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  1. CASE PRESENTATION July 7, 2005 Trevor Langhan PGY-3

  2. OUTLINE • Case seen while on plastic surgery this spring • Brief case presentation • As interactive as possible, ask some questions if you like, and I may ask one or two of you! • Diagnosis • Review of current literature

  3. CASE • May 17, 19:20 • 43 year female unrestrained driver in MVC at 60 km/h • Frontal collision with no airbags • Steering wheel deformity • Extracted by fire/EMS at scene • C-spine protected in collar • Talking at scene • Copious oral/pharyngeal blood from facial smash • Multiple EMS attempts to intubate – 3rd attempt successful • Transported to RGH for treatment

  4. CASE • Arrival at RGH in C- spine collar and intubated • Vitals on arrival to trauma bay • HR 110 • BP 124/70 • Sats 99% (intubated) • Temp 37.0 • GCS – 11 (E4,V1,M6) • Primary survey adjuncts?

  5. PRIMARY SURVEY Airway Breathing Circulation Disability Exposure Full Vitals ADJUNCTS CXR, PXR, C-spine NG, foley, ECG Monitors, trauma panel FAST if needed SECONDARY AMPLE hx Full head-to-toe ADJUNCTS CT, FAST, DPL Extremity Xrays Angiography Endoscopy Contrast studies CASE

  6. CASE • Secondary survey • Start at head and work down • Ears/nose/eyes/dentition/scalp etc… • Complicated facial laceration extending from mid-brow toward nose • ? Medial canthus involvement • Tarsal plate OK • Appears to have full EOM and pupils are equal and reactive

  7. CASE • Lab work – all normal • Injuries include: • Right rib fractures • Complex facial laceration • Complex nasal bone #’s • ? Aspiration • Blood in and around oral pharynx • Superficial lip laceration

  8. CASE • May 18, 7 am (approx 16 hours post MVC) • Was kept intubated overnight as C-spines not cleared radiographically • On monitor in ICU: • ? ST changes • 12 lead EKG • Troponin 0.3 • Talk to the husband – only CAD risk factor is smoking

  9. CASE • 43 year lady: • BP 125/65 HR 80 • Intubated, ventilating OK • New EKG changes, +ve troponin • What now? • Would you heparinize this lady? • CT head/chest/abdo/pelvis – normal • Hemoglobin this am 110 (down from 140 on admit)

  10. CASE • CCU consulted • Troponin 0.05 • ASA, IV heparin and Beta blocker • Echo: • Apex and Anterior wall severely hypokinetic • ? Aneurysmal formation at heart apex • No pericardial effusion • DDx: • Coronary dissection • Myocardial stunning due to contusion • Ischemic heart disease • Left ventricular aneurysm

  11. Normal coronary arteries

  12. Normal coronary arteries

  13. diastole systole

  14. Tako-tsubocardiomyopathy

  15. Tako-tsubo • Takotsubo: a Japanese pot for fishing for octopus • Tako – octopus • Tsubo - pot

  16. Tako-tsubo cardiomyopathy • First described by Satoh et al. in 1990 • Recently recognized reversible form of heart failure • Clinically resembles acute myocardial infarction but normal coronary arteries • Characterized by: • transient left ventricular dysfunction with chest pain • electrocardiographic changes • minimal release of myocardial enzymes

  17. Tako-tsubo • 250 cases have been reported in Japan since 1990 • Defined as: • Occurrence of heart failure similar to acute myocardial infarction • Takotsuboshaped hypokinesis of left ventricle on echo/ventriculography • Normal coronary arteries despite continued ST segment abnormalities • Complete normalization of LV dysfunction in a few weeks

  18. Tako-tsubo • More prevalent among women than men (7 : 1) • Average age mid 60’s • 68.6±12.2 in women and 65.9±9.1 years in men • Women are 6–12 times more likely to be affected than men • Clinical features derived from case reports: • Symptoms at onset mimic MI • Ventricular dysfunction looks like a takotsubo • Coronary arteries are disease free • Dysfunction improves rapidly over few weeks • Mean time to resolution 17.4 days in one study (N=7) • Data on recurrence rate is unknown

  19. Tako-tsubo • Most common presenting symptom is chest pain • Often acute pulmonary edema from decreased left ventricular systolic function • Dyspnea, shock may also be presenting complaints • May have associated tachy or brady dysrhythmias • EKG findings classically ST elevation in V3 and V4 • ST depression • T wave inversion • Abnormal Q waves • Small or moderate elevation of cardiac enzymes (large elevations unusual)

  20. Tako-tsubo • Most case reports (some case series): • elderly women over 60 years of age • some physical or mental stress precedes the onset of thesymptom • associated with several clinical events: • Myocardial stunning • Pneumothorax • Trauma • subarachnoid haemorrhage • Phaeochromocytoma • Guillain-Barré syndrome • Emotional stress (death of loved one, panic d/o)

