Example of Pain and Suffering Documentation in the Case of an Auto Accident

RESEARCH REPORT
TRAUMATIC ASPHYXIATION

Privileged and Confidential Work Product

Case (Patient) Name: JDC
Marital Status: UNK
Date of Birth: ../../74
Date of Death: ../../97
Age: 2.
Social Security #: ...
Occupation: Police Officer
Social History: ...
Alcohol: UNK
Tobacco: UNK
Weight: ~180
Height: 72" (6")
Allergies: UNK
Hospital Records: NONE
Physicians: NONE

Issues: What pain and suffering were experienced in the time period between the accident and the patient losing consciousness? How long might this have been?

Case Summary
On 8-21-97 Mr. JDC died as the result of an automobile accident. The cause of death was determined, on autopsy, to be "traumatic asphyxiation." Other injuries verified by autopsy were:

• Fracture of symphysis pubis
• Contusions of lung
• Abrasions of face and neck
• Numerous fine petechial hemorrhages of the face, conjunctivae and larynx
• Congestion of viscera

Pain is a universal accompaniment of trauma. "Pain has a very deleterious effect in prolonging the metabolic response to trauma." Pain increases the expenditure of energy and increases the need for oxygen. Under the influence of pain, the heart beats more rapidly. Small vessels in the skin and extremities will constrict to conserve the blood and oxygen supply for the vital organs and brain. This serves to reduce bleeding from extremities, but will increase internal bleeding. As a result, blood pressure rises somewhat throughout the body. This rise in blood pressure would have exacerbated the effects of the weight of the vehicle on his body.

Traumatic asphyxia is a distinctive clinical syndrome characterized by cervicofacial cyanosis and edema, multiple petechiae , and subconjunctival hemorrhage after a severe crush injury of the thorax or of the upper part of the abdomen. Fear response (a sense of impending doom or death, often accompanied by panic), tachypnea (rapid breathing, usually very shallow), and dyspnea (difficulty breathing) have also been associated with this injury.

Note: Although blunt trauma to the thorax (chest) or abdomen has been documented to frequently cause a tear in the diaphragm, there was no description of the condition of the diaphragm in the autopsy report.

According to a witness on the scene, Mr. C was alive and conscious immediately after the accident, and was trying to talk and move purposefully.

During the time between sustaining the injuries and the time help arrived, Mr. C______ experienced extreme suffering as he fought to breathe and stay alive. The time frame for retaining consciousness during the process of traumatic asphyxiation (in the absence of trauma-caused unconsciousness) can be as long as 6 minutes, with an average time of 4 minutes. Mr. C______ was alive and conscious for some time after the accident. He made purposeful movements and attempted to speak to people on the scene. The indented, italicized portions of this report are the logical extensions of the descriptions of injuries found in the autopsy report and the eye-witness report along with the known physiology of hypoxia (lack of oxygen) and asphyxiation (death from lack of oxygen).

The automobile was on top of him, pinning him down with its full weight. The pressure from the vehicle caused the blood pressure in his head, neck and chest to increase. The pressure was so high in these areas that tiny small blood vessels in the lining of his eyelids, in his voice box, and in the skin of his face broke, causing pinpoint hemorrhages called petechiae (pee-tee-kee-aye).

The weight and movement of the vehicle as it had rolled over him had fractured and then separated his pelvis (the pubic bone in the front) nearly 1/2 inch. There is severe pain associated with this kind of injury.

Severe pain (from the pubic break and separation) knifed through his pubic bone and seemed to twist and pull terribly each time that part of his body moved. This pain continued throughout the ordeal.

There was a contusion (bruise) on the right lung and contusions on the pleura (lining of the lungs) on both sides. The pain caused by a bruised lung increases with each attempt to breathe in. Pleural pain is excruciatingly sharp, making it nearly impossible to inhale. Once air is inhaled, the excruciating pleural pain makes it difficult to exhale.

Each time he attempted to breathe in, there was a deep, severe, aching pain in his lung. Trying to minimize the pain, he breathed less deeply, but then felt overpowering hunger for air, and had to try to breathe more deeply despite the pain.

