzodiazepines Administration: Rapid bolus intravenousinjection For anxiolysis and sedation where acatastrophic bleed occurs, give 5mg as a fastbolus. (If no IV access is available give 5 10mg as a Subcutaneous or Intramuscularinjection. Further doses may be given untilthe patient is fully sedated. Morphine is not indicated unless: Patient complains of pain and or breathlessness 40. Caring for the patient at home Many patients may wish to go home and maynot wish to stay in hospital, waiting tobleed. The approach of death can evokefeelings of loss in a dying patient. Loss of control may be the mostoverwhelming and distressing feeling, whichis often further intensified byhospitalization. Being at home may give the patient andfamily privacy, control over theirsurroundings, and may help the patient toretain their own identity.Bourne, V. Frogge, M.H. (1999) Grief, in Yarbro CH, Frogge MH, Goodman (eds) Cancer symptom management (ed 2). The team should discuss a management planSudbury, MA Jones and Bartlett, 618-626 41. Thank youQuestions? 42. Sometimes, it may be necessary to block off a bloodvessel as the primary means of treating a problem. Ifthat blood vessel supplies the brain, doing so mightresult in a stroke. However, at the base of the brain,there can be connecting vessels which can take over theblood supply. Because we are not certain, in somepatients, that these connections are sufficient, we do atest beforehand. This testing involves temporarilyblocking off the blood flow in the vessel we areinterested in permanently blocking. We do this with a small, soft balloon placed in theartery. With the balloon in place and inflated, we canthen perform a neurological examination on the patientto make sure there is no problem. If the blood flow isinsufficient, the patient will start to developneurological impairment, such as weakness, loss ofsensation, speech problems, etc. When this happens, theballoon is deflated to restore the normal blood flow.Depending upon these results, we can then decide on the


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