  21. Tako-tsubo • Onset is associated with: • Acute medical illness • Emotional or physical stress • Animal models support idea that it is likely the result of catecholamine induced microvascular spasm • Also supported by elevated serum norepinephrine levels in patients with disease • Myocardial perfusion studies support this theory

  22. Tako-tsubo • Many authors debate the actual pathophysiology • Primarily argue vasospasm vs. a less well known effect of elevated catecholamines • Provocative testing using ergonovine • Did not show coronary spasm • 0 out of 20 cases in one study • Ergonovine testing proved positive in some series’ • 21% of cases in one series • 30% of cases in a second series

  23. Tako-tsubo • Akashi et al. The clinical features of takotsubo cardiomyopathy. Q J Med. 2003: 96:563-573 • 472 patients with sudden onset of heart failure, acute MI like abnormal Q wave and ST changes admitted • 463 with acute MI from CAD, 2 viral myocarditis • 7 (1.5%) with takotsubo defined as: • Acute heart failure similar to MI • Boat shaped hypokinesis on echo and LV ventriculograph • Normal coronary angio with continuous ST changes • Normalization of LV function in 3 weeks

  24. Tako-tsubo • Akashi et al. The clinical features of takotsubo cardiomyopathy. Q J Med. 2003: 96:563-573 • 5 had Hx of HTN, none had CAD Hx • Possible triggers included • Pneumothorax • Common cold (2) • Idiopathic ventricular fibrillation • Exercise • Emotional care giver stress • ST elevation in 6 of 7 persisted for 1 week • Plasma norepinephrine level elevated in 4 of 7 • Serial levels showed highest value in first sample • 1 – 4 year follow up - 6 had no further cardiac illnesses, 1 died of non-cardiac cause

  25. Tako-tsubo • Seth et al. A syndrome of Transient Left Ventricular Apical Wall Motion Abnormality in the Absence of Coronary Disease: A perspective from the the United States. Cardiology 2003;100:61-66. • Over 2 ½ year period 12 (11 women) patients presented with chest pain, ECG changes, abnormal cardiac enzymes, echo findings of apical wall motion abnormality • All inverted T waves in precordium, 1/3 had ST elevation • 10 had angiography (all had non-critical lesions) • All 12 had a definitive precipitating ‘trigger’ • 5 emotional, 5 resp distress, 2 post-op • Follow up echocardiography revealed normalization of LV function • Concluded that Takotsubo phenomenon described in Japan occurs in the U.S. • Increasing use of echo will result in more frequent diagnosis

  26. Tako-tsubo • In-hospital mortality rate is less than 1% • Fatality rate Takotsubo less than acute myocardial infarction • 10 of 250 patients in one study • 1 of 88 patients in another • 0 of 7 in a third • The 2-year recurrence rate is less than 3% • reversible left ventricular dysfunction

  27. Questions raised by case? • Another cause of non-ischemic ST elevation to add to the list? • Role of troponins and/or EKG in setting of blunt thorax injury? • Anti-coagulation of a trauma patient? • Angiography of a trauma patient +/- stenting?

  28. References • Sato H, Tateishi H, Uchida T, Dote K, Ishihara M. Tako-tsubo-like left ventricular dysfunction due to multivessel coronary spasm. in: Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure. Kodama K, Haze K, Hori M, Eds. Kagakuhyoronsha Publishing Co., Tokyo, 1990: 56–64 (in Japanese). • Kawai S, Suzuki H, Yamaguchi H, et al. Ampulla cardiomyopathy ('Takotsubo' cardiomyopathy). −Reversible left ventricular dysfunction with ST segment elevation. Jpn Circ J 64: 156–159, 2000 (Erratum in Jpn Circ J 64: 237, 2000). • Kawai S. Ampulla-shaped ventricular dysfunction or ampulla cardiomyopathy? Respiration and Circulation 48: 1237–1248, 2000 (in Japanese). • Ogura R, Hiasa Y, Takahashi T, et al. Specific findings of the standard 12-lead ECG in patients with 'Takotsubo' cardiomyopathy. −Comparison with the findings of acute anterior myocardial infarction. Circ J 67: 687–690, 2003. • Kawabata M, Kubo I, Suzuki K, et al. 'Tako-tsubo cardiomyopathy' associated with syndrome malin. −Reversible left ventricular dysfunction. Circ J 67: 721–724, 2003.) • Kurisu S, Inoue I, Kawagoe T, et al. Myocardial perfusion and fatty acid metabolism in patients with Tako-tsubo-like left ventricular dysfunction. J Am Coll Cardiol 41: 743–748, 2003. • Abe Y, Kondo M, Matsuoka R, et al. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 41: 737–742, 2003. • Amaya K, Shirai T, Kodama T, et al. Ampulla cardiomyopathy with delayed recovery of microvascular stunning: a case report. J Cardiol 42: 183–188, 2003 (in Japanese).