Congestion of the viscera (internal organs) resulted from the pressure of the vehicle which landed on Mr. C. Similar petechial (small, pinpoint) hemorrhages (bleeding points) occur when someone takes a deep breath in and holds it while strongly trying to exhale (a Valsalva Maneuver). (These pinpoints of bleeding in the skin occur frequently in women during childbirth as they work to push the baby down and out of the birth canal. The same kind of pinpoint bleeding may occur in someone attempting to move an object too heavy to lift.) In the case of Mr. C, they indicate not only the severe pressure of the vehicle on top of him, but that he was attempting to breathe out, and was unable to do so.

Breathing in (inhaling) requires contraction of diaphragm and intercostal (between the ribs) muscles to increase the size of the chest and decrease the pressure in the chest so the lungs will expand. Exhaling normally is passive, but may become active during labored breathing or when air movements out of the lungs is impeded. Forced expiration requires contraction of the intercostal and abdominal muscles. Being under the car with its weight on his chest and abdomen prevented Mr. C______ from breathing with ease. The pain also interfered with his breathing movements and patterns.

The increased pressure in his chest from the weight of the vehicle and as he tried to breathe in and out made his head and face, especially his eyes, feel as though they were full to exploding. Tiny blood vessels in the skin of his face and neck burst under the pressure, adding a stinging sensation to the pain of the scrapes and abrasions.

He experienced extreme "air hunger" under the automobile. His body desperately needed oxygen, but was not getting it. He tried to breathe in, but experienced severe pain, both aching and sharp pain. When he managed to drag some air in, he tried to breathe out, but the air wouldn't leave his lungs because of the chest injuries. He spent much effort trying to breathe out. His lungs were aching and crying out for fresh air. It was like being underwater and not being able to get to the surface. He couldn't breathe. Air wouldn't come in, and when, with supreme effort he managed to bring air into his lungs, he couldn't get it out. Each time he tried to expand his chest, the weight of the vehicle pressed down. Each time he tried to breathe out, the swelling in his throat prevented the air from getting out. He was frightened, panicked. He couldn't get enough air. His whole body was screaming for oxygen, but he couldn't breathe.

Pain was everywhere. It was overwhelming. Not just the irritation of the abrasions on his face and neck, but the knife-like pain in his pelvis and his chest with the underlying deep ache of the bruised lung.

Someone came to him, getting down under the vehicle with him. In agony, he reached out and tried to touch the person. The person took his hand and he held on tight. He desperately tried to tell the person what was happening, what had happened, but only inarticulate, squeaking noises came out. He was panicky, trying to explain what he needed - air - and trying to breathe.

Because of the injuries to the lungs and increased congestion, fluid was beginning to seep into the air spaces in his lungs further impeding his ability to breathe. He experienced hypoxia (oxygen deficiency) of 2 different types: hypoxic hypoxia (low pressure of oxygen in arterial blood related to his obstructed airway) and stagnant hypoxia (inability to carry oxygen to tissues fast enough related to shock). Hypoxia creates a sensation of suffocation and air hunger through 2 mechanisms: carbon dioxide levels in the blood rise and the pH decreases. Receptors in the arteries, heart, lungs and brain urgently stimulate the body to breathe. The hormonal "fight or flight" mechanism comes into play, urging the body to escape from the situation at any cost. Inability to escape and inability to get air lead to overwhelming fear, anxiety, and in some people, anger - more of the "fight or flight" responses.

He pulled at the hand of the person under the car as hard as he could, but he couldn't move himself. The car was holding him down, pinning him, keeping him from being able to breathe. His lungs felt stuffy and he tried to breathe some more. The person kept telling him that help was coming. He tried to stay conscious, to stay alive, to breathe, but lack of air was sapping his strength, taking him far away.

Panic was overtaking him. He fought to escape, to get away. He fought to breathe. He fought to stay awake and alive despite the agonizing pain which accompanied each breath. After about 4 minutes, however, he began to feel more distant from the event. He may have thought about his family, his friends, or his uncompleted professional duties during those last few minutes before he finally lost consciousness. Or, he may have been completely consumed with the sensations of pain from his pubic bone and chest, the desperate need for air that he was experiencing, and the urgent need to get out of the situation.. Gradually, over the next 2 to 5 minutes, he lost more and more awareness. The last thing he heard was someone's voice saying help was on its way, but he couldn't wait any longer.

