Transcript CASE PRESENTATION

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
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
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 midbrow 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 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
Normal
coronary arteries
Normal
coronary arteries
diastole
systole
Tako-tsubo
cardiomyopathy
Tako-tsubo
Takotsubo: a Japanese
pot for fishing for
octopus
Tako – octopus
Tsubo - pot
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-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
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
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)
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)
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
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
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
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
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
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
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?
References
1.
2.
3.
4.
5.
6.
7.
8.
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).
References
9.
10.
11.
12.
13.
14.
15.
16.
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 infarctionlike 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
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 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
Results
 44 (13%) significant BCI


80 patients with abnormal ECG and TnI


27 (34%) developed SigBCI
131 with normal serial ECG and TnI


Admission ECG or TnI was abnormal in 43 of 44 patients
with SigBCI
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
47 (25%)
Abnormalities
Echo/ecg
124
(–ve TnI)
16 (9%)
no other
abnormality
All had
–ve echos
and EKG’s
TnI levels:
Lower on admit
Lower peak
Resolved sooner
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