File photo
Posted: Thursday, August 18, 2016 1:37 pm
Danville Register & Bee
Goodyear employee William “Billy” Scheier was killed at the Danville plant last Friday by blunt injuries to the chest and mechanical asphyxiation, according to the medical examiner’s office in Roanoke.
Tracie Cooper, district administrator with the office, declined to elaborate .
Scheier’s death was the fourth to occur at the Goodyear plant in the past year. The incident remains under investigation.
Scheier, 47, lived in Halifax County and had worked as an electrician at the Goodyear plant.
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Matt Bell/Register & Bee
The Goodyear plant in Danville
Posted: Friday, August 12, 2016 10:57 am
Danville Register & Bee
Another worker has died at Goodyear’s plant in Danville.
"We regret to report that early this morning, a death occurred in the Goodyear-Danville manufacturing facility," Goodyear spokeswoman Laura Singleton said in a statement Friday morning.
Goodyear's on-site emergency response team and local emergency personnel responded immediately and all parties are cooperating in the investigation into the cause of the incident, Singleton said.
The company has reported the incident to the Occupational Safety and Health Administration and will cooperate with the organization, Singleton said.
"Our hearts go out to the family, friends and co-workers of the employee during this very difficult time," Singleton said.
Singleton did not release the name of the employee who died, but it marked the fourth worker death at Danville’s largest private employer in a year.
On April 12, Greg Cooper, 52, a maintenance mechanic at the plant died on the job. He had worked at Goodyear for 18 years.
On March 31, Kevin Edmonds, 54, of Penhook, died during his work shift.
And in August 2015, Jeanie Lynne Strader, 56, of Chatham, died in an accident at the plant.
Danville’s Goodyear plant also had a fatality in 2007.
=============
Cause of death released for Danville Goodyear employee
By Colter Anstaett - Reporter Published: April 15, 2016, 11:46 am Updated: April 15, 2016, 6:07 pm
DANVILLE (WSLS 10) – The Medical Examiner’s Office in Roanoke has released the cause of death for the man who died earlier this week at the Goodyear plant in Danville.
He died as a result of drowning and thermal injuries. Greg Cooper died while working at the plant Tuesday morning and is the second person to die on the job in two weeks.
The Goodyear plant in Danville opened on Friday for the first time after the death. As the investigation into what happened continues, United Steelworkers, the union that represents the workers at the plant, wants some answers.
USW Director of Health, Safety & Environment Michael Wright said it is standard for them to assist the plant and OSHA in the investigation.
Wright said given that three people have died there in the last eight months, union representatives will be extra thorough with their investigation and plan to talk with representatives from the plant and Goodyear.
“When we understand the root causes, we would talk to the company through a negotiating process and say ‘these are things that need to be addressed’ and we would hopefully work with them to do that,” said Wright.
The plant voluntarily closed on Tuesday after Cooper’s death in order to conduct a thorough investigation of the incident.
Goodyear says that at the start of each shift, plant associates participated in a two-hour safety meeting where they were given the opportunity to ask questions and share any comments they may have.
Counselors will also continue to be provided on-site throughout the week, according to Goodyear.
=====================
Goodyear, USW continue investigation of death at plant
By Mike McNulty Follow Author
A Goodyear worker inspects truck tires at the plant in Danville, Va.
DANVILLE, Va.—At least three investigations into the death of a worker, the second in two weeks and the third in eight months, are being conducted at the Danville tire production plant.
Goodyear and the United Steelworkers union are conducting one probe while the Virginia Occupational Safety and Health agency and local police officials are conducting their own investigations.
The latest death occurred on April 12 when Greg Cooper, who had worked at the factory for 18 years, died from burns and drowning, according to the office of the chief medical examiner in Roanoke, Va.
A maintenance mechanic, Cooper was 52 years old, a company spokeswoman said.
In a prepared statement issued shortly after the latest accident, Goodyear said the plant's “on-site emergency response team, as well as local emergency personnel responded immediately, and all parties are cooperating in the investigation into the root cause of the incident.”
It said the company “is taking this matter very seriously” and reported the death to OSHA, which in turn launched its inspection of the facility.
Goodyear response
Goodyear temporarily closed the Danville plant to complete a full evaluation of the factory and thoroughly investigate the incident, it said. The shutdown occurred April 12, and the plant reopened on April 15.
“Our hearts go out to the family, friends and co-workers of the employee during this very difficult time,” the company said.