Mr. C. died from:
a. not being able to breathe,
b. the broken pelvis and
c. the bruise to his lung.
If he were the least claustrophobic, he would have experienced additional overpowering fear and anxiety from the automobile being on top of him and crushing him.

The saddest thing about this case is that had paramedics arrived sooner and had the vehicle been removed from his body sooner there was a chance he might have been saved. There is no mention of broken ribs, no mention of a diaphragmatic tear, no mention of cardiac trauma. The trauma literature indicates that there are good results in the majority traumatic asphyxiation cases when medical assistance is given rapidly.

References

• Gasnet: Global Textbook in Anesthesiology
• C______, L______, Summary Witness Statements Mr. L_____ B_____
• Hagan, Daniel, (1998) Biology of Aging. Course Curriculum. Athens & Carrolton, GA: University of Georgia, Georgia Southern University. (Personal Communication)
• Jongewaard, W.R., Cogbill, T.H., & Landercasper, J. (1992) Neurologic consequences of traumatic asphyxia. J Trauma, 32:1, 28-31. (Abstract attached)
• Lee, M.C., Wong, S.S., Chu, J.J., Chang, J.P., Lin, P.J., Shieh, M.J., & Chang, C.H. (1991) Traumatic asphyxia. Ann Thorac Surg. 51:1, 86-8. (Abstract attached)
• Lowe, L., Rapini, R.P., & Johnson, T.M. (1990) Traumatic asphyxia. J Am Acad Dermatol, 23:5 Pt 2, 972-4.
• Moore, Keith L. (1985). Clinically oriented anatomy. Baltimore: Williams & Wilkins. 269-274.
• Newquist, M.J., & Sobel, R.M. (1990) Traumatic asphyxia: an indicator of significant pulmonary injury. Am J Emerg Med. 8:3, 212-5. (Abstract attached)
• R____, L_____ S. (8-22-97) Autopsy Report: JDC
• Lesh, RVirginia Health Sciences Center.E. (1998) Control of Respiration. University of
• Schlimgen, M. (1994) Hypoxia, physiology of. University of Wisconsin Department of Anesthesia.

Abstracts

• DeAngeles, D., Schurr, M., Birnbaum, M., & Harms, B. (1998) Traumatic asphyxia following stadium crowd surge: stadium factors affecting outcome. WMJ, 97:9, 42-5
  Abstract: BACKGROUND: Stadium crowd surges frequently occur following major athletic events. A recent crowd surge injured more than 80 persons by trampling and/or crushing. This incident was reviewed to identify injury patterns consistent with crush-related injury. In addition, the incident was reviewed to determine which stadium policy and design factors may have potentiated this event. METHODS: A recent crowd surge occurred following a college football game. This resulted in 86 people being transported to the University of Wisconsin and other area hospitals. All charts were reviewed to evaluate patient outcomes. The stadium was examined as were security system video tapes to evaluate stadium factors that contributed to this event. Current policies were obtained through the university sports administration. RESULTS: Of 86 patients transported for evaluation of stadium-related injuries, 10 were treated for traumatic asphyxia. Other injuries requiring hospital admission included musculo-skeletal trauma in two patients and one grade II liver injury. Six others were admitted overnight for observation. Several stadium factors were identified that contributed to the event, and appropriate changes in crowd control policies and stadium design were instated to prevent recurrence. CONCLUSIONS: This report details the largest single report of traumatic asphyxia second to the England Hillsborough disaster. Several stadium factors were identified that resulted in crush-related injury. Cooperative review and modification of stadium policies and design may prevent such events in the future.

Language of Publication English
Unique Identifier 99027952

• Jones, M.J., & James, E.C. (1976) The management of traumatic asphyxia: case report and literature review. J Trauma, 16:3, 235-8
  Abstract: Traumatic asphyxia is not as benign as has been indicated in the literature and may represent a life-threatening process. A thorough understanding of the involved pathophysiology coupled with aggressive cardiopulmonary management is essential for patient survival. In cases with severe pulmonary injury, the judicious employment of respirator and PEEP therapy is emphasized.

