CASE PRESENTATION

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CASE PRESENTATION

• July 7, 2005
• Trevor Langhan PGY-3

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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

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CASE

• May 17, 1920
• 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

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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?

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CASE

• 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

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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

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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

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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

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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)

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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

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Normal coronary arteries
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Normal coronary arteries
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diastole
systole
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Tako-tsubocardiomyopathy
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Tako-tsubo

• Takotsubo a Japanese pot for fishing for octopus
• Tako octopus
• Tsubo - pot

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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

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Tako-tsubo

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

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Tako-tsubo

• More prevalent among women than men (7 1)
• Average age mid 60s
• 68.612.2 in women and 65.99.1 years in men
• Women are 612 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
  (N7)
• Data on recurrence rate is unknown

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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)

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Tako-tsubo

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

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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

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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

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Tako-tsubo

• Akashi et al. The clinical features of takotsubo
  cardiomyopathy. Q J Med. 2003 96563-573
• 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

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Tako-tsubo

• Akashi et al. The clinical features of takotsubo
  cardiomyopathy. Q J Med. 2003 96563-573
• 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

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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 200310061-66.
• 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

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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

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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?

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References

1. 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
   5664 (in Japanese).
2. Kawai S, Suzuki H, Yamaguchi H, et al. Ampulla
   cardiomyopathy ('Takotsubo' cardiomyopathy).
   -Reversible left ventricular dysfunction with ST
   segment elevation. Jpn Circ J 64 156159, 2000
   (Erratum in Jpn Circ J 64 237, 2000).
3. Kawai S. Ampulla-shaped ventricular dysfunction
   or ampulla cardiomyopathy? Respiration and
   Circulation 48 12371248, 2000 (in Japanese).
4. 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 687690, 2003.
5. Kawabata M, Kubo I, Suzuki K, et al. 'Tako-tsubo
   cardiomyopathy' associated with syndrome malin.
   -Reversible left ventricular dysfunction. Circ
   J 67 721724, 2003.)
6. 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 743748, 2003.
7. Abe Y, Kondo M, Matsuoka R, et al. Assessment of
   clinical features in transient left ventricular
   apical ballooning. J Am Coll Cardiol 41 737742,
   2003.
8. Amaya K, Shirai T, Kodama T, et al. Ampulla
   cardiomyopathy with delayed recovery of
   microvascular stunning a case report. J
   Cardiol 42 183188, 2003 (in Japanese).

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References

1. Osa S, Abe M, Ueyama N, et al. A case of ampulla
   cardiomyopathy caused by dysfunction of coronary
   microcirculation. Heart 35 117123, 2003 (in
   Japanese).Yamashita E, Numata Y, Sakamoto K, et
   al. Clinical analysis of 21 patients so-called
   tako-tsubo like cardiomyopathy. Heart 35
   379385, 2003 (in Japanese).
2. 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 1118, 2001.
3. Ishihara M, Sato H, Tateishi H, et
   al. "Takotsubo"-like cardiomyopathy. Respiration
   and Circulation 45 879885, 1997 (in Japanese).
4. 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 636640, 1994.
5. Dote K, Sato H, Tateishi H, et al. Myocardial
   stunning due to simultaneous multivessel coronary
   spasms a review of 5 cases. J Cardiol 21
   203214, 1991 (in Japanese).
6. 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 639653, 1985 (in
   Japanese).
7. Sassa H, Tsuboi H, Sone T, et al. Clinical
   significance of transitory myocardial
   infarction-like ECG pattern in postoperative
   patients. Heart 15 669678, 1983.
8. Kuramoto K, Matsushita S, Murakami M. Acute
   reversible myocardial infarction after blood
   transfusion in the aged. Jpn Heart J 18 191201,
   1977.

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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)

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Blunt Cardiac Injury

• Nagy KK, Krosner SM, Roberts RR, et al (Cook
  County Hospital, Chicago, IL Rush University,
  Chicago, IL) World J Surg. 200125108-111
• 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

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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

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• Prospective and consecutive major blunt chest
  patients. N333.
• 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

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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

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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 mug/L in asymptomatic patients
at within the first 6 hours rule out myocardial
injury Tn levels above 1.05 mug/L mandate
further cardiologic workup
124 (ve TnI)
63 (34) ve TnI
All had ve echos and EKGs
16 (9) no other abnormality
47 (25) Abnormalities Echo/ecg
TnI levels Lower on admit Lower peak Resolved
sooner
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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

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