In a second statement, plant Manufacturing Director Greg Kerr said the company's “immediate priority is to provide support and assistance to Greg's family, as well as the entire team of associates in the Danville plant as we cope with the loss of a teammate.”
On the day the factory resumed normal operations, Goodyear issued another statement in which it noted that the investigations are ongoing.
“As associates return to their jobs,” the tire maker said in the statement, “the plant team will be keeping the safety and well-being of our associates as the highest priority.
“At the start of each shift, plant associates participated in a two-hour safety meeting where they were given the opportunity to ask questions and share any comments they may have.”
Goodyear also continued to provide counselors onsite throughout the following week.
The Goodyear spokeswoman said the company will not provide further comment on the active investigations or the first accident at the factory in August 2015.
Mike Wright, director of health, safety and environment for the United Steelworkers, said the union was conducting a joint investigation with the tire maker into what caused the latest fatality and the accident that led to the death of another plant employee—54-year-old Kevin Edmonds—March 31 in an industrial accident.
An autopsy revealed that the cause of Edmonds death was asphyxiation.
The USW sent an investigator to the Danville plant immediately after it learned about the accident, he said.
“We look at root causes and other contributing factors,” Wright said. OSHA, on the other hand, is primarily looking at violations of standards.
“There are lots of issues that must be reviewed,” he said, adding that he could not supply further specifics about the probe at this point. The investigation, while not complete, will be thorough, he added. He did not have a timetable on when he thought the probe would be complete.
Continuous inspection
Jennifer L. Rose, Virginia Occupational Safety and Health safety compliance director with the Virginia Department of Labor and Industry, said after VOSH was notified of the death at the Danville factory, it too initiated another inspection at the facility.
The agency was already in the midst of conducting an inspection of the plant following the March 31 death of Edmonds. That investigation has not been closed.
“I cannot comment on the status of any open inspections, such as this one,” Rose said. Once the investigation has been closed, VOSH will post any citations issued on the federal Occupational Safety and Health Administration web page.
She said the agency has up to six months from the opening of the inspection to issue any citations.
On Aug. 31, 2015, the Danville facility suffered the first of the three deaths when 56-year-old Jeanie Strader, a 15-year veteran of the company, was killed after being caught in machine rollers, according to an OSHA document. She was employed at Goodyear as a windup operator and roll changer.
Goodyear recently was fined $16,975 by OSHA for three serious violations at the Danville factory following an inspection after Strader's death.
==================================
Traumatic asphyxia due to blunt chest trauma: a case report and literature review
1
This article has been cited by other articles in PMC.
Abstract
Introduction
Crush
asphyxia is different from positional asphyxia, as respiratory
compromise in the latter is caused by splinting of the chest and/or
diaphragm, thus preventing normal chest expansion. There are only a few
cases or small case series of crush asphyxia in the literature,
reporting usually poor outcomes.
Case presentation
We
present the case of a 44-year-old Caucasian man who developed traumatic
asphyxia with severe thoracic injury and mild brain edema after being
crushed under heavy auto vehicle mechanical parts. He remained
unconscious for an unknown time. The treatment included oropharyngeal
intubation and mechanical ventilation, bilateral chest tube
thoracostomies, treatment of brain edema and other supportive measures.
Our patient’s outcome was good. Traumatic asphyxia is generally
under-reported and most authors apply supportive measures, while the
final outcome seems to be dependent on the length of time of the chest
compression and on the associated injuries.
Conclusion
Treatment
for traumatic asphyxia is mainly supportive with special attention to
the re-establishment of adequate oxygenation and perfusion; treatment of
the concomitant injuries might also affect the final outcome.
Introduction
Asphyxia is defined as any condition that leads to tissue oxygen deprivation [1].
Traumatic asphyxia is a type of mechanical asphyxia, where respiration
is prevented by external pressure on the body, at the same time
inhibiting respiratory movements and compromising venous return from the
head. Conditions like compression of the chest and/or abdomen under a
heavy weight and wedging of the body within a narrow space or large
crowds have been reported [2]. A Valsalva maneuver is necessary before thoracic compression for development of the syndrome [3].
Usual autopsy findings include intense purple facial congestion and
swelling with hemorrhagic petechiae of the face, the neck and upper
chest, craniocervical cyanosis and subconjunctival hemorrhage.
Case presentation
A
44-year-old Caucasian man was working under a car when the vehicle’s
transmission system fell on his chest, squeezing his torso between the
heavy item and the ground. After an unknown time, he was found in an
unconscious state by a relative, who called for medical aid. It was
estimated that at least one hour elapsed before our patient received
medical care.
