Gregg Peery v. Mid Continent Industrial

(Affirming Award and Decision of Administrative Law Judge)

Injury No.: 04-084324

Employee: Gregg Allen Peery, deceased

Dependent: Diane L. Peery

Employer: Mid Continent Industrial

Insurer: Hartford Underwriters Insurance Company

Date of Accident: July 12, 2004

Place and County of Accident: St. Joseph, Buchanan County, Missouri

The above-entitled workers' compensation case is submitted to the Labor and Industrial Relations Commission (Commission) for review as provided by section 287.480 RSMo. Having reviewed the evidence and considered the whole record, the Commission finds that the award of the administrative law judge is supported by competent and substantial evidence and was made in accordance with the Missouri Workers' Compensation Act. Pursuant to section 286.090 RSMo, the Commission affirms the award and decision of the administrative law judge dated July 27, 2007, and awards no compensation in the above-captioned case.

The award and decision of Administrative Law Judge Robert B. Miner, issued July 27, 2007, is attached and incorporated by this reference.

Given at Jefferson City, State of Missouri, this 25th day of February 2008.

LABOR AND INDUSTRIAL RELATIONS COMMISSION

William F. Ringer, Chairman

Alice A. Bartlett, Member

John J. Hickey, Member

Attest:

Secretary

AWARD

Employee: Gregg Allen Peery

Injury No.: 04-084324

Employer: Mid Continent Industrial

Dependent: Diane L. Peery

1. Second Injury Fund liability: None. (Second Injury Fund is not a party in this case.

TOTAL: None.

1. Future requirements awarded: None.

Employee: Gregg Allen Peery

Injury No: 04-084324

Dependent: Diane L. Peery

Employer: Mid Continent Industrial

Insurer: Hartford Underwriters Ins. Co. Checked by: RBM

A final hearing was held in this case in St. Joseph, Missouri on April 23, 2007. Diane L. Peery, ("Claimant"), dependent widow of deceased Employee, Gregg Allen Peery ("Employee"), who died on July 4, 2005, appeared in person. Attorney Nickolas A. Marshall, appeared on behalf of Claimant. Employer, Mid Continent Industrial ("Employer") and its insurer, Hartford Underwriters Ins. Co. ("Insurer") appeared by and through their attorney, J. Sean Dumm. The Second Injury Fund is not a party in this case.

Counsel for Employer/Insurer advised at the beginning of the hearing that he had intended to call Mike Tate, supervisor of Employer, as a witness at the hearing, but that Mike Tate was unavailable, according to Employer, because of his wife's illness. Counsel for Employer/Insurer requested that the record in the case be left open for up to thirty days from the date of the April 23, 2007 hearing (which was May 23, 2007) to permit him to offer additional deposition testimony of Mike Tate, regarding his observations of Employee and causation. Counsel did not request a continuance of the scheduled April 23, 2007 hearing. Claimant's counsel did not object to the request, with the understanding that he be permitted to depose additional witnesses within the thirty day period relating to the testimony of Mike Tate. The request to keep the record open for up to an additional thirty days from April 23, 2007 was granted. Counsel for Employer/ Insurer wrote a letter dated May 22, 2007 that was received by the Division on May 23, 2007 advising that they were unable to take or schedule the deposition of Mike Tate, and that the case was now ready for submission and determination. The record in this case was closed on May 23, 2007. Claimant's attorney requested that the Administrative Law Judge take judicial notice of the Division of Workers Compensation's file in this case.

Nicholas A. Marshall requested a 25\% attorney's fee from all compensation awarded.

Stipulations

It was stipulated between Claimant and Employer/Insurer that:

1. On or about July 12, 2004, Mid Continent Industrial was an employer operating under the provisions of the Missouri Workers' Compensation law and that their liability under said Law was fully insured by Hartford Underwriters Ins. Co.
2. On or about July 12, 2004, Gregg Allen Peery was an employee of Mid Continent Industrial and was working under the provisions of the Missouri Workers' Compensation Law.
3. Employer had notice of the alleged injury, and a Claim for Compensation was filed within the time

prescribed by law.

1. The average weekly wage was agreed to be $\ 992.05, and the weekly compensation rate for temporary total disability, permanent total disability, and death is $\ 661.37, and the weekly compensation rate for permanent partial disability is $\ 354.05.
2. Compensation in the amount of $\ 33,068.50, representing temporary total disability benefits at the rate of $\ 661.37 per week for the period July 13, 2004 to June 26, 2005, had been paid by Employer/Insurer.
3. Medical aid in the amount of $\ 16,504.17 had been furnished by Employer/Insurer.

Issues

It was stipulated between Claimant and Employer/Insurer that the issues in dispute to be determined in this case were:

1. Was Employee's death medically causally related to an accident or occupational disease that arose out of and in the course of his employment for Employer, resulting in Claimant being entitled to death benefits, including burial expenses?
2. What is Employer/Insurer's liability, if any, for permanent partial disability benefits?
3. What is Employer/Insurer's liability, if any, for past medical bills?

Claimant offered the following Exhibits which were admitted in evidence without objection:

Exhibit A—September 19, 2005 letter from Dr. Allen Parmet.

Exhibit C—Employee's Death Certificate.

Exhibit D-Employee's and Claimant's Marriage Certificate.

Exhibit F—Heartland Regional Medical bill.

Exhibit I— Medical records.

Exhibit J—Dr. Parmet's CV dated 6-30-05.

Exhibit K—Dr. Parmet's CV dated 1-1-07.

Exhibit L—Answer to Amended Claim for Compensation.

Exhibit M—Answer to Claim for Compensation.

Claimant offered the following Exhibit which was admitted in evidence over the objection of Employer/Insurer: Exhibit N—Photograph of Employee.

Claimant also offered Exhibit B, a letter dated September 19, 2005 from Dr. Parmet, and Exhibit H, a section from the Code of Federal Regulations. Claimant also asked the Administrative Law Judge to take judicial notice of Section 201.322 of the Code of Federal Regulations set forth in Exhibit H.

Employer/Insurer's counsel objected to the admission of Exhibit B and Exhibit H, and to the Court taking judicial notice of Section 201.322 of the Code of Federal Regulations. The Court took under advisement the

offers of these Exhibits and the request to take judicial notice of this federal regulation. Employer/Insurer's objections are overruled. Exhibits B and H are admitted, and judicial notice is taken of Section 201.322 of the Code of Federal Regulations.

Employer/Insurer offered the following Exhibits which were admitted in evidence without objection:

Exhibit 1—Deposition of Dr. Howard Worman.

Exhibit E—Deposition of Dr. Allen Parmet.

Exhibit 2—Dr. Worman Notice of Filing of Medical Report.

