Cardiac tamponade is a medical and surgical emergency, which needs early recognition and treatment. Myocardial perforation leading to cardiac tamponade is a rare complication after pace maker insertion. We are reporting a case of cardiac tamponade after removal of temporary pace maker in a multidisciplinary intensive care unit

Khan, Muhammad Faisal

Zubairi, Ali Bin Sarwar

eCommons@AKU

eCommons@AKUDepartment of Anaesthesia Medical College, PakistanMay 2008Cardiac tamponade after removal of temporarypace maker in multidiscipinary intensive care unitMuhammad Faisal KhanAga Khan UniversityAli Bin Sarwar ZubairiAga Khan UniversityFollow this and additional works at: http://ecommons.aku.edu/pakistan_fhs_mc_anaesthPart of the Anesthesiology CommonsRecommended CitationKhan, M., Zubairi, A. (2008). Cardiac tamponade after removal of temporary pace maker in multidiscipinary intensive care unit.Journal of the Pakistan Medical Association, 58(5), 270-2.Available at: http://ecommons.aku.edu/pakistan_fhs_mc_anaesth/36population in SHI, which may make this system morecomplicated rather than helpful. ConclusionGiven present human resource constraints andinstitutional capacities, operationalizing anygovernment funded SHI scheme on a national levelensuring universal coverage is a huge challenge.Positive vibes are a rising national economy, politicalwill to carry out health sector reforms and the creation ofdistrict health system after devolution. The currentscenario is ideal to pilot small initiatives, may be atdistrict levels, and then up scale by learning lessonsfrom these pilot projects. Policy makers, health systemsspecialists and other stakeholders must capitalize onthese opportunities and windows to find a way out. References1. Conn CP, Walford V. An introduction to health insurance for low incomecountries. Health Systems Resource Centre. Department for InternationalDevelopment, London: 1998.2. World Health Organization & European Commission. Highlights on health inGermany. WHO Regional Office for Europe, Copenhagen: 1999. 3. World Bank. Health care financing in low-income countries. In: HealthFinancing revisited.  Washington DC: 2006.4. Schneider P. Why should the poor insure? Theories of decision-making in thecontext of health insurance. Health Policy Plann 2004; 19: 349-55. 5. Stefan G.  Competition in Social Health Insurance: A Three-CountryComparison. Discussion Paper No. 135. Universität Duisburg-Essen,Duisburg: 2004. 6. Hussey P, Anderson GF. A comparison of single- and multi-payer healthinsurance systems and options for reform. Health Policy 2003; 66:215-28.7. Komamura K, Yamada A. Who bears the burden of social insurance?Evidence from Japanese health and long-term care insurance data. J Jap  IntEconom 2004; 18: 565-81.8. Selbmann HK, Flohi R, Volk HD, Rothmund M, Reinauer H, Konze-ThomasB, et al. Country profile Germany: Health care. Lancet 1996; 348:1631-9.9. Fukawa T. Public health insurance in Japan. World Bank Institute. WashingtonDC:  2002. 10.  Ruger JP, Kim H-J. Out-of-pocket healthcare spending by the poor andchronically ill in the Republic of Korea. Am J Public Health 2007; 97:804-11.11. Oliver A, Mossialos E. Equity of access to health care: outlining thefoundations for action. J Epidemiol Community Health 2004; 58: 655-8.12. Sreshthaputra N, Indaratna K. The universal coverage policy of Thailand: anintroduction. Asia-Pacific Health Economics Network (APHEN); Bangkok:2001.13. Asian Development Bank. Technical Assistance to the Islamic Republic ofPakistan for the Developing Social Health Insurance Project. Islamabad 2005.14. Nishtar S. Social Health Insurance in NWFP-the steps ahead. Islamabad:Heartfile 2006. 