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, 19:2043 year female unrestrained driver in MVC at 60 km/hFrontal collision with no airbagsSteering wheel deformityExtracted by fire/EMS at sceneC-spine protected in collarTalking at sceneCopious oral/pharyngeal blood from facial smashMultiple EMS attempts to intubate – 3rd attempt successfulTransported to RGH for treatment

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?

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

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

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

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

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)

CASE

CCU consultedTroponin 0.05ASA, IV heparin and Beta blockerEcho: 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

Normalcoronary arteries

Normalcoronary arteries

diastole systole

Tako-tsubocardiomyopathy

Tako-tsuboTakotsubo: a Japanese pot for fishing for octopus

Tako – octopus

Tsubo - pot

Tako-tsubo cardiomyopathy

First described by Satoh et al. in 1990Recently recognized reversible form of heart failureClinically 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-tsubo250 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

Tako-tsuboMore 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-tsuboMost 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-tsuboMost 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)

Tako-tsuboOnset 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-tsuboMany 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-tsuboAkashi 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 admitted463 with acute MI from CAD, 2 viral myocarditis7 (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-tsuboAkashi et al. The clinical features of takotsubo cardiomyopathy. Q J Med. 2003: 96:563-573

5 had Hx of HTN, none had CAD HxPossible triggers included Pneumothorax Common cold (2) Idiopathic ventricular fibrillation Exercise Emotional care giver stress

ST elevation in 6 of 7 persisted for 1 weekPlasma 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-tsuboSeth 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 abnormalityAll inverted T waves in precordium, 1/3 had ST elevation10 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 functionConcluded that Takotsubo phenomenon described in Japan occurs in the U.S. Increasing use of echo will result in more frequent diagnosis

Tako-tsuboIn-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?

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?

References1. 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).

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: 156–159, 2000 (Erratum in Jpn Circ J 64: 237, 2000).

3. Kawai S. Ampulla-shaped ventricular dysfunction or ampulla cardiomyopathy? Respiration and Circulation 48: 1237–1248, 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: 687–690, 2003.

5. 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.)

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: 743–748, 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: 737–742, 2003.

8. 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).

References9. 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).

10. 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.

11. Ishihara M, Sato H, Tateishi H, et al. "Takotsubo"-like cardiomyopathy. Respiration and Circulation 45: 879–885, 1997 (in Japanese).

12. 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.

13. 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).

14. 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).

15. 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.

16. 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

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 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 Injury

Meta analysis of BCI literature by Maenza et al. 25 prospective (2210 pts), 16 retrospectiveCardiac complications requiring treatment in 2.6% of patients – dysrhythmiasAbnormal ER EKG and +ve CK-MB correlated with developing BCI related complications100% 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 TnIEcho prnOutcome = sigBCI = heterogeneous definition Hypotension presumed to be cardiogenic in origin Arrhythmia abnormal post-traumatic TTE with low Cardiac Index

Myocardial ContusionResults

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.

16 (9%) no other

abnormality

47 (25%)Abnormalities

Echo/ecg

124 (–ve TnI)

63 (34%)+ve TnI

187 pts

All had–ve echosand EKG’s

TnI levels:Lower on admit

Lower peakResolved sooner

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

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