Claimant's counsel called Claimant and Dr. Allen Parmet as witnesses at the hearing. No deposition testimony of Employee was offered at the hearing.

This case is brought by Diane L. Peery ("Claimant"), widow of Gregg Allen Peery ("Employee"), a carpenter, who sustained a back injury on July 12, 2004 in the course of his employment for Employer. Employee had conservative treatment until December 28, 2004 when he had an L4-5 microdiscectomy on the left. He continued to have pain and radiculopathy after surgery, and saw two physical medicine and rehabilitation doctors in March and April 2005. He was hospitalized in April 2005 for end stage liver disease. He died on July 4, 2005 at the age of forty-five from liver failure before he had completed treatment of his back injury. He had a history of drinking several beers a day over many years. Employee was prescribed pain medication containing acetaminophen to treat his back injury. Claimant asserts that Employee died from liver failure caused by his taking acetaminophen to treat his back injury, and that she is entitled to compensation for Employee's death. She also alleges that she is entitled to receive permanent partial disability benefits resulting from Employee's back injury. For the following reasons, I deny Claimant's claim for benefits.

Gregg Allen Peery ("Employee") was hired by Employer as a carpenter on June 29, 2004.[1] His wife, Diane L. Peery, ("Claimant"), testified that she took Employee to work on July 12, 2004 and dropped him off. He walked into work with the other guys. He called her before noon and said he needed to go to the clinic because he was hurt. He complained about his rear and down into his leg. He was not able to sit. He had to recline in his seat in the car on the way to the clinic.

Exhibit I contained medical treatment records pertaining to Employee.

Employee went to Heartland Occupational Medicine on July 12, 2004 complaining of cramping in left leg carrying heavy panels at work. He saw Mike Stroud, NP, whose impression was left sciatica. Employee was taken off work and given a prescription for Medrol Dosepak, Skelaxin, and Lortab,[2] one every six hours as needed for pain. Employee returned and saw Richard Campbell, NP, on July 14, 2004. His chief complaint was lumbar spine and left lower extremity. The diagnosis was lumbar strain/pain with left radiculopathy. The plan was to schedule an MRI of the lumbar spine. Medications were continued. Employee saw Dr. David Cathcart at Heartland Occupational Medicine on July 19, 2004. Dr. Cathcart noted that Employee had been having some pain in his back radiating down his left leg and it started after a work-related injury. His impression was lumbosacral strain with probably L5-S1 ruptured disk to the left. He needed an MRI scan. He refilled Lortab 5 mg one or two every four hours as needed for pain. He noted that Employee was unable to work at that time. No history of liver disease was noted in these Heartland Occupational Medicine records.

A handwritten Neurological Examination for Employee dated September 16, 2004 of Patricia Waddell, RN, of Heartland Neurosurgery, noted that on July 12, 2004 Employee was carrying panels, lost his footing and went down and fell on his left hip-buttocks. Medications were noted to be Skelaxin and Lortab 5mg "po Q4."[3] The record noted an MRI of the lumbar spine dated July 26, 2004 revealed a bulge left L4-5. Assessment plan was Celebrex, Neurontin, and physical therapy. Patricia Waddell's September 15, 2004 typewritten report noted that Employee's MRI demonstrated a left disc bulge at L4-5 and degenerative disc disease at L2-3. The Neurologic Patient Self Assessment Form in this record noted that Employee was working at the onset of this problem. He was noted to have been a carpenter for twenty-five years with a tenth grade education. A history of kidney stones was noted.

Heartland Health's Physical Therapy Notes document that Employee had ten physical therapy sessions there between September 27, 2004 and October 28, 2004 that included ultrasound, therapeutic exercise, and spinal traction.

Patti Waddell's October 18, 2004 Clinic Note stated that she saw Employee on that date. He had improved with physical therapy. The Clinic Note stated that Employee was currently taking the Celebrex 200 mg one po bid, and was also taking the Neurontin 300 mg one "po at his", and Lortab prn.[4] The diagnosis was low back pain with left leg radiculopathy and a disc bulge on the left at L4-5. Patti Waddell's November 5, 2004 Clinic Note stated that physical therapy had helped, but Employee was continuing to complain of left foot and left lateral leg pain. The note said that Employee was going to continue his current medications. Dr. John Olson's November 22, 2004 Heartland Neurosurgery Clinic Note stated that Employee came to the clinic that day and complained of pain and paresthesias radiating from his sciatic notch down his left leg. Employee had a focal disc herniation at L4-5 on the left. He was noted to have had several months of physical therapy without any lasting relief. Dr. Olson offered Employee a microdiscectomy at L4-5 on the left.

Dr. John Olson performed L4-L5 microdiscectomy on the left on Employee on December 28, 2004 at Heartland Health in St. Joseph, Missouri. Dr. Olson's diagnosis in the Operative Report dated December 28, 2004 was disc herniation L4-L5 on the left. Dr. Olson's December 28, 2004 Post-op/Discharge Order noted: "5. Discharge medication(s) to be called to patient pharmacy of choice. [X] Hydrocodone 7.5 mg Acetaminophen 500 mg one po every 4-6 hours PRN pain. \#60-0 refills" and "7. [X] Continue home medication." Dr. Olson's Surgeon's History \& Physical dated 12-27-04 noted Medications: "Celebrex 200 mg daily, Neurontin 300 TIP, Lortab 5/500 PRN." A Clinical Lab report dated December 28, 2004 noted that Employee's Alcohol Level was .052\%.

Dr. Olson saw Employee on January 19, 2005. His January 19, 2005 Clinic Note stated that Employee had had no change in his symptoms since his surgery. His symptoms still radiated from his sciatic notch posteriorly down his leg and included the entire leg below the knee as they did preoperatively. The Clinic Note stated that Employee's surgery went well, and Dr. Olson did not see any reason to believe that there was any residual disc or recurrent disc material. Dr. Olson stated that it may have been that the L4-5 abnormality was not really contributing to his symptoms, and he may have direct injury to the area of his sciatic notch. Employee told Dr. Olson that was actually where he fell, and Dr. Olson noted that it may be that Employee had a contused sciatic nerve or musculotendonal injuries in that area that caused further compression of the sciatic nerve in that area. Dr. Olson recommended that Employee see a physiatrist for further evaluation and treatment.