15. World Health Organization. Reaching universal via social health insurance.Discussion paper No.2. Geneva: 2004.Case ReportCardiac Tamponade after removal of temporary pace maker in multidiscipinaryIntensive Care UnitMuhammad Faisal Khan1,  Ali Bin Sarwar Zubairi2Department of Anesthesiology1, Pulmonary and Critical Care Medicine2, Aga  Khan University Hospital, Karachi.AbstractCardiac tamponade is a medical and surgicalemergency, which needs early recognition and treatment.Myocardial perforation leading to cardiac tamponade is arare complication after pace maker insertion. We arereporting a case of cardiac tamponade after removal oftemporary pace maker in a multidisciplinary intensivecare unit.IntroductionCardiac tamponade is a medical emergency which ischaracterized by the accumulation of fluid in the pericardialspace, resulting in reduced ventricular filling andsubsequent haemodynamic compromise. Myocardialperforation leading to cardiac tamponade is a rarecomplication after pace maker insertion. This conditionrequires urgent recognition since the prompt drainage of thepericardial fluid may be lifesaving. We present a case reportof myocardial perforation complicated by cardiactamponade after removal of a pacemaker which wassuccessfully managed surgically.Case ReportA 60 year-old female with hypertension, diabetesmellitus and ischaemic heart disease with mild to moderatesystolic dysfunction, was admitted through emergencyroom with cardiogenic shock due to Non-ST elevated MI(Troponin I >3), hyponatraemia (Na = 123 Meq/L)  andsevere metabolic acidosis. She was intubated in emergencyroom due to respiratory distress. Post intubation, she wentinto cardiac arrest. Temporary pacemaker was inserted inthe emergency room (Figure) and she was transferred tointensive care unit (ICU). She was successfully extubatedon day 4. Patient regained her own heart rhythm 24 hoursafter insertion of pacemaker as shock and metabolicacidosis improved. Within one hour of removal ofpacemaker she complained of dizziness and difficulty inbreathing. Blood pressure was 60/40 mmHg and heart rate270 J Pak Med Assoc90/min. Pulse was weak. EKG showed low voltage waveswith ST depression in V3 to V5. Urgent echocardiogramshowed large pericardial effusion with tamponade. She wasresuscitated with IV fluids and immediatepericardiocentesis was performed and 400 ml of clottedblood was removed. Pericardial window was made. Patientbecame haemodynamically stable and was extubated on thenext day and shifted to special care unit. She was dischargedhome seven days after the event.DiscussionMyocardial perforation is a rare complicationfollowing pacemaker implantation that may cause cardiactamponade. If it does occur, it is usually at the time of leadinsertion.1 Tamponade usually takes place due to arrowhead endocardial electrode.2 Fatal myocardial perforationcan occur with this electrode and the apex of the rightventricle should be avoided as the site of insertion3. Thiscondition requires urgent recognition since the promptdrainage of the pericardial fluid may be lifesaving.The pericardium consists of a thin serous membranecovering the epicardial surface (visceral pericardium) and aserous membrane-lined fibrous sac (parietal pericardium),which has limited elastic properties. The pericardial spaceseparates the two layers and contains approximately 25-35ml of serous fluid.1 An acute accumulation of pericardialfluid of greater than 100 ml will produce haemodynamiceffects of tamponade whereas a chronic pericardialcollection of fluid up to 2000 ml may occur withoutimposing any effect upon cardiac output.2Cardiac tamponade is defined as ahaemodynamically significant cardiac compression causedby pericardial fluid.3 The fluid may be blood, pus, effusionor air.4 Pericardial tamponade may arise from multipletraumatic and non traumatic etiologies, resulting inunrecognized rapid deterioration and often death.Traumatic pericardial tamponade occurs in only 2% of allpenetrating chest injuries5, and rarely is the result of blunttrauma. Mortality exceeds 60% if cardiac arrest occurs.6Non traumatic causes of pericardial tamponade includehaemopericardium due to anticoagulant therapy or as a rarecomplication of acute myocardial infarction. In addition,various non- traumatic causes such as infection, drugs,neoplasm, uraemia, myxoedema, collagen vascular disease,and hypersensitivity states may produce large effusion withtamponade. Pericardial tamponade has resulted fromcardiac catheterization, central venous catheterization,pericardiocentesis, intracardiac injection, cardiac surgery,and sternal bone biopsy and transvenous pacemakerinsertion.7 Common sites of perforation are the right atriumand right ventricle followed by superior