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CASE PRESENTATION. July 7, 2005 Trevor Langhan PGY-3. 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. CASE. May 17, 19:20

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case presentation


July 7, 2005

Trevor Langhan PGY-3

  • 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
  • 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
  • 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?






Full Vitals


CXR, PXR, C-spine

NG, foley, ECG

Monitors, trauma panel

FAST if needed



Full head-to-toe



Extremity Xrays



Contrast studies

  • 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
  • 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
  • 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
  • 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)
  • 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


coronary arteries



coronary arteries




tako tsubo
  • Takotsubo: a Japanese pot for fishing for octopus
  • Tako – octopus
  • Tsubo - pot
tako tsubo cardiomyopathy1
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
tako tsubo1
  • 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
tako tsubo2
  • 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
tako tsubo3
  • 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)
tako tsubo4
  • 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)
tako tsubo5
  • 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
tako tsubo6
  • 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
tako tsubo7
  • 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
tako tsubo8
  • 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
tako tsubo9
  • 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
tako tsubo10
  • 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
questions raised by case
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?
  • 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).
  • 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.
blunt cardiac injury
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)
blunt cardiac injury1
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
blunt cardiac injury2
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
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
myocardial contusion
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

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


(–ve TnI)

All had

–ve echos

and EKG’s

47 (25%)



16 (9%)

no other


TnI levels:

Lower on admit

Lower peak

Resolved sooner

my take home points
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