On March 7, 2005, Employee saw Dr. Jennifer Finley, a doctor board certified in Physical Medicine and Rehabilitation, according to her report's letterhead. The section of her report titled "History of Present Illness" noted Employee's history and continued complaints of pain. It also noted, "He has been taking Celebrex and doesn't feel that it is helping at all. He started on Neurontin a couple of months ago and he feels it is helpful. The dose has not been adjusted from his initial prescription and he is tolerating it reasonably well." That section of the report did not mention Lortab. The section of her report titled, "Current Medications" noted "Celebrex 200 mg q day, Neurontin 300 mg tid, Lortab 7.5/500 4 q day." The Social

History noted, "He smokes cigarettes and drinks beer." Dr. Findley's Impression was: "1. Status post left L45 microdiscectomy. 2. Probable chronic left L4-5 radiculopathy. 3. Possible left sciatica secondary to contusion." Her Plan was for him to have EMG testing done of his left lower extremity to distinguish between sciatica and L4 and L5 radiculopathy. She stated that she would like for him to discontinue Celebrex as it had not been helpful, and he had a history of bleeding ulcers and current indigestion. She said she would like him to increase his Neurontin to 300 mg qid. The Plan did not mention Lortab.

The handwritten Confidential Patient Information Sheet Medical History dated March 7, 2005 in Dr. Finley's records contained a section that stated: "Please list all current medications, including dosage, frequency, and duration of use:" The handwritten response was: "Celebrex 200 mg .1 day not helping; neurontin 300 mg 3 day is helping-on / (illegible); lor tab (sic) 7.54 day." Duration of use of lor tab (sic) was not addressed. It was not clear whose handwriting was on the Medical History. The Medical History form also had a section asking if the patient had tried any of certain listed drugs, including ibuprofen, Tylenol, Tylenol \#3, and Lortab. The record did not indicate that he had tried any of those drugs, or any other listed drugs. The Social History part of the form asked, "Alcohol use? (Indicate Quantity). "Yes" was checked and "Beer" was checked, but no quantity was indicated. The form answered "No" to the question, "Have you ever been treated for drug or alcohol addiction?"

Dr. Findley's records contained a report of St. Joseph Imaging Center dated March 21, 2005 of an MRI of the lumbar spine. The MRI report noted that a residual soft tissue defect was seen within the spinal canal in the antero left portion which was displacing the thecal sac posteriorly. There was also a broad based component which extended into the neural foramen and narrowed it mildly. The report noted that it may be touching the nerve. The Impression was postoperative changes at L4-5 on the left with probable residual or recurrent disc material in the antero left bony canal. A handwritten notation on the MRI report dated 3/24/05 noted that Employee needed to follow up with surgeon.

Dr. Finley's Medication Record for Employee identified two medications for Employee in the following table:

The Medication Record did not list or mention Lortab. The Medication Record contained the phone number: "816 232 9096", followed by the word: "(Pharm)."

Employee saw Dr. James Zarr, a Physical Medicine and Rehabilitation doctor, according to his report's letterhead, on April 4, 2005. Employee complained of low back pain that radiated down his left lower extremity. Dr. Zarr's report noted that on July 12, 2004, Employee was performing his usual job duties when he slipped and fell, landing on a concrete wall. Dr. Zarr summarized Employee's medical treatment in his report. He noted that the follow-up MRI scan ordered by Dr. Finley showed a residual disc fragment in the spinal canal at the L4-5 level, which may be touching on the nerve root. He recommended that Employee be reevaluated by Dr. Olson to see if any further surgery was indicated. He stated he would be willing to see Employee after surgery if that was indicated. He stated that if no surgery was indicated, he would recommend a series of lumbar steroid epidural injections at a pain management clinic, followed by a work

hardening program and a functional capacity assessment. He noted that Employee would then be at maximum medical improvement. Dr. Zarr renewed Employee's prescription for Ultram and Lortab. The Lortab renewal was for " 7.5 mg , Disp: 40 (forty), Sig: T po q 4-6 hrs prn pain." The prescription form noted renewal 3 times. Employee was to remain off work until seen by Dr. Olson.

Employee was admitted to the Heartland Health Emergency Room on April 18, 2005. Employee complained of abdominal discomfort since starting Ultram two weeks ago. It was noted to be getting worse. His belly was distended so bad that he could not take a breath now. The Emergency Department Clinical Record noted current medications were: "Ultram prn, Neurontin qid, and Lortab prn." A supplement to the Emergency Department Record dated April 18, 2005 of Dr. Michael Dunlap noted that Employee's chief complaint was abdominal swelling and pain. The record noted current medications were Ultram P.R.N., Lortab P.R.N., and Neurontin. The record stated, "He said he does not take the pain pills excessively." Extremities were noted to be grossly unremarkable except for poor skin turgor, and a suggestion of jaundice. Blood alcohol level was noted to be "62". Dr. Dunlap's impression was acute ascites, [5] etiology to be determined.

Heartland's History and Physical dated April 18, 2005 of Dr. Ronald Kempton noted that Employee presented to the emergency room with abdominal pain and swelling, and had increased swelling of the abdomen over the last three or four weeks. The record stated, "He does admit that he drinks eight to ten beers most nights and sometimes more, sometimes less . . . and has been drinking like this for at least the last decade." Medications prior to admission were noted to be Ultram, Lortab, and Neurontin. Dr. Kempton's impressions were: 1. Abdominal pain; 2. Ascites; 3. Hyponatremia;[6] and 4. Electrolyte imbalance to include hypokalemia.[7]

A Heartland Health Physician Order dated April 18, 2005 stated: "Do not start Neurontin or Lortab." Heartland's Health Information Report for medications and IV's for the period April 18 to April 25, 2005 did not identify Lortab or acetaminophen. Heartland Health's Health Information Report Admission Profile dated April 18, 2005 refers to "meds taken at home: medication history: Neurontin 500 mg a(?)ID, Lortab 7.5 every four hours for pain, Ultram 50 mg every four hours pain." The Admission Profile also refers to "Home Health Patterns/Miscellaneous History: Alcohol: Yes, How many drinks per week? 42 (six daily)." Heartland Health's April 18, 2005 Radiology Report-- Abdominal Ultrasound Findings noted, "The liver is echogenic and relatively small. Suspect that this represents cirrhosis." The impression was: 1. Probable hepatic cirrhosis; 2. Moderate free-flowing ascites. Heartland Health's April 18, 2005 CT of the abdomen noted an impression of: "Hypodensity and irregularity of the liver. There is a large amount of ascites. These findings are most likely secondary to hepatic failure. No definite focal masses are visualized."

Dr. McCormick's Consultation Report dated April 18, 2005 in the Heartland Health records noted that Employee sits around home most days and drinks admittedly six to eight beers on a day, maybe ten to twelve on weekend. The Consultation Report noted that in general, Employee was an ill-appearing, jaundiced white male. Dr. McCormick's impression was: "1. probable alcoholic cholestatic hepatitis, cirrhosis, and ascites. 2. New-onset ascites probably from his alcoholic cholestatic cirrhosis, but we want to rule out any kind of peritonitis spontaneous. 3. Subclinical encephalopathy. 4. Hyponatremia and hypokalemia probably due to his fluid overload. Protein-calorie malnutrition. 5. Chronic back pain."