vena cava.8Perforation has also been reported in the left atrium (patentforamen ovale) and the left pericardiophrenic vein.Endocardial injury is thought to be caused by eithermovement of the catheter tip, by movements of cardiacchambers and lower superior vena cava (cardiac cycle) orby direct trauma. Injury causes thrombus formation andeventually adherence of the wire to the endocardium.Erosion occurs which may lead to perforation. Early recognition and treatment of cardiactamponade is essential to prevent fatal outcome. Symptomsand signs are usually sudden and include nausea, fatigue,light-headedness, dyspnoea, retrosternal chest pain,cyanosis, venous engorgement, pulsus paradoxus andconfusion. The most common findings noted by Nasim andcolleagues9 from case reports were hypotension (88%),raised central venous pressure (70%) and a disturbance incardiac rhythm (67%) mainly tachycardia. However in 29%of these cases death occurred suddenly after 'vaguepremonitory signs'. Diagnosis of cardiac tamponade isdifficult in sedated, ventilated and post-operative patients.EKG and chest radiograph findings may not alwaysassist the diagnosis. EKG findings such as low voltage QRScomplex or electrical alternans may not always be present.Chest radiograph may not show abnormalities untilconsiderable fluid has accumulated in the pericardial sac.Transthoracic or transesophageal echocardiography isdiagnostic. These techniques are unfortunately not alwaysavailable and delaying treatment to obtain theseinvestigations may be fatal.The patient is initially resuscitated with intravenousfluids to promote maximum filling of the heart. In general,inotropic agents that increase the stroke volume and supportFigure 1. Portable Chest X-Ray showing ET tube, right IJ swan sheath and temporary pacemakerin appropriate position. Lung fields show mild bilateral pleural effusions, silhouetting of left hemidiaphragm and haze over both lower lung zones consistent with pulmonary edema.Vol. 58, No. 5, May 2008 271systemic resistance are used, although some recommendisoprenaline, as it reduces the cardiac size and diminishes theeffective degree of tamponade while increasing cardiacoutput.2 The definitive treatment of cardiac tamponade is theremoval of cardiac diastolic restriction by eitherpericardiocentesis or thoracotomy. Pericardiocnetesis isusually performed for urgent management of an acutetamponade (the acute removal of as little as 50 ml of fluid isoften sufficient to correct the hypotension). A thoracotomy isoften required when a tamponade exists following coronaryartery bypass grafting, penetrating or closed cardiac traumaand aortic dissection. It is also indicated whenpericardiocentesis has failed to relieve the tamponade. ConclusionCardiac tamponade is a life-threatening emergency.Immediate recognition and treatment are imperative if adisastrous outcome is to be prevented.References1.  Barriales AV, Alvavez Tamargo JA, Garcia AM, Martin FM, Morales C.Delayed myocardial perforation following pacemaker implantation. Int JCardiol 2004; 93: 89-91.2. Collins D. Aetiology and management of acute cardiac temponade. Crit Care Resusc 2004; 6: 54-8.3. Hancock EW. Cardiac temponade. Med Clin North Am 1979; 63:223-37.4. Spodick DH. Pathophysiology of cardiac temponade. Chest 1998;113:1372-8.5. Costa IV, Soto B, Diethem L, Zarco P. Air pericardial temponade. Am JCardiol 1987; 60:1421-2.6. Beall AC Jr, Diethrich EB, Crawford HW, Cooley DA, De Bakey ME.Surgical management of penetrating cardiac injuries. Am J Surg1966;112:686-92.7. Fisch GW, Sherz RG. Neck vein catheter and pericardial temponade.Pediatrics 1973;52:8628. Booth S.A, Nortam B, Mulvey DA. Central venous catherization and fatalcardiac temponade. Br J Anaesth 2001; 87 : 298-302.9. Nasim A, Cooper GG, Ah-see AK. Caridac temponade to central venouscatheterization. J R Coll Surg Edinb 1992; 37:337-9.Case ReportDe novo primary squamous cell carcinoma of the ovary: A case of a raremalignancy with an aggressive clinical courseAli Imran Amjad, Inam PalDepartment of Surgery, Aga Khan Univeristy Hospital, Karachi, Pakistan.AbstractOvarian squamous cell carcinoma is a raremalignancy and the occurrence is attributable to malignanttransformation