Download Cardiac lesions associated with cardiopulmonary

Rom J Leg Med [19] 1-6 [2011]
DOI: 10.4323/rjlm.2011.1
© 2011 Romanian Society of Legal Medicine
Cardiac lesions associated with cardiopulmonary resuscitation
George Cristian Curcă1, Dan Dermengiu2, Mihai Ceaușu3, Adriana Francisc4, Mugurel Constantin Rusu5,
Sorin Hostiuc6
___________________________________________________________________________________________________________
Abstract: Cardiac arrest is a major cause of morbidity and mortality across the world despite the fact that significant
advances were made in basic and advanced life support techniques. Cardiac lesions during CPR are rare, and usually are not
involved in thanatologic chains. They can however lead to severe or even lethal complications and may be difficult to differentiate
from non-iatrogen trauma, especially in traumatic deaths. We present in this article four cases of cardiac lesions associated with
resuscitated cardiac arrest, discuss their forensic significance and review the most important iatrogen cardiac lesions associated
with cardiopulmonary resuscitation.
Keywords: cardiac contusion, myocardial lesions, cardiopulmonary resuscitation
C
ardiac arrest is a major cause of morbidity and mortality across the world despite
the fact that significant advances were made in basic and advanced life support
techniques. Even though cardiopulmonary resuscitation has an overall success rate of 30-40%[1],
over 50% of all resuscitated patients die before leaving the hospital, usually due to cardiovascular
or CNS complications[2]; many successful resuscitations are in turn associated with a series of
post cardiac arrest syndromes (PCASs) or iatrogenic traumas determined by the CPR technique.
According to Nolan et al there are three main types of post-cardiac arrest syndromes: (1) postcardiac arrest brain injury, which encompasses impaired cerebrovascular auto-regulation, cerebral edema,
and postischemic neurodegeneration and is clinically associated with coma, myoclonies, seizures, variable
degree of cognitive dysfunctions, ischemic or hemorrhagic stroke, persistent vegetative state or brain death;
(2) post cardiac arrest myocardial dysfunction, which encompasses global hypokinesis, reduced cardiac
output, and ischemic heart disease and is clinically associated with acute cardio-circulatory insufficiency,
hypotension, arrhythmias; (3) systemic ischemia/ reperfusion, which encompasses systemic inflammatory
response syndrome, impaired vasoregulation, altered coagulation, adrenal suppression, impaired tissue oxygen
delivery and utilization, impaired resistance to infection and is clinically associated with sepsis, hypotension,
hyperglycemia, pyrexia, acidosis, and organ dysfunction[3-8]. Iatrogenic trauma may add to the severity of
1) Assoc.Professor, PhD, National Institute of Legal Medicine “Mina Minovici”
2) Corresponding author: Professor, MD, PhD, National Institute of Legal Medicine “Mina Minovici”,
Sos. Vitan Birzesti 9, Sector 4, 042122 – Bucharest, Romania, [email protected]
3) Assistant Professor, PhD, Chair of Pathology, University of Medicine and Pharmacy “Carol Davila”
4) MD, PhD, National Institute of Legal Medicine “Mina Minovici”
5) MD, PhD, PI, Senior Lecturer, Chair of Anatomy, University of Medicine and Pharmacy “Carol Davila
6) MD, National Institute of Legal Medicine “Mina Minovici”
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Dermengiu D et al
Cardiac lesions associated with cardiopulmonary resuscitation
the PCASs but usually they are mild and, if found at the autopsy, have little relevance in tanathogenesys.
Their medical-legal importance resides in the need of a differential diagnosis with either non-iatrogenic
trauma, especially in violent deaths, or morphologically similar non-violent pathologies. [4-6,9-19]. CPR
trauma can be divided in resuscitative injuries related to ventilation procedure (RIVP) and due to chest
compression (RICC) [15]. RIVPs are usually associated with respiratory tract lesions (larynx, pharynx, trachea,
lungs), but stomach lesions or bruisings/abrasions on the face and neck can be also found. RICCs are less often
described, affecting the face (petechiae), eye (retinal hemorrhages, petechiae on the eyelids and conjunctiva),
brain (subarachnoidal hemorrhages), skeletal structures (sternum and ribs fractures, bone marrow embolism),
heart (cardiac rupture, myocardial hemorrhages, epicardial petechiae, air invasion into ventricles, coronary
lacerations and hematomas), liver and spleen (ruptures, hematomas), hemo- or pneumoperitoneum, etc.
We present in this article four cases of myocardial hemorrhages associated with resuscitated cardiac arrest
and discuss their forensic significance.