Employee was discharged from Heartland Health on April 25, 2005. Heartland's Discharge Summary of Dr. Kempton dated May 15, 2005 identified the following discharge diagnoses: 1. abdominal pain; 2. ascites; 3. hyponatremia; 4. electrolyte imbalance; 5. end-stage liver disease; 6. electrolyte imbalance; 7. anemia; 8. confusion; 9. portal systemic encephalopathy; 10. alcoholic cholestatic hepatitis; 11. subacute bacterial peritonitis; 12. cirrhosis; 13. hypokalemia. The Discharge Summary noted that Employee had a long history of alcohol abuse. He was admitted and continued to have severe pain. An EGD, as well as abdominal ultrasound, and CT of the abdomen, were all noted to be consistent with end stage liver disease.

He was placed on medical management with poor prognosis, and discharged to home with hospice.

Dr. Olson saw Employee on May 9, 2005. Dr. Olson's record noted that Employee continued to have the same pain he had preoperatively in the back and his leg roughly in the L5 distribution. Repeat MRI scan showed excellent anatomical results. Dr. Olson noted that there did not appear to be any entrapment of the nerve root or any remaining compression. The record noted that he thought the MRI showed excellent anatomical results. Dr. Olson stated that he suspected Employee had injury to the sciatic nerve in the location of his sciatic notch when he fell backwards, and the spinal canal abnormalities were actually not the cause of his problems. Dr. Olson did not have any further surgical treatment to offer Employee on May 9, 2005. He noted that Employee had not had any clinical improvement at all since his surgery. He assessed persistent radiculopathy, but offered no further treatment for that.

Dr. Olson's May 9, 2005 Clinic Note also stated that unfortunately Employee had had liver failure develop in the interim, and still uncertain as to the etiology of that liver failure. Dr. Olson's Note stated that it did not appear that Employee had had either any previous alcoholism or substance abuse by the history he gave them. The note stated that in terms of a cause of his liver failure, he was really not sure what had caused that. Dr. Olson noted that Employee was taking Lortab for an extended period of time. He noted that it appeared from his records that Employee had a safe dose of Lortab, and only took it on an occasional basis, albeit for several months. Dr. Olson noted that Employee did take less than the maximum dose of acetaminophen with that medication during that time. His May 9, 2005 Clinic Note stated that, "Unless he had previous liver injury, I do not see that the amount of Tylenol we gave him in his Lortab was related to his liver failure, so I am really at a loss at this point as to what the cause of his liver failure actually is." Dr. Olson stated that he did not have any further surgical treatment to offer Employee, and he apparently had disabling pain in the sciatic distribution, and that appeared to have resulted from his fall at work, so he thought that was clearly related. His May 9, 2005 Clinic Note further stated, "Unfortunately his liver failure, the origin of this is unknown."

Before his work injury, Employee was treated for back complaints in June 2004 by Dr. Harold Turley. Exhibit 1 also included records of the Plattsburg Medical Clinic and Dr. Harold Turley. Dr. Turley's record dated June 4, 2004 noted that Employee was 44 years old and weighed 170 pounds. The record noted under "chief complaint": "moving hide-a-bed 8d ago-felt "something" c/o sharp pain $\downarrow$ left leg all the way to the foot." Employee was noted to have complained of pain down posterior left lower extremity and paresthesia into the left foot. He denied weakness. He had marked tenderness in the lower lumbar region. The doctor's assessment was lumbar disc process with nerve involvement. He prescribed Celebrex bid and Lortab 7.5 \#20 PRN. Employee was to return in two weeks. Hydrocodone, generic for Lortab, was prescribed with one fill authorized. Directions were take one tablet by mouth every eight hours as needed. Dr. Turley saw Employee on June 22, 2004. His record noted that the Lortab was gone. Pain and numbness continued down the left lower extremity but were less. Employee reported no pain in foot but continued paresthesia. Dr. Turley's assessment was lumbar disc disease, improved. The record noted that Employee was to continue Celebrex and Lortab. The record stated, "Of note, patient had not picked up last RF from 6/15 yet."

Employee treated with several doctors from June 4, 2004 through May 9, 2005. Prescriptions were provided for medication containing acetaminophen by various providers. [8]

Claimant testified that she was the widow of Employee. She had not remarried. She and Employee were married on May 30, 1999 in Stewartsville Missouri. Employee built a house for them over three years beginning in 2000. They had no children. Employee had no children. In 2004 and 2005, Employee had no dependents other than her. No one was financially dependent on Employee besides her. She and Employee were best friends and spent all of their time together when they were not working. She observed him daily.

She stated that before July 12, 2004, Employee was great and felt fine. After July 12, 2004, he was hurt, could not control his bowels, and was unable to have marital relations. He did not have those problems before July 12, 2004. Before July 12, 2004 he was six feet tall, weighed 170 pounds, was healthy, and was handsome and muscular. He was very proud of his body and wore short sleeve shirts. He was a union carpenter. Before his July 12, 2004 injury, he helped friends build things, including porches, in his free time. She and Employee fished, took walks, and trapped raccoons. After his injury, he was slower to get around. He stretched out on a recliner. He still went for rides, but bumps in the road hurt him.

Claimant stated that Employee usually drank at least eight beers per night and averaged between eight beers and ten beers per night. She said that he usually drank five nights per week. He did not drink alcoholic beverages other than beer. He did not show physical effects from drinking. It loosened him up. He was able to throw a tomahawk into a tree and make it stick while drinking. After he had surgery December 2004, he gradually went downhill. He was not as muscular. He had swelling in his abdomen in April 2005, and the pressure hurt him. He did not have yellowing of his skin before April 2005. His beer consumption did not change after the July 12, 2004 accident. He went to the hospital on April 18, 2005. He drank less after that.

Claimant stated that Employee took his medications as prescribed. She filled his prescriptions for him at Wal-Mart. No prescription records from Wal-Mart were offered in evidence. She identified Exhibit F, Employee's funeral bill in the amount of $\ 7,653.10, and testified that she paid that bill.

On cross examination, Claimant stated that Employee hurt the middle of his back in June 2004 while he was moving a bed. He saw Dr. Turley for that. That injury did not keep him from doing anything. He was not working in June 2004, but he was able to work. He had only two visits with Dr. Turley. She did not recall if he was taking prescription medications in June 2004. Some days he drank less than eight to ten beers per day, and other days he drank more than eight to ten beers in a day. Employee did not take more Lortab than was prescribed by the doctor. Claimant was not aware of any prior back injury of Employee besides the June 2004 bed lifting incident. He had not had back surgery before December 2004. He had not had any prior workers' compensation claims. He was very careful. She had no knowledge of Employee drinking on the job. Employee had worked for Employer prior to the July 12, 2004 injury, but she did not recall exactly when he started working for Employer. Employee was still having back problems prior to April 2005. Between July 2004 and April 2005, Employee could not do household chores. Before July 2004, he was very helpful. He moved furniture while she swept carpets.