of an existing ovarian dermoid cyst. The denovo occurrence of squamous cell carcinoma of the ovary,in the absence of an antecedent ovarian dermoid, isextremely rare. The case of a 31 year old Asian woman,evaluated for abdominal distension and discomfort ispresented. Abdominal CT was suggestive of a malignantneoplastic process. Laparotomy confirmed a malignanttumour with involvement of the right adnexa and extensioninto the omentum and bowel. Surgical debulking,hysterectomy, bilateral salpingo-ophorectomy and totalomentectomy and bowel resection was performed.Histopathology demonstrated squamous cell carcinomaarising from the right ovary with no co-existing ovariandermoid. The postoperative period was significant fordisease progression despite adjuvant chemotherapy. IntroductionSquamous cell carcinoma of the ovary is a rareclinical entity, accounting for less than 1% of all malignanttumours of the ovary.1 Malignant transformation of a pre-existing mature cystic teratoma (dermoid cyst) isappreciated as the underlying pathophysiologicalmechanism, and this phenomenon is considered rare, asonly 1-2% of teratomas demonstrate this change.1 The denovo development of a primary squamous carcinoma, in anotherwise healthy ovary is an extremely rare occurrence.2-5We present a case of this rare malignancy, not beenpreviously reported in the Southeast Asian population, witha review of literature.Case ReportA 31 year old, para 2, Asian female (Pakistaniheritage) was referred to the general surgery clinic with aone year history of progressive abdominal discomfort anddistension.  She had a history of weight loss with no changein appetite, bowel habit or menstrual flow. A recent papsmear was negative for dysplasia. On examination, she wasanaemic with no jaundice, lymphadenopathy and hadnormal breast examination. Abdominal examinationrevealed a firm, mildly tender, mobile mass occupying mostof the lower abdomen. There was no clinical evidence ofascites. Pelvic and rectal exams were unremarkable. Pre-operative evaluation showed anaemia withnormal cell counts, and normal kidney and liver functions.272 J Pak Med Assoc

Cardiac tamponade after removal of temporary pace maker in multidiscipinary intensive care unit

eCommons@AKUDepartment of Medicine Department of MedicineMay 2008Cardiac tamponade after removal of temporarypace maker in multidiscipinary intensive care unit.Muhammad Faisal KhanAga Khan UniversityAli Bin Sarwar ZubairiAga Khan University, ali.zubairi@aku.eduFollow this and additional works at: http://ecommons.aku.edu/pakistan_fhs_mc_med_medPart of the Pulmonology CommonsRecommended CitationKhan, M. F., Zubairi, A. (2008). Cardiac tamponade after removal of temporary pace maker in multidiscipinary intensive care unit..JPMA. The Journal of the Pakistan Medical Association, 58(5), 270-272.Available at: http://ecommons.aku.edu/pakistan_fhs_mc_med_med/312population in SHI, which may make this system morecomplicated rather than helpful. ConclusionGiven present human resource constraints andinstitutional capacities, operationalizing anygovernment funded SHI scheme on a national levelensuring universal coverage is a huge challenge.Positive vibes are a rising national economy, politicalwill to carry out health sector reforms and the creation ofdistrict health system after devolution. The currentscenario is ideal to pilot small initiatives, may be atdistrict levels, and then up scale by learning lessonsfrom these pilot projects. Policy makers, health systemsspecialists and other stakeholders must capitalize onthese opportunities and windows to find a way out. References1. Conn CP, Walford V. An introduction to health insurance for low incomecountries. Health Systems Resource Centre. Department for InternationalDevelopment, London: 1998.2. World Health Organization & European Commission. Highlights on health inGermany. WHO Regional Office for Europe, Copenhagen: 1999. 3. World Bank. Health care financing in low-income countries. In: HealthFinancing revisited.  Washington DC: 2006.4. Schneider P. Why should the poor insure? Theories of decision-making in thecontext of health insurance. Health Policy Plann 2004; 19: 349-55. 5. Stefan G.  Competition in Social Health Insurance: A Three-CountryComparison. Discussion Paper No. 135. Universität Duisburg-Essen,Duisburg: 2004. 6. Hussey P, Anderson GF. A comparison of single- and multi-payer healthinsurance systems and options for reform. Health Policy 2003; 66:215-28.7. Komamura K, Yamada A. Who bears the burden of social insurance?Evidence from Japanese health and long-term care insurance data. J Jap  IntEconom 2004; 18: 565-81.8. Selbmann HK, Flohi R, Volk HD, Rothmund M, Reinauer H, Konze-ThomasB, et al. Country profile Germany: Health care. Lancet 1996; 348:1631-9.9. Fukawa T. Public health insurance in Japan. World Bank Institute. WashingtonDC:  2002. 10.  Ruger JP, Kim H-J. Out-of-pocket healthcare spending by the poor andchronically ill in the Republic of Korea. Am J Public Health 2007; 97:804-11.11. Oliver A, Mossialos E. Equity of access to health care: outlining thefoundations for action. J Epidemiol Community Health 2004; 58: 655-8.12. Sreshthaputra N, Indaratna K. The universal coverage policy of Thailand: anintroduction. Asia-Pacific Health Economics Network (APHEN); Bangkok:2001.13. Asian Development Bank. Technical Assistance to the Islamic Republic ofPakistan for the Developing Social Health Insurance Project. Islamabad 2005.14. Nishtar S. Social Health Insurance in NWFP-the steps ahead. Islamabad:Heartfile 2006. 15. World Health Organization. Reaching universal via social health insurance.Discussion paper No.2. Geneva: 2004.Case ReportCardiac Tamponade after removal of temporary pace maker in multidiscipinaryIntensive Care UnitMuhammad Faisal Khan1,  Ali Bin Sarwar Zubairi2Department of Anesthesiology1, Pulmonary and Critical Care Medicine2, Aga  Khan University Hospital, Karachi.AbstractCardiac tamponade is a medical and surgicalemergency, which needs early recognition and treatment.Myocardial perforation leading to cardiac tamponade is arare complication after pace maker insertion. We arereporting a case of cardiac tamponade after removal oftemporary pace maker in a multidisciplinary intensivecare unit.IntroductionCardiac tamponade is a medical emergency which ischaracterized by the accumulation of fluid in the pericardialspace, resulting in reduced ventricular filling andsubsequent haemodynamic compromise. Myocardialperforation leading to cardiac tamponade is a rarecomplication after pace maker insertion. This conditionrequires urgent recognition since the prompt drainage of thepericardial fluid may be lifesaving. We present a case reportof myocardial perforation complicated by cardiactamponade after removal of a pacemaker which wassuccessfully managed surgically.Case ReportA 60 year-old female with hypertension, diabetesmellitus and ischaemic heart disease with mild to moderatesystolic dysfunction, was admitted through emergencyroom with cardiogenic shock due to Non-ST elevated MI(Troponin I >3), hyponatraemia (Na = 123 Meq/L)  andsevere metabolic acidosis. She was intubated in emergencyroom due to respiratory distress. Post intubation, she wentinto cardiac arrest. Temporary pacemaker was inserted inthe emergency room (Figure) and she was transferred tointensive care unit (ICU). She was successfully extubatedon day 4. Patient regained her own heart rhythm 24 hoursafter insertion of pacemaker as shock and metabolicacidosis improved. Within one hour of removal ofpacemaker she complained of dizziness and difficulty inbreathing. Blood pressure was 60/40 mmHg and heart rate270 J Pak Med Assoc90/min. Pulse was weak. EKG showed low voltage waveswith ST depression in V3 to V5. Urgent echocardiogramshowed large pericardial effusion with tamponade. She wasresuscitated with IV fluids and immediatepericardiocentesis was performed and 400 ml of clottedblood was removed. Pericardial window was made. Patientbecame haemodynamically stable and was extubated on thenext day and shifted to special care unit. She was dischargedhome seven days after the event.DiscussionMyocardial perforation is a rare complicationfollowing pacemaker implantation that may cause cardiactamponade. If it does occur, it is usually at the time of leadinsertion.1 Tamponade usually takes place due to arrowhead endocardial electrode.2 Fatal myocardial perforationcan occur