On arrival to our emergency department,
our patient had a gasping breath without foreign bodies in his oronasal
cavities, palpable regular pulses with a rate of 130 beats per minute
and an arterial pressure of 80/40mmHg. On pulse oxymetry he had a
saturation of 80% on room air. His Glasgow Coma Scale score was 8
(absent eye opening, unintelligible voice responses and limp withdrawal
to painful stimuli), his papillae were isochoric and light reflexes were
bilaterally present. Because of his altered consciousness and impending
respiratory failure, our patient was urgently intubated and put under
controlled mechanical ventilation.
The rest of the
physical examination revealed that his face, the front part of his neck
and the upper part of his chest were congested, edematous and covered
with numerous petechiae, especially on the conjunctivae and the
periorbital skin. In a later bedside ophthalmologic examination, mild
bilateral periorbital swelling, severe bilateral subconjunctival
hemorrhages, chemosis, mild exophthalmos and mild optic disc edema were
observed. Ecchymotic bruises were also noted on the back part of his
neck and the upper part of both shoulders. His tympanic membranes were
clear and there were no mucosal hemorrhages of his upper airways.
Absence
of breathing sounds over both lung apices in combination with palpable
subcutaneous emphysema over his neck pointed towards the existence of
bilateral pneumothorax. Moreover, bloody fluid was drained through the
endotracheal tube, indicating possible lung contusions. The physical
examination of his heart and abdomen was unremarkable and
electrocardiogram was normal. Thoracic X-ray examination revealed
bilateral pneumothorax and multiple rib fractures (Figure 1).
In this respect, bilateral tube thoracostomies were inserted, draining
air and blood and eliciting major improvement in his hemodynamic
parameters. In subsequent X-rays, bilateral lung opacities were evident,
which were consistent with the clinical suspicion of lung contusions.
Fiberoptic bronchoscopy was not performed due to the bilateral
pneumothorax. Subsequently, our patient was transferred to our intensive
care unit (ICU). Arterial blood gases on admission to our ICU were: pH
7.246; partial pressure of carbon dioxide: 58.3mmHg; partial pressure of
oxygen: 441mmHg; bicarbonate: 21.9mEq/L; oxygen saturation: 99.9%; and
lactate: 1.1mmol/L while our patient was ventilated with a frequency of
15 breaths/min; tidal volume: 700mL; positive end-expiratory pressure:
5cmH2O; and fraction of inspired oxygen: 100%. His Acute
Physiology and Chronic Health Evaluation II score was 14, while his past
medical history was noted to be non-significant.
Chest X-ray taken after tube thoracostomies were inserted.
Note multiple rib fractures, subcutaneous emphysema, multiple lung
opacities, particularly on the right, corresponding to sites of lung
contusion and residual pneumothorax on the left side.
Further
work-up included radiological evaluation of his spine and limbs, which
was unremarkable, a normal echocardiography, and head, neck, chest and
abdomen computed tomography (CT). On the CT scan, a mild brain edema
without signs of hemorrhage was observed, while CT of his chest revealed
bilateral hemopneumothorax and sizeable bilateral lung contusions,
particularly on his right lung (Figure 2).
Computed tomography scan of the chest showing bilateral hemopneumothorax and multiple lung contusions, especially on the right.
Serum
biochemistry included elevated levels (ten times above the upper limits
of normal) of creatine phosphokinase, lactic dehydrogenase, aspartate
aminotransferase and alanine aminotransferase. A urine analysis was
normal (Table 1).
In
the ICU, our patient was ventilated with volume-control mode, with a
tidal volume of 7mL/kg, frequency 10 to 12 per minute, positive
end-expiratory pressure not exceeding 5cmH2O and a gas
mixture that was quickly tapered to a fraction of inspired oxygen of
40%. The unimpeded ventilation, the swift restoration of hypercapnia,
hypoxia and hemodynamics, the spontaneous containment of the
tracheobronchial hemorrhage, the rapid radiographic improvement in the
following days (disappearance of the opacities) and the quick recovery,
simply by placing thoracostomies tubes, made the event of a potential
rupture of major bronchial or arterial branch less plausible. Therefore,
we did not proceed to further invasive diagnostic procedures, such as
bronchoscopy, which would have added no more information towards the
appropriate management of our patient and would even pose some risks.