Claimant's and Employee's Marriage Certificate, Exhibit D, noted that they were married on May 30, 1999. Employee's Certificate of Death, Exhibit C, noted that Employee died on July 4, 2005. The immediate cause of death identified on the Certificate of Death was "liver failure."

Medical Experts

Dr. Allen Parmet

Dr. Allen Parmet testified in person on behalf of Claimant at the April 23, 2007 hearing in this case. Dr. Parmet's deposition taken on April 2, 2007 was admitted as Exhibit E. He is board certified in aerospace medicine and in occupational medicine, and is certified as a medical review officer by the Department of Transportation. He is a member of the AMA, the American College of Occupational and Environmental Medicine, Euro Space Medical Association, and the American College of Public Health. He is on staff at St. Luke's Hospital in Kansas City, and consultant at Research. He is on the faculty at the University of Missouri Kansas City, the University of Kansas, and Wright State University in Ohio. He has completed all of the course work for his Ph.D. in toxicology, but has not submitted his thesis. He does primarily occupational and aerospace medicine and consulting. He has testified on behalf of employers and employees in workers compensation cases. He reviewed the medical records pertaining to Employee that are contained in Exhibit

Dr. Parmet was aware that Employee died on July 4, 2005 at the age of forty-five. He identified Employee's death certificate, Exhibit C. Exhibit C identified the immediate cause of Employee's death as: "Liver failure." Dr. Parmet stated that within a reasonable degree of medical certainty, the cause of Employee's death was liver failure due to hepatic toxicity. He stated that hepatic toxicity is a term for poisons that disable and destroy the liver. He stated that there can be more than one toxin or a single toxin doing that, but the result is liver cells dying, and because this is an essential organ, if the liver dies, you die.

Dr. Parmet described the history of Employee's medical treatment beginning on June 4, 2004. He testified that Lortab is a pain reliever, and the only reason to prescribe that is pain control. He testified that what happened on July 12, 2004 was a substantial factor in what caused Employee's pain. He was not sure which diagnosis was correct. He noted there were two being entertained at the end--one, the herniated disc, and the other, direct trauma to the sciatic nerve, which anatomically can take place within about an inch or so of each other. Employee did not get pain relief after the surgery, which you normally do after a successful surgery. The anatomical correction was quite good. There may have been an injury directly to the sciatic nerve, although sometimes they do see a disk herniation that does not improve even when you correct it.

Dr. Parmet testified that if you have an alcoholic with pain, they often drink more after surgery or after whatever is causing pain. He did not disagree with Dr. Olson's May 9 conclusion and opinion where he stated, "In any case, I do not have any further surgical treatment to offer him. He apparently has disabling pain in the sciatic distribution and this appears to have resulted from his fall at work so I think that is clearly related." Dr. Parmet noted that the surgery did not relieve Employee's pain.

Dr. Parmet testified that this hepatotoxin would cause damage greater than what you would get from just alcohol, and alcohol and acetaminophen caused more damage than either one alone. He stated that alcohol and acetaminophen are liver toxins, and that acetaminophen is a much more potent toxin than alcohol, and they are synergistic in their effect. He stated that Employee's liver was functioning normally at the time of surgery in December 2004. He noted that the enzymes were not elevated and the other body functions regulated by the liver were in order. He said the signs and symptoms of decreased liver function and liver abnormalities were first really detected in April 2005. He thought that Employee's chronic intake of prescribed acetaminophen was a very substantial factor of his death and an accelerator of his liver failure. He stated it was not the sole cause, but it certainly accelerated it. He thought the damage was on top of the prior damage, and was synergistic with a continuing alcohol use. He stated that acetaminophen created damage in and of itself.

Dr. Parmet also testified that it was impossible to say to what extent acetaminophen contributed to the end stage liver disease versus the alcohol. He stated he could not, to a reasonable degree of medical certainty, apportion how much was alcohol and how much was acetaminophen. He thought it was substantial, and noted that Employee's decline was unusually a rapid. He stated that when an alcoholic goes into liver failure, they usually almost invariably go in and out, over a series of years. He stated they do not present as Employee did with normal liver functions, and four months later, have liver functions of end stage failure and cirrhosis, and then die two months later. He acknowledged that he did not have specific training in hepatology. He stated he had seen patients with chronic hepatitis, but he was not actively treating patients for alcohol induced cirrhosis. He stated that it would be difficult to know one way or another whether Employee was taking the prescribed dosages of acetaminophen. He said he did not see evidence of Employee running out early and going in for refills.

He defined the term "substantial factor" to mean "a significant percentage." He stated he would not quantify it, but thought a significant amount of Employee's liver damage and the acceleration of his liver failure was due to consumption of the acetaminophen during this period while he was also consuming alcohol. When asked what was significant, Dr. Parmet responded that Employee's decline was immensely

rapid. He stated you do not see people go down the tubes this fast. He thought the only reasonable explanation was the acceleration caused by the synergy with acetaminophen. He said he did not think it was fifty percent, but it would be more than ten. He also stated that a low BUN would not catch anybody's attention at the time of surgery. He also stated that acetaminophen is a renal toxin and kills kidney cells.

Dr. Parmet agreed that Employee was felt to have alcoholic cirrhosis when he appeared in the emergency room on April 18, 2005. He agreed that alcoholic cirrhosis comes from many years to decades of heavy drinking rather than just a year's period of time. By definition, alcoholic cirrhosis is due to chronic alcohol use. He thought that Employee's cirrhosis probably was long-standing. He stated there was no other way to explain his demise except that he had cirrhosis for a very long time. Employee also developed kidney failure, and that would also be common in individuals with cirrhosis and end stage liver disease.

Dr. Parmet agreed that there was no evidence to suggest that Employee was taking an amount of acetaminophen in excess of what was prescribed. He noted that from the medical records, three grams per day appeared to be about the prescribed dosage. He stated that acute exposure meant something taken with a single dose within the course of about twenty-four hours. He said most of his personal work had not been looking at acute doses. Chronic dosing meant exposure for more than two weeks to any particular agent. The effects of chronic dosing of more than two weeks exposure are not understood because the toxin continues to be converted. He said that acetaminophen is synergistic with alcohol. On an acute basis the lethal dose is much, much lower. On a chronic basis, alcoholics with liver disease will have liver failure. He stated that basically acetaminophen should not be given to alcoholics, or the dose absolutely minimized. He noted that the interaction of continuing use of acetaminophen, at the less than lethal acute dose, undoubtedly led to a chronic hepatoxicity (sic) due to the toxic metabolites formed by acetaminophen in the presence of the cirrhosis. He stated that the toxin was going to accelerate the liver disease, and that had never been quantified. He said it is going to accelerate the liver disease, but the increased degree of damage that is occurring is not exactly precisely known. He stated that he could not offer within a reasonable degree of medical certainty to what extent the ingestion of Lortab combined with the alcohol would have led to the end stage liver disease, or accelerated the end stage liver disease. He said he could not be precise as to how much additional damage occurred, but he could say it was contributing.