  29. References • Osa S, Abe M, Ueyama N, et al. A case of ampulla cardiomyopathy caused by dysfunction of coronary microcirculation. Heart 35: 117–123, 2003 (in Japanese).Yamashita E, Numata Y, Sakamoto K, et al. Clinical analysis of 21 patients so-called tako-tsubo like cardiomyopathy. Heart 35: 379–385, 2003 (in Japanese). • Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol 38: 11–18, 2001. • Ishihara M, Sato H, Tateishi H, et al. "Takotsubo"-like cardiomyopathy. Respiration and Circulation 45: 879–885, 1997 (in Japanese). • Kono T, Morita H, Kuroiwa T, et al. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol 24: 636–640, 1994. • Dote K, Sato H, Tateishi H, et al. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases. J Cardiol 21: 203–214, 1991 (in Japanese). • Tokioka M, Miura H, Masaoka Y, et al. Transient appearance of asynergy on the echocardiogram and electrocardiographic changes simulating acute myocardial infarction following non-cardiac surgery. J Cardiograph 15: 639–653, 1985 (in Japanese). • Sassa H, Tsuboi H, Sone T, et al. Clinical significance of transitory myocardial infarction-like ECG pattern in postoperative patients. Heart 15: 669–678, 1983. • Kuramoto K, Matsushita S, Murakami M. Acute reversible myocardial infarction after blood transfusion in the aged. Jpn Heart J 18: 191–201, 1977.

  30. Blunt Cardiac Injury • Definition is heterogeneous in various specialties • Encompasses mild cardiac bruise to cardiac rupture and death • Due to difficulty defining injury incidence can range from 19% - 75% in blunt chest trauma • No gold standard • Practical diagnosis is by good mechanism and altered cardiac function (wall motion or arhyth)

  31. Blunt Cardiac Injury • Nagy KK, Krosner SM, Roberts RR, et al (Cook County Hospital, Chicago, IL; Rush University, Chicago, IL) World J Surg. 2001;25:108-111 • Patients at risk for BCI admitted to ICU for serial ECGs, monitoring, serial enzymes and Echo. N= 171 (group 1). • Group 2 = no risk factors and hemodynamically stable. • Results: • normal ECG, normotensive and no dysrhythmias on admission had benign outcomes. • Those with ST segment changes, dysrhythmias, or hypotension after blunt chest trauma need to be monitored for 24 hours; they occasionally need further treatment for complications of BCI. • No additional information was gained by using ECHO for screening

  32. Blunt Cardiac Injury • Meta analysis of BCI literature by Maenza et al. • 25 prospective (2210 pts), 16 retrospective • Cardiac complications requiring treatment in 2.6% of patients – dysrhythmias • Abnormal ER EKG and +ve CK-MB correlated with developing BCI related complications • 100% sensitive if use any and all dysrhythmias (including sinus tach, a fib, conduction delays) • Normal EKG and –ve troponin on admit and at 6 and 12 hours, very low probability of clinically significant BCI

  33. Prospective and consecutive major blunt chest patients. N=333. • All had serial ECGs and TnI • Echo prn • Outcome = sigBCI = heterogeneous definition • Hypotension presumed to be cardiogenic in origin • Arrhythmia • abnormal post-traumatic TTE with low Cardiac Index

  34. Myocardial Contusion • Results • 44 (13%) significant BCI • Admission ECG or TnI was abnormal in 43 of 44 patients with SigBCI • 80 patients with abnormal ECG and TnI • 27 (34%) developed SigBCI • 131 with normal serial ECG and TnI • none developed SigBCI • Abnormal ECG only or TnI only, 22% and 7%, respectively, developed SigBCI • one patient had initially normal ECG and TnI and developed abnormalities 8 hours after admission • Concluded: • PPV and NPV 29%/98% for ECG • 21% and 94% for TnI • 34% and 100% for the combination

  35. Rajan GP, Zellweger R.Cardiac troponin I as a predictor of arrhythmia and ventricular dysfunction in trauma patients with myocardial contusion.J Trauma. 2004 Oct; 57(4):801-8; discussion 808. 187 pts TnI below 1.05 [mu]g/L in asymptomatic patients at within the first 6 hours rule out myocardial injury Tn levels above 1.05 [mu]g/L mandate further cardiologic workup 63 (34%) +ve TnI 124 (–ve TnI) All had –ve echos and EKG’s 47 (25%) Abnormalities Echo/ecg 16 (9%) no other abnormality TnI levels: Lower on admit Lower peak Resolved sooner

  36. My Take home points • ECG is the best screening test • Optimal period of observation is unknown • Enzymes have no role alone, but in conjunction with EKG can improve negative predictive value • not predictive of disease or absence of disease • Echo is not a screening test • Positive echo does not predict clinical complications • Use echo to r/o tamponade or cardiac rupture or to aid in diagnosis of unexplained hypotension