with this electrode and the apex of the rightventricle should be avoided as the site of insertion3. Thiscondition requires urgent recognition since the promptdrainage of the pericardial fluid may be lifesaving.The pericardium consists of a thin serous membranecovering the epicardial surface (visceral pericardium) and aserous membrane-lined fibrous sac (parietal pericardium),which has limited elastic properties. The pericardial spaceseparates the two layers and contains approximately 25-35ml of serous fluid.1 An acute accumulation of pericardialfluid of greater than 100 ml will produce haemodynamiceffects of tamponade whereas a chronic pericardialcollection of fluid up to 2000 ml may occur withoutimposing any effect upon cardiac output.2Cardiac tamponade is defined as ahaemodynamically significant cardiac compression causedby pericardial fluid.3 The fluid may be blood, pus, effusionor air.4 Pericardial tamponade may arise from multipletraumatic and non traumatic etiologies, resulting inunrecognized rapid deterioration and often death.Traumatic pericardial tamponade occurs in only 2% of allpenetrating chest injuries5, and rarely is the result of blunttrauma. Mortality exceeds 60% if cardiac arrest occurs.6Non traumatic causes of pericardial tamponade includehaemopericardium due to anticoagulant therapy or as a rarecomplication of acute myocardial infarction. In addition,various non- traumatic causes such as infection, drugs,neoplasm, uraemia, myxoedema, collagen vascular disease,and hypersensitivity states may produce large effusion withtamponade. Pericardial tamponade has resulted fromcardiac catheterization, central venous catheterization,pericardiocentesis, intracardiac injection, cardiac surgery,and sternal bone biopsy and transvenous pacemakerinsertion.7 Common sites of perforation are the right atriumand right ventricle followed by superior vena cava.8Perforation has also been reported in the left atrium (patentforamen ovale) and the left pericardiophrenic vein.Endocardial injury is thought to be caused by eithermovement of the catheter tip, by movements of cardiacchambers and lower superior vena cava (cardiac cycle) orby direct trauma. Injury causes thrombus formation andeventually adherence of the wire to the endocardium.Erosion occurs which may lead to perforation. Early recognition and treatment of cardiactamponade is essential to prevent fatal outcome. Symptomsand signs are usually sudden and include nausea, fatigue,light-headedness, dyspnoea, retrosternal chest pain,cyanosis, venous engorgement, pulsus paradoxus andconfusion. The most common findings noted by Nasim andcolleagues9 from case reports were hypotension (88%),raised central venous pressure (70%) and a disturbance incardiac rhythm (67%) mainly tachycardia. However in 29%of these cases death occurred suddenly after 'vaguepremonitory signs'. Diagnosis of cardiac tamponade isdifficult in sedated, ventilated and post-operative patients.EKG and chest radiograph findings may not alwaysassist the diagnosis. EKG findings such as low voltage QRScomplex or electrical alternans may not always be present.Chest radiograph may not show abnormalities untilconsiderable fluid has accumulated in the pericardial sac.Transthoracic or transesophageal echocardiography isdiagnostic. These techniques are unfortunately not alwaysavailable and delaying treatment to obtain theseinvestigations may be fatal.The patient is initially resuscitated with intravenousfluids to promote maximum filling of the heart. In general,inotropic agents that increase the stroke volume and supportFigure 1. Portable Chest X-Ray showing ET tube, right IJ swan sheath and temporary pacemakerin appropriate position. Lung fields show mild bilateral pleural effusions, silhouetting of left hemidiaphragm and haze over both lower lung zones consistent with pulmonary edema.Vol. 58, No. 5, May 2008 271systemic resistance are used, although some recommendisoprenaline, as it reduces the cardiac size and diminishes theeffective degree of tamponade while increasing cardiacoutput.2 The definitive treatment of cardiac tamponade is theremoval of cardiac diastolic restriction by eitherpericardiocentesis or thoracotomy. Pericardiocnetesis isusually performed for urgent management of an acutetamponade (the acute removal of as little as 50 ml of fluid isoften sufficient to correct the hypotension). A thoracotomy isoften required when a tamponade exists following coronaryartery bypass grafting, penetrating or closed cardiac traumaand aortic dissection. It is also indicated whenpericardiocentesis has failed to relieve the tamponade. ConclusionCardiac tamponade is a life-threatening emergency.Immediate recognition and treatment are imperative if adisastrous outcome is to be prevented.References1.  