Dr. Parmet said in his deposition that he had reviewed the medical report of Dr. Howard Worman. He stated most people would disagree with Dr. Worman's opinions of the safety of acetaminophen being non-toxic. He stated it is a hepatic toxin. He did not agree that it was safe for an active alcoholic to take acetaminophen. He said he was aware of numerous reports demonstrating that ingestion of acetaminophen by alcoholics causes and precipitates liver failure. He agreed that he did not cite any specifically in his report. He was surprised that somebody would decide that acetaminophen was not even a liver toxin. He acknowledged that he had not had any specific studies in hepatology.

Dr. Parmet's September 19, 2005 report, Exhibit A, summarized his review of the medical treatment records of employee. The report noted Dr. Parmet's diagnosis was "liver failure due to haptic toxicity." He noted in his report that Dr. Olson discharged employee on a prescription for Lortab, which contains 500 mg of acetaminophen, equivalent to one extra strength Tylenol. The report stated that acetaminophen is a liver toxin. The report stated that the acute lethal dose of acetaminophen falls to four grams in individuals who consume alcohol. The report noted that if taken as prescribed when discharged from hospital, on December 28, 2004, Employee would have been taking as much as three grams of acetaminophen daily. The report stated,

However, the interaction of continuing use of acetaminophen, at the less than lethal acute dose, undoubtedly led to a chronic hepatotoxicity due to the toxic metabolites formed by acetaminophen in the presence of the cirrhosis. The continuous pain following surgery would have caused Mr. Peery to take his prescribed analgesic medications and undoubtedly, as all alcoholics do, to have increased his alcohol consumption. By the time Dr. Zarr was apprised of the alcohol situation, I think the continued use of acetaminophen as an

analgesic was far too late to have affected any outcome, since the admission two weeks later indicated that he was already at the endstage liver failure.

In conclusion, the chain of events that began with his on-the-job injury of July 12, 2004 lead to reasonable medical treatment at the time, which, unbeknownst to his providers, complicated the pre-existing but concealed alcohol abuse history. Thus, the treatment for his occupational condition inexorably contributed to his demise.

Dr. Parmet authored two reports dated September 19, 2005, Exhibits A and B. Dr. Parmet's second report further stated that the acetaminophen in Employee's medications used to treat his pain contributed to his liver injury and ultimate death. The report stated that Dr. Parmet could not quantify the degree of acceleration or increased the injury due to his use of acetaminophen. The report stated that there is no proven safe dose of acetaminophen in an active alcoholic.

Dr. Parmet's supplemental report, Exhibit B, which was authored in February 2007, was incorrectly dated September 19, 2005. The permanent partial disability rating contained in Exhibit B was given within a reasonable degree of medical certainty. The objections to Exhibit B are overruled, and Exhibit B is admitted in evidence.

Dr. Parmet testified at the hearing that there was a range of twenty to thirty percent body as a whole permanent partial disability concerning Employee's back injury. He based that on years of doing these kinds of disability evaluations. He said he had many thousands of cases in Missouri. He said his rating was within a reasonable degree of medical certainty. Dr. Parmet stated the range of twenty to thirty percent body as a whole disability was based on a number of factors. First, it was the range of the sort of symptom complex and physical findings that Employee had compared to individuals that he had seen, treated or supervised over many years, and understanding how the workers' compensation works in this state. He noted that Dr. Turley suspected the disc. He noted that Dr. Olson operated on the disc, but some of the symptoms were now suggestive to come from the nerve, from later trauma. Employee may have had both at the same time. Employee did have a herniated disc. You can have a herniated disc with no symptoms, or with symptoms, and you can have sciatic trauma with symptoms, same time, same place causing so-called "double crush." Employee reported in June to Dr. Turley's office describing lower extremity pain. That could be consistent with lumbar problems such as at the L4-L5 level, or potential sciatic nerve problems.

Dr. Parmet stated that he was not prepared to offer any opinion to a reasonable degree of medical certainty as to what portion of the disability would be related to any sciatic conditions. His range of disability was based upon the range that he would see within an individual with this symptom complex and physical limitations. He stated that Employee was not fully evaluated and treated at the time of his demise. He said that it was conceivable with additional treatment Employee might have reached a level and plateaued in the area that far reduced the terms of disability.

Dr. Parmet testified on cross-examination in his deposition that he was not referred to this case until after Employee was deceased, and that all of his opinions were based purely on medical records review. He was not precisely clear as to what Dr. Turley meant when he said on January 4, 2004 (sic) that he felt Employee had lumbar disc process. He did not apportion any of Employee's disability to a pre-existing component prior to July 12, 2004 because he did not have any indication that it was continuing to exist at the time of the July 12, 2004 injury. Dr. Parmet also testified on cross-examination that on the date of his death, Employee was still temporarily and totally disabled based solely on his back conditions. He felt that further treatment was warranted. He testified that additional treatment would potentially cause Employee to be less disabled. He stated that the twenty to thirty percent range assumed that Employee's condition would not improve. He agreed that additional treatment could potentially decrease the level of Employee's disability. He said that if Employee's condition was purely a disc, Employee should have been relieved of symptoms. He said that happens ninety percent of the time. He noted that Employee still had some symptoms when he saw Dr.

Turley on June 22, 2004.

Dr. Parmet's second report, Deposition Exhibit 2, stated that the permanent partial disability was difficult to assess since he did not personally examine Employee. He stated that Employee had ongoing pain and limitations which prevented him from returning to duty continuously up to the time of his death. Had those clinically remained stabilized and not improved, Employee would have had a residual permanent partial disability in the range of twenty to thirty percent of the body as a whole. He stated further, "It is conceivable that with further treatment, he would have been much less disabled, but I would be speculating beyond reasonable certainty to assign a value to an ultimate outcome."