Cases presentation
Case 1
A 32 years old female without a positive personal history of either cardiac or non-cardiac pathologies
collapsed at work. The ambulance crew found it in ventricular fibrillation and successfully resuscitated
her. She was admitted with the diagnosis of post CPR status, cardiac arrest under mechanical ventilation,
and survived for another four days with a GSC=4. At the autopsy we found a left forth costal fracture
and two contusive myocardial areas of 6/4/0.4 cm in the anterior wall of the left ventricle extended in
the interventricular septum (Figure 1) and in an anterior left papillary muscle. A few epicardial petechiae
were also identified. Histological examination revealed multiple myocardial contusions on the anterior
and anteroseptal walls of the left ventricle (Figures 2, 3) and one papillary muscle, a small fibrino-hematic
thrombus in the atriventricular node artery, and myxoid degenerescence of the mitral valve (Figure 4).
Figure 1. Myocardial contusions on the left ventricle
Figure 2. Areas of hemorrhagic necrosis on the antero-septal
wall of the left ventricle, HE, 10x
Figure 3. Contraction band necrosis (arrows) of the
cardiomyocytes in the left ventricle, PTAH stain, 40x
Figure 4. Myxoid degenerescence of the mitral valve; acid
mucopolysaccharides revealed by combined stain PAS – AB
pH 2.5, 20x
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Romanian Journal of Legal Medicine Vol. XIX, No 1(2011)
Case 2
A nineteen old female, was found at home in cardiac arrest; after a successful resuscitation she was
hospitalized in a third degree coma. She was previously healthy but had a history of birth control pills for a
couple of months before the event. She was transferred to an emergency hospital where she died seven days
later. During hospitalization the evolution was extremely severe, with hypoxic encephalopathy, acute renal
failure, hepatic dysfunction, acute cardio-circulatory insufficiency on maximal vasopressor and inotrope
support, and CID. The autopsy proved inconclusive for the cause of death. Gross pathological examination
revealed a partially organized thrombus in the left auricle, dated about seven days before death (Figure
5), a subendocardial hemorrhagic necrosis of the left ventricle, occurring most likely two days before death
Figure 5. Thrombosis of the left auricula (mixture of fibrin,
erythrocytes and leucocytes), HE, 5x
Figure 6. Extensive subendocardial hemorrhagic necrosis
(Figure 6,7), a few epicardial petechiae, a
pulmonary artery thrombosis dated also about
two days before death, bronchopneumonia
and renal infarct. All except the auricle
thrombosis and possibly the epicardial
petechiae were considered to be terminal
events, associated with MOSF and CID.
The auricle thrombosis was considered
to be either the cause of the initial cardiac
arrest or a resuscitation - related lesion.
As the patient hadn’t a personal history
of atrial fibrillation, chronic mitral valve
pathology or other predisposing cardiac,
hematological or thrombophilia disease, the Figure 7. Extensive subendocardic hemorrhagic necrosis, HE & Lie, 5x
cause of the thrombosis was related to CPR.
Case 3
A 28 years old male was admitted to the hospital with the diagnosis of acute hemorrhagic and necrotic
pancreatitis. During hospitalization he developed a deep coma (GCS=3), fever, acute respiratory, renal, and
cardio-circulatory insufficiency. On the seventh day, after un unsuccessfully resuscitated cardiac arrest, is
pronounced dead. Coagulative status was slightly decreased but fibrinogen levels were normal until the day he
died (332 mg/dl). During the necropsy cardiac examination revealed multiple subepicardial petechiae with the
absence of petechiae in other locations which made us conclude they were CPR-related.
Case 4
A 57 years old male was hospitalized for undetectable arterial tension, dizziness, and severe altered
mental state. The symptoms had started eight days before the admission. Clinical examination revealed
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Cardiac lesions associated with cardiopulmonary resuscitation
peritoneal irritation, diminished vesicular murmur, breathing difficulties, gastric stasis. Acute abdomen is
suggested by clinical, radiological and echographic investigations, but the patient developed bradicardia
and asystole before a surgical intervention could be performed. The patient was resuscitated but developed a
second, irresuscitable cardiac arrest after one hour and a half. Gross pathological examination found the cause
of death to be acute hemorrhagic and necrotic pancreatitis. Secondary to CPR attempts the patient had costal
fractures on the right (5th-7th ribs) and a hemorrhagic myocardial area in the of 1/0.8/0.8 cm below the right side
coronary artery at about 1 cm from the origin caused by the CPR attempts.
Discussions
Cardiac lesions during CPR are rare, and usually not involved in thanatologic chains. Krischer [20],
on a study of 705 deaths after CPR found cardiovascular lesions to occur in 10.6% of cases ( a total of 72
lesions), the majority of which were hemoperitoneum (8.4%), epicardial hematoma (2.7%), and myocardial
hemorrhages (1.3%), including ventricular subendocardial contusions and atrial lesions. He also noticed in six
patients great vessel complications – bubbles in the vena cava, laceration of small abdominal vessels, aortic
adventitial hemorrhage, superior vena cava perforation and inferior vena cava contusion[20].
Hemopericardium is, according to Krischer, the most frequent cardiac complication following CPR,
and may be caused by small myocardial contusions, tears in coronary branches, rib fractures with posterior
displacement tearing the pericardial sac, etc. The most frequent cause however seems to be the administration of
cardiac injections during CPR. Davison found, from 53 patients which suffered CPR, 17 cases with pericardial
effusion during echography and 8 (out of 28) cases of hemopericardium during the autopsy[21]. Usually the
hemopecardium in these cases is small, only rarely being cited quantities of over 100 ml[21,22]. Fatal cases are
also cited but they are extremely rare [23]. Schonefelder for example found four fatal hemopericardium cases out
of 340 autopsies with a history of intra-cardiac injections as a resuscitative measure[23].
Petechiae are small hemorrhages produced by rupture of small vessels (usually venules)[24]; epicardial
petechiae are usually caused by abrupt increases in intravascular pressure with subsequent over distension and
rupture. Hashimoto found them in 40% of autopsies in cases which previously suffered CPR [15], located as
follows: 52% on the anterior side of the heart, 17% on the posterior wall and in 30% on both the anterior and
the posterior side of the heart. Epicardial hematomas are rare [20,25-28] and usually determined by the force
applied by the ribs/sternum moving towards the epicardium, but may be caused by cardiac injections as well[21].
Myocardial contusions and hemorrhages are usually caused by a direct mechanism, as described above. There
are however cases in which the water-hammer effect may play an important role [29,30], as are the eight cases
described by Hashimoto [15] with septal myocardial hemorrhages, and possible subendocardial hemorrhages.
CPR with associated myocardial contusions seem to have a poorer prognosis than the ones without myocardial
contusions [15] as it is leads to additional hypotension, arrhythmias, hypoxia, etc. [30]
Cardiac rupture or laceration occur only exceptionally [1, 15, 22, 25, 31-35], and are usually associated
with a preexistent myocardial pathology [15]. A greater prevalence seems to be associated with open chest direct
cardiac massage [36] – Baldwin et al found them in six out of 16 cases analyzed. In patients without preexistent
myocardial pathology the rupture/laceration may be caused by a fractured sternum/rib [13,37-39], or by an acute
hemorrhage when there is a decrease in blood quantity in the heart chambers, permitting a stronger compression
of the heart between the anterior thoracic wall and the vertebral column[15]. Other possible mechanism for CPRassociated right ventricular rupture is the increased pressure in the right cardiac chambers when compressed
pulmonary valves affect the blood flow during resuscitation[15]. Increased risk for CPR-associated cardiac
rupture seems to be associated with the use of active compression-decompression devices like the Cardio-Pump®
[40,41]
Valvular lesions are only exceptionally described. Buschmann et al [41] for example found a rupture
of a highly calcified mitral valve ring after CPR with subsequent migration of the calcified fragments into the
myocardium and cardiac tamponade. Chatson described the development of a ventricular pseudoaneurism
associated with CPR six weeks after mitral valve replacement [42] Gerry et al. described two cases of rupture of
a papillary muscle followed by a tricuspid insufficiency following CPR [43].
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Cardiac thrombosis associated with CPR was previously described by Milstoc and Berger[44]; they
described a patient with cor pulmonale which had a thromboembolic mass in the right atrium, right ventricle and
pulmonary artery. The thromboembolic mass contained bone marrow emboli and bone spicules probably due
to a fractured rib after external cardiac massage. Barringer et al described a bone marrow embolus adherent to a
mural thrombus in the right atrium after CPR.[45] Andriessen et al. described a CPR complicated with cardiac air
emboli and a vena cava thrombosis which occluded the entry of the right ventricle.[46] As in the above described
situations our case had a predisposing condition (the use of birth control pills) which could favor an increased
thrombotic state. The particularity of our case is however the lack of direct or local causes for the development
of the atrial thrombosis.
Another cardiac structure which is sometimes affected by CPR but is often overlook in routine autopsy
cases is the cardiac electrical conduction system (ECS). Rossi et.al found a hemorrhage in the bundle of His
associated with CPR and suggested as a possible mechanism an excessive squeezing of the heart between the
sternum and the vertebral column[47]. Frink and Rose described direct blunt injuries of the coronary arteries or
the ECS in 44% (35 cases) of patients who received CPR prior to their death[48]. Nishida found lesions of the
ECS in seven out of 80 patients, suggesting their frequency is much higher than previously suggested[49]; the
distribution of hemorrhages in his study is as follows – six cases had hemorrhages in the conduction tissue (three
had hemorrhages in the sinus node, one had a hemorrhage in the proximal bundlw of His, two in the distal left
branch), and one had a focal dissection of the atrioventricular node artery.
The histological pattern of CPR related hemorrhages is similar to the classical traumatic cardiac
contusion morphology, and is very similar to the one found in myocardial infarction, with a more preeminent and
individualized hemorrhagic area. Histological examination reveals contraction band necrosis, myocardial cell
segmentation, bundles of contracted myocardiu alternating with bundles of distended myocardium, a widening
of the intercalated disks, granular myocitar disruption [30], fibrillar eosinophilia, elongated nuclei and sarcomers,
depleted troponin I, C, and myosin [50].
Aknowledgements
This work was supported by CNCSIS –UEFISCSU, project number PNII – IDEI 2642/2008
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