Fluid
resuscitation with crystalloids was copious, in order to prevent renal
complications of a potential traumatic rhabdomyolysis. Special care for
the brain edema was taken with mannitol administration and frequent
neurologic assessments. Regarding his respiratory function, our patient
improved swiftly, resulting in an uneventful extubation on the second
day of ICU hospitalization. However, his neurologic status lagged
behind, as he remained disoriented and agitated until the fourth day.
Facial and thoracic petechiae gradually faded within the next three
days. Serum aspartate aminotransferase, alanine aminotransferase,
creatine phosphokinase and lactic dehydrogenase levels decreased to
normal on the seventh day and our patient was discharged from the ICU
and transferred to the thoracic surgical ward.
Discussion
Crush
asphyxia is caused by a sudden compressive trauma to the
thoracoabdominal region and presents with facial cyanosis and edema,
hyposphagmata and petechial hemorrhages of the face, neck and upper
chest [4]. It is typically associated with transient ischemic neurological deficits and injuries to the thorax, abdomen and limbs.
Traumatic
asphyxia was first described over 170 years ago, by Ollivier in his
observations on the cadavers of people trampled upon during crowd
upheavals in Paris on Bastille day [1].
Later, Perthes added some other characteristics, such as mental
dullness, hyperpyrexia, hemoptysis, tachypnea and ‘contusion pneumonia’
to the initial description [1].
Other terms for this condition are Ollivier’s syndrome, Perthes’
symptom complex, compression cyanosis, traumatic cyanosis, cervicofacial
static cyanosis and cervicofacial cutaneous asphyxia.
A
review of the literature indicates that traumatic asphyxia is a rare
condition, since it might go unrecognized or not be even reported. Laird
and Borman found only seven cases out of 107,000 hospital and clinic
patients in a 30-month period, of whom 75,000 had been involved in major
accidents [5]. Dwek reported only one case out of a total of 18,500 accident victims in an area with heavy military traffic [6].
Our
patient suffered from traumatic asphyxia due to prolonged compression
between the ground and a sizeable heavy object, a mechanism quite common
in similar published reports. In particular, cases of crush asphyxia
are mainly a consequence of motor vehicle crashes, crushing among other
bodies in a panicked crowd, entrapment beneath vehicles or falling down
in a narrow space [7].
Other causes include injuries from machines and furniture, blast
injury, a python tightened around the thorax and, rarely, deep-sea
diving, weightlifting, epileptic seizures, difficult obstetric delivery
and asthmatic attack. The typical range of the duration of compression
is between two and five minutes [8].
The duration and the amount of pressure affect the outcome after
traumatic asphyxia. Significant weight can be tolerated for a short
time, whereas a relatively modest weight applied for a longer period may
result in death [8].
In our case, the duration of compression could not be confirmed, but it
is estimated as fairly long, although this is loosely consistent with
the rapid and full recovery of the patient.
The diagnosis is reached from the physical appearance, clinical examination, history and trauma mechanism [3].
Superior vena cava (SVC) obstruction and basilar skull fracture have
features that closely resemble the appearance of traumatic asphyxia.
Yet, the history of traumatic injury should rule out SVC obstruction,
while skull fractures are rare in traumatic asphyxia, unless the force
of compression is applied to the head [7]. Our patient had no head injury, as verified by the imaging studies.
The
exact pathophysiologic mechanism of traumatic asphyxia remains
controversial. It is generally considered that a compressive force to
the thoracoabdominal region together with the ‘fear response’ (deep
breath and closing of the glottis) cause a huge increase in the central
venous pressure. This induces reversal of venous blood flow from the
heart through the SVC into the innominate and jugular veins of the head
and neck. The back transmission of the elevated central venous pressure
to the head and neck venules and capillaries, while arterial flow is
continued, results into capillary stasis and rupture, producing the
characteristic upper body petechial and subconjunctival hemorrhages [1]. These features are often more prominent on the eyelids, nose and lips [4].
The lack of petechiae in the lower body may be due to the compressive
obstruction of the inferior vena cava in the chest or abdomen.
Furthermore, the fact that the lower part of the body is protected from
back transmission of venous pressure by a series of valves could be
another mechanism, since the SVC, innominate and jugular veins have no
valves [4].
Associated
injuries, such as pulmonary, cardiac, neurologic, ophthalmic, abdominal
and orthopedic trauma, were not apparent in our patient. As has been
concluded from Rosato et al., cardiac injuries during traumatic
asphyxia are extremely rare. Only two cases of cardiac contusion and
one of ventricular rupture have been reported so far, within the last
three years [9].
A normal electrocardiogram does not rule out blunt cardiac injury.
Another rare consequence of traumatic asphyxia is delayed myocardial
infarction due to coronary artery contusion [1].
Myoglobinuria, rhabdomyolysis and acute renal tubular necrosis (crush
syndrome) present only in cases of associated injury and ischemia of
large muscle groups [3].
After
awakening and despite the normal findings on brain imaging, our patient
was in a state of agitation and confusion that lasted for four days.
According to Perthes, neurological injury in traumatic asphyxia includes
cerebral hypoxia or anoxia, ischemia, venous hypertension, cerebral
vascular congestion, rupture of small vessels, petechial hemorrhages and
hydrostatic edema [2].
However, the rapid full recovery discouraged us from requesting further
brain imaging studies, such as magnetic resonance imaging, that were
not expected to influence the treatment plan. The vision may be affected
with the same mechanism: retinal hemorrhage, retrobulbar hemorrhage and
vitreous exudates (Purtscher’s retinopathy) [10].
A hearing deficit can be caused by edema of the Eustachian tubes, or a
hemotympanum. Other neurologic manifestations of the syndrome are loss
of consciousness, prolonged but self-limiting confusion, disorientation,
agitation, restlessness, seizures, visual disturbances, blurred vision,
papillary changes, optic nerve atrophy, exophthalmos, diplopia and
hearing loss [10]. Often, the neurologic status improves during transfer to the emergency room [8].
The suggested mechanism for loss of consciousness and prolonged
confusion associated with traumatic asphyxia includes cerebral hypoxia,
ischemia and venous hypertension, which lead to cortical dysfunction.
This dysfunction resolves within the following 24 to 48 hours.
Intracranial hemorrhage has seldom ever been evident in a patient [8].
CT scans of the brain are usually normal, whereas in fatal cases,
autopsy shows only petechiae and congestion, suggesting brain injury at
the cellular level [1].
Despite
the dramatic appearance of the ‘ecchymotic mask’, mortality in crush
asphyxia is low. However, it may be influenced by the severity, nature
and duration of the compressive force and the presence of concomitant
injuries, which can be useful markers of the severity of compression [2].
The proposed algorithm for the management of all trauma patients on
arrival and during the initial phases of treatment is the ABCDE (Airway,
Breath, Circulation, Disability, Environment) algorithm, described in
the Advanced Trauma Life Support guidelines by the American College of
Surgeons Committee on Trauma. The outcome is improved by airway control
and cervical spine protection, rapid restoration of ventilation,
oxygenation and circulation by thoracic decompression, fluid
resuscitation and prevention of renal complications secondary to
rhabdomyolysis and other secondary causes [1].
Management of these patients may be complicated by severe upper airway
edema, and the possibility of a difficult intubation should thus be
considered early. The prognosis is good if the patient survives the
initial few hours following injury, although a prolonged thoracic
compression could lead to cerebral anoxia and permanent neurological
sequelae [3].
Conclusion
Optimal
management of traumatic asphyxia must focus on early recognition of
this entity based upon the classic physical signs and the mechanism of
injury. Resuscitation efforts should include rapid administration of
oxygen with effective ventilation and fluid resuscitation, and must
focus on reversing hypoxia and prevent further tissue damage.
Consent
Written
informed consent was obtained from the patient for publication of this
case report and accompanying images. A copy of the written consent is
available for review by the Editor-in-Chief of this journal.
Authors’ contributions
ES,
GK and VT managed the patient, reviewed the literature and contributed
to the preparation of the manuscript; VP and IP reviewed the manuscript
and contributed to its final form. All authors read and approved the
final manuscript.
Authors’ information
Eleni
Sertaridou, MD is a Surgeon-Intensivist at the ICU University Hospital
of Alexandroupolis, Alexandroupolis, Greece. Vasilios Papaioannou, MD,
MSc, PhD is an Assistant Professor of Critical Care Medicine at the ICU
University Hospital of Alexandroupolis, Alexandroupolis, Greece.
Georgios Kouliatsis, MD is a Pulmonologist-Intensivist at the ICU
University Hospital of Alexandroupolis, Alexandroupolis, Greece.
Vasiliki Theodorou, MD is an Anaethesiologist-Intensivist at the ICU
University Hospital of Alexandroupolis, Alexandroupolis, Greece. Ioannis
Pneumatikos, MD, PhD, FCCP is a Professor of Critical Care Medicine at
the Democritus University of Thrace and Head of ICU, University Hospital
of Alexandroupolis, Alexandroupolis, Greece.
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