Dr. Howard Worman evaluated this case for Employer and Insurer. His deposition taken on April 5, 2007, Exhibit 1, was admitted in evidence. Objections contained in Exhibit 1 are overruled. Dr. Worman's report dated February 2, 2007 contained in Exhibit 2 was also admitted in evidence. Dr. Worman is employed by Columbia University, New York, New York as associate professor in the department of medicine and the department of anatomy and cell biology. His teaching responsibilities at Columbia include teaching fellows hematology in the liver clinic, lecturing first-year medical students on the liver and biliary system, and lecturing second year medical students on various aspects of liver disease. His curriculum vitae ("CV') and bibliography were marked as Deposition Exhibit 1. His CV is twenty-five pages long. He received a bachelor's degree from Cornell University in 1981, and was Phi Beta Kappa. He received an M. D. degree from the University of Chicago in 1985. He is board certified in internal medicine. He has been active in the American Association for the Study of Liver Diseases since 1991, and was on the editorial board of their journal Hepatology from 1994-2006. He directs care for patients roughly twenty percent of his time. Most of his inpatient care is liver disease, including end stage liver disease. That includes acute or sudden liver failure cases.

Dr. Worman has been a web master and editor for the online publication, Diseases of the Liver. He has served as a committee member for the American Association of the Study of Liver Disease. His CV identifies thirty-eight Research Grants, Contracts, and Fellowships. It identifies three sponsored clinical trials in which he had participated as an investigator. He has been an Ad-Hoc Reviewer for numerous medical journals and foundations. The CV identifies seventy-nine original peer reviewed articles that he has co-authored, eight case reports/short clinical studies that he has authored or co-authored, and fifty reviews, chapters and editorials that he has authored or co-authored, including Worman, H. J. Cellular intermediate filament networks and their derangement in alcoholic hepatitis. IAlchol. Clin. Exp. Res. 1990;14:789-804. He is the senior author or co-senior author of three books, namely, The Liver Disorders Sourcebook (1999), The Hepatitis C Sourcebook (2002), and The Liver Disorders and Hepatitis Sourcebook (second edition)(2006). The CV identifies forty-eight featured speaker or section chair at national/international meetings, including, for example, World Chinese Congress of Digestion, invited plenary speaker on "Molecular Biology and the Diagnosis and Treatment of Liver Diseases," Oct. 1998, Beijing, China. The CV also identifies 124 invited lectures from 1988 to 2007 on a variety of topics including primary biliary cirrhosis, Hepatitis C, and autoimmune liver diseases.

Dr. Worman reviewed Employee's medical records. His report noted Employee's medical and employment history and past medical history. It noted that Employee likely consumed alcohol at an amount of approximately six to twelve drinks a day. The report discussed Employee's medical treatment beginning on June 4, 2004 to his death on July 4, 2005.

Dr. Worman's report stated that Employee had alcoholic liver disease. Dr. Worman noted that Employee had alcoholic cirrhosis, and in April of 2005, also alcoholic hepatitis. The alcoholic cirrhosis was noted to be a result of many years, probably decades, of heavy drinking. He noted that Employee reported drinking six to eight and sometimes ten to twelve beers a day.

Dr. Worman noted that alcohol generally leads to three pathological processes in the liver, which can occur together and at the same time in the same patient. These are fatty liver, alcoholic hepatitis, and cirrhosis. Hepatitis is inflammation of the liver. Alcoholic hepatitis can range from mild to significant liver dysfunction with complications such as jaundice, hepatic encephalopathy (neurological dysfunction caused by liver failure), ascites (fluid accumulation in the abdomen), esophageal varices, abnormal blood clotting, and coma. He noted that alcoholic hepatitis very frequently occurs in alcoholics who have underlying cirrhosis of the liver, especially during times of increased drinking. He noted that cirrhosis is fibrosis (scar tissue) combined with widespread nodules in the liver. He noted that cirrhosis develops only over many years and can lead to end stage liver disease, in which the liver irreversibly fails to function properly. He noted that kidney failure also often occurs in individuals with advanced cirrhosis.

Dr. Worman stated that, "To the highest degree of medical certainty, Mr. Peery had cirrhosis prior to his seeking medical attention in 2004." He noted that Employee had a blood urea nitrogen (BUN) concentration of $1 \mathrm{mg} / \mathrm{dl}$ on December 28, 2004. He noted that one of the few causes, if not the only cause, of a low BUN concentration is severe liver disease. He stated that Employee had alcoholic cirrhosis and concurrent alcoholic hepatitis in March 2005. He had alcohol in his blood, demonstrating that he was actively drinking. Dr. Worman noted that several factors supported the fact that Employee had long-standing cirrhosis in March 2005. Ultrasound and CT imaging both showed a small liver. He had a significantly low blood albumin concentration which usually becomes so low with long-standing liver dysfunction. He also had muscle wasting and abnormal connections between the veins draining the gut and the veins draining the skin, both of which occur in long-standing cirrhosis.

Dr. Worman stated that there was no evidence that chronic use of acetaminophen, especially at recommended doses as prescribed to Employee, causes or contributes to chronic liver disease. He stated there was no evidence that the hydrocodone at the doses prescribed to Employee caused or contributed to chronic liver disease. He said there was no data proving that taking Tramadol at the doses prescribed to Employee could be a contributing factor in the development of end stage liver disease. He stated that the prescribed intake of Lortab and the other pain management drugs did not contribute to Employee's death. He stated Employee's death resulted from alcoholic liver disease. He noted that although overdose of acetaminophen, generally at a dose of $250 \mathrm{mg} / \mathrm{kg}$, can cause liver damage and acute liver failure, there are no studies demonstrating that chronic intake of acetaminophen or any of the other medications Employee received contribute to the development of end stage liver disease in an individual with another chronic liver disease, such as alcoholic cirrhosis. He said there are no studies showing that taking acetaminophen for a year at recommended doses (up to 4 grams a day) leads to the development of end stage liver disease. He said the only randomized, double-blind clinical trial has shown the opposite, that a daily dose of 4 grams of acetaminophen for a year is safe. He noted that it is well established that 10 drinks a day can cause alcoholic hepatitis, and over the long term, cirrhosis.

Dr. Worman stated that assuming Dr. Parmet's diagnosis was liver failure due to hepatotoxicity due to acetaminophen or other drugs Employee was taking, Dr. Parmet's diagnosis was incorrect. He stated that while overdose of acetaminophen (generally $250 \mathrm{mg} / \mathrm{kg}$ dose) can be hepatotoxic and cause acute liver failure, there is no credible scientific evidence that recommended doses of acetaminophen can cause liver failure. He also stated that there is no credible evidence that chronic consumption of acetaminophen at recommended doses is harmful to the liver. Dr. Worman also stated that he was unaware of any data to support Dr. Parmet's statement, "In individuals who consume alcohol, the cytochrome P-450 system is activated and becomes the predominant method of metabolizing acetaminophen." He also stated that he was unaware of any study showing that the "acute lethal dose" of acetaminophen is four grams under any circumstances. Dr. Worman cited a study supporting the statement that there is credible scientific evidence proving that four grams of acetaminophen a day is a safe dose in individuals who consume alcohol. He also noted that Employee did not suffer from "acute lethal" liver disease, but from a chronic progressive liver disease.