Barriales AV, Alvavez Tamargo JA, Garcia AM, Martin FM, Morales C.Delayed myocardial perforation following pacemaker implantation. Int JCardiol 2004; 93: 89-91.2. Collins D. Aetiology and management of acute cardiac temponade. Crit Care Resusc 2004; 6: 54-8.3. Hancock EW. Cardiac temponade. Med Clin North Am 1979; 63:223-37.4. Spodick DH. Pathophysiology of cardiac temponade. Chest 1998;113:1372-8.5. Costa IV, Soto B, Diethem L, Zarco P. Air pericardial temponade. Am JCardiol 1987; 60:1421-2.6. Beall AC Jr, Diethrich EB, Crawford HW, Cooley DA, De Bakey ME.Surgical management of penetrating cardiac injuries. Am J Surg1966;112:686-92.7. Fisch GW, Sherz RG. Neck vein catheter and pericardial temponade.Pediatrics 1973;52:8628. Booth S.A, Nortam B, Mulvey DA. Central venous catherization and fatalcardiac temponade. Br J Anaesth 2001; 87 : 298-302.9. Nasim A, Cooper GG, Ah-see AK. Caridac temponade to central venouscatheterization. J R Coll Surg Edinb 1992; 37:337-9.Case ReportDe novo primary squamous cell carcinoma of the ovary: A case of a raremalignancy with an aggressive clinical courseAli Imran Amjad, Inam PalDepartment of Surgery, Aga Khan Univeristy Hospital, Karachi, Pakistan.AbstractOvarian squamous cell carcinoma is a raremalignancy and the occurrence is attributable to malignanttransformation of an existing ovarian dermoid cyst. The denovo occurrence of squamous cell carcinoma of the ovary,in the absence of an antecedent ovarian dermoid, isextremely rare. The case of a 31 year old Asian woman,evaluated for abdominal distension and discomfort ispresented. Abdominal CT was suggestive of a malignantneoplastic process. Laparotomy confirmed a malignanttumour with involvement of the right adnexa and extensioninto the omentum and bowel. Surgical debulking,hysterectomy, bilateral salpingo-ophorectomy and totalomentectomy and bowel resection was performed.Histopathology demonstrated squamous cell carcinomaarising from the right ovary with no co-existing ovariandermoid. The postoperative period was significant fordisease progression despite adjuvant chemotherapy. IntroductionSquamous cell carcinoma of the ovary is a rareclinical entity, accounting for less than 1% of all malignanttumours of the ovary.1 Malignant transformation of a pre-existing mature cystic teratoma (dermoid cyst) isappreciated as the underlying pathophysiologicalmechanism, and this phenomenon is considered rare, asonly 1-2% of teratomas demonstrate this change.1 The denovo development of a primary squamous carcinoma, in anotherwise healthy ovary is an extremely rare occurrence.2-5We present a case of this rare malignancy, not beenpreviously reported in the Southeast Asian population, witha review of literature.Case ReportA 31 year old, para 2, Asian female (Pakistaniheritage) was referred to the general surgery clinic with aone year history of progressive abdominal discomfort anddistension.  She had a history of weight loss with no changein appetite, bowel habit or menstrual flow. A recent papsmear was negative for dysplasia. On examination, she wasanaemic with no jaundice, lymphadenopathy and hadnormal breast examination. Abdominal examinationrevealed a firm, mildly tender, mobile mass occupying mostof the lower abdomen. There was no clinical evidence ofascites. Pelvic and rectal exams were unremarkable. Pre-operative evaluation showed anaemia withnormal cell counts, and normal kidney and liver functions.272 J Pak Med Assoc

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Cardiac tamponade after removal of temporary pace maker in multidiscipinary intensive care unit

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