Language of Publication English
Unique Identifier 76146830

• Jongewaard WR; Cogbill TH; Landercasper J (1992) Neurologic consequences of traumatic asphyxia. J Trauma, 32:1, 28-31
  Abstract: Patients with traumatic asphyxia treated at a single institution during a 10-year period were studied to determine the incidence and sequelae of neurologic impairment associated with this entity. Traumatic asphyxia was identified in 14 patients from 4 to 73 years old. Each had sustained thoracic crush injuries from objects weighing more than 1,000 pounds. The mechanism of injury was crush by farm implement in six patients, entrapment beneath a vehicle in five, compression by a large hay bale in one, crush by a farm animal in one, and a ditch cave-in in one. Craniocervical cyanosis and subconjunctival hemorrhage were apparent in all patients. Associated chest wall and intrathoracic injuries were present in 11 (79%) patients. Neurologic abnormalities included loss of consciousness in eight patients, prolonged confusion in five, seizures in two, and pronounced visual disturbances in two. There were no deaths in this series and no long-term neurologic sequelae were evident. However, careful serial neurologic assessment should be performed in these patients and other causes of neurologic symptoms excluded.

Language of Publication English
Unique Identifier 92122339

• Lee, M.C., Wong, S.S., Chu, J.J., Chang, J.P., Lin, P.J., Shieh, M.J., Chang, C.H. (1991) Traumatic asphyxia. Ann Thorac Surg, 51:1, 86-8
  Abstract: During a 5-year period, we treated 14 cases of traumatic asphyxia. There were 12 male and 2 female patients ranging in age from 2 to 32 years. Most suffered crushing injuries at work or were run over by motor vehicles. Mild to severe cervicofacial cyanosis and petechiae developed in all patients. A fear response was reported by 12 of the patients. Subconjunctival hemorrhage was also found in 12 patients. Nine patients had tachypnea and 7 complained of dyspnea. Most of the patients suffered some associated injuries including 8 head injuries, 7 pulmonary contusions, and 6 cases of blunt abdominal trauma. Less-associated injuries were rib fractures, brachial and radial nerve injuries, hemothorax, and pneumothorax. The hospital stay ranged from 4 to 28 days (mean, 14 days) and follow-up from 10 to 60 months (mean, 32 months). Treatment for traumatic asphyxia included measurement of arterial blood gases, oxygen supplementation, and intubation with mechanical ventilation. The patients' recovery conditions were relative to the severity of injury and the associated injuries.

Language of Publication English
Unique Identifier 91090525

• Lowe, L., Rapini, R.P., & Johnson, T.M. (1990) Traumatic asphyxia. J Am Acad Dermatol, 23:5 Pt 2, 972-4
  Abstract: Traumatic asphyxia is a distinctive clinical syndrome characterized by cervicofacial cyanosis and edema, multiple petechiae, and subconjunctival hemorrhage after a severe crush injury of the thorax or of the upper part of the abdomen. A case of traumatic asphyxia is reported, and its clinical and pathophysiologic features are discussed.

Language of Publication English
Unique Identifier 91036237

• Newquist, M.J., & Sobel, R.M. (1990) Traumatic asphyxia: an indicator of significant pulmonary injury. Am J Emerg Med, 8:3, 212-5
  Abstract: Traumatic asphyxia has often been described as a rare syndrome with little prognostic significance. In the authors' series, however, all cases secondary to deceleration injury or compression of the anterior thorax were associated with pulmonary injury. The signs of venous congestion of the face and anterior thorax are not always recognized in the emergency department where they should be most clinically evident. Increased awareness of this syndrome by emergency physicians will result in better reporting and understanding of its clinical implications.

Language of Publication English
Unique Identifier 90234054

• Nunn, C.R., Bass, J.G., Nastanski, F., & Morris, J.A., Jr. (1997) Traumatic asphyxia syndrome. Tenn Med, 90:4, 144-6
  Abstract: Although the craniofacial changes associated with TAS are usually not life threatening, the syndrome is not benign. The mechanism of injury needed to create TAS is sufficient to warrant extreme caution in the approach to these patients. It is vital for the physician to recognize the pathophysiology of the injury pattern and to remain cognizant of the high likelihood of potentially lethal associated injuries. Aggressive and directed management of the cardiopulmonary systems coupled with prompt recognition and treatment of associated injuries is essential for optimal patient outcome.

Language of Publication English
Unique Identifier 97243248

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