Dr. Worman stated that it was pure speculation for Dr. Parmet to write, "The interaction of continuing use of acetaminophen at the less than lethal acute dose, undoubtedly led to a chronic hepatotoxicity due to the toxic metabolites formed by acetaminophen in the presence of the cirrhosis." He noted that Dr. Parmet did not specify what those "toxic metabolites" were, nor did he provide a rational scientific explanation as to how they can cause "chronic" hepatotoxicity.

Dr. Worman concluded that to the highest degree of medical certainty, Employee died from complications of cirrhosis, which developed as a result of many years of excessive alcohol consumption. He noted that the natural history of Employee's liver disease was typical for someone with alcoholic hepatitis and cirrhosis. He further concluded, "Based on the available medical records, there were no factors other than excessive consumption of alcohol that contributed to his developing end stage liver disease or that led to his death."

Dr. Worman identified Deposition Exhibit 2, his Medical Opinion pertaining to Employee. He discussed Employee's medical treatment noted in the records. Employee had a low BUN concentration at the time of his surgery. That indicated that the liver was not functioning, was not able to turn the nitrogen into urea. He noted that Dr. Zarr's record of his April 4, 2005 examination indicated that Employee reported drinking eight to ten beers a day. He discussed lab findings from Employee's April 18, 2005 hospitalization and noted that he had slightly elevated white blood count which can be elevated for many reasons, including alcoholic hepatitis or inflammation of the liver from alcohol. Employee's hemoglobin was slightly low because he had alcoholic liver disease. His prothrombin time was slightly prolonged which was suggestive that the liver might not be functioning properly. His blood alcohol concentration was sixty-two milligrams per deciliter. He had elevation of AST and ALT enzymes. The AST was more than two times the ALT which indicated that the liver damage was from alcohol. He had albumin concentration that was quite low. The albumin is usually low in a chronic liver disease. Dr. Worman testified that if your liver just failed three or four days ago, your albumin may be normal, but it becomes usually low in cirrhosis, where the liver is not working over time. He had a low sodium concentration. One reason for that is liver failure, when the liver is not working well.

Dr. Worman testified that chronic liver disease is liver disease lasting longer than six months. He said that Employee had an underlying serious liver disease. He had longstanding liver disease that was for years, and probably progressive over years and decades. He testified that Employee's case is almost a medical school presentation. Someone drinks and drinks and never realizes he is sick, and then presents in the emergency room with abdominal swelling, with fluid in the abdomen from the failing liver. He noted that Employee had muscle wasting which you see in people who have chronic liver disease. If your liver failed now, your muscles would not be wasting in days or weeks. Dr. Kempton had noted capul medusa which develops in chronic liver disease, almost always in people with cirrhosis. Employee's liver was small. That was consistent with chronic, not acute, liver disease. The CT scan showed a small and irregular liver which is suggestive of cirrhosis. Employee had very significant and advanced liver disease at that time. Dr. Worman thought this was one hundred percent text book case of alcoholic hepatitis and cirrhosis. He found nothing from the medical record which that suggested that Employee was using acetaminophen above the prescribed dose, which would be the safe dose. He stated that lab findings on May 9 indicated a combination of failing liver and failing kidneys. He agreed with the death certificate listing the cause of death as liver failure. He also stated that Employee probably had failing kidneys secondary to a failing liver.

Dr. Worman testified that his main conclusion was that Employee had cirrhosis secondary to excessive alcohol consumption, and that he very likely had cirrhosis for several years. He also believed that when Employee presented in March or April to the emergency room, he had a component of increased hepatitis, on top of cirrhosis, which was probably caused by increased alcohol consumption, a little bit before that time. He testified that there is no evidence in the literature or elsewhere from scientific studies that he had heard of where chronic use of acetaminophen contributes to the development or the progression of a chronic liver disease. He also considered the other drugs Employee was taking, and he did not think that Tramadol

contributed. He concluded that alcohol contributed one hundred percent to Employee's liver disease. He also testified that acetaminophen causes or can cause liver disease in acute overdoses. He noted that was well established to people who take established doses, maybe in the range of fifteen to twenty grams, as overdose 250 milligrams per kilogram is the number often cited in the literature that can cause acute liver disease in some people. He defined acute to mean "all of a sudden, fast." He stated that it meant like, if right now you took twenty grams of acetaminophen, there was a chance that three days later your liver would be failing.

When asked if Employee took Lortab at or below the prescribed level, would that be a significant contributing factor to the acceleration of development of the liver disease, Dr. Worman testified that he did not believe so. He stated that there is no evidence or data to say that can happen or how that can happen. When asked if Employee was taking Lortab and acetaminophen, which would have been for a year prior to his death, in conjunction with alcohol, did that increase or accelerate the possibility for development of end stage liver disease or liver failure, Dr. Worman stated that there is no literature to say that can happen or how that can happen. He stated that he could not see how that could have affected his progression. He stated that the dosages that Employee took should not be harmful.

Dr. Worman testified that it was pure speculation for Dr. Parmet to state that the continuing use of acetaminophen at a less than lethal acute dose undoubtedly lead to a chronic hepatotoxicity due to the toxic metabolites formed by acetaminophen in the presence of the cirrhosis. He noted that Dr. Parmet had not specified the toxic metabolite. Dr. Worman stated there was no study, data, or experience that Dr. Parmet could give to support that speculation. He said he agreed that there is no way to quantify if there is any damage done from taking alcohol and represented doses of acetaminophen over time. He did not think one ethically could. The anecdotal reporting was uncontrolled. Dr. Worman stated that there was no data, no experience, nothing to support Dr. Parmet's statement that the interaction of continuing use of acetaminophen, at the less than lethal acute dose, undoubtedly led to chronic hepatotoxicity due to the toxic metabolites formed by acetaminophen in the presence of the cirrhosis. He stated that was speculation.

Dr. Worman concluded that, within a reasonable degree of medical certainty, Employee died from liver failure, which was secondary to alcoholic cirrhosis, and that there were no other contributing factors.

Dr. Worman testified on cross-examination that in the records he had, there were no documented physical exams or history signs that Employee had cirrhosis prior to his surgery on December 28, 2004. There was no record prior to the surgery of portal hypertension, jaundice, encephalopathy, cachexia, muscle wasting, or esophageal varices. Employee had worsening symptoms approximately three months after the surgery in April 2005. He acknowledged that a low protein diet can lower your BUN, but not to a level of one. He acknowledged that severe malnutrition can lower your BUN. He agreed that BUN can be affected by things other than the liver. He acknowledged that the liver can be damaged in multiