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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

Case presentation

  • 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

Case presentation

  • 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?

Case presentation







Full Vitals


CXR, PXR, C-spine

NG, foley, ECG

Monitors, trauma panel

FAST if needed



Full head-to-toe



Extremity Xrays



Contrast studies


Case presentation

  • 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

Case presentation

  • 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

Case presentation

  • 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

Case presentation

  • 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)

Case presentation

  • 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

Case presentation


coronary arteries

Case presentation


coronary arteries

Case presentation



Tako tsubo cardiomyopathy

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

Case presentation

Myocardial contusion
Myocardial Contusion N=333.

  • 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

  • Case presentation

    Rajan GP, Zellweger R. N=333.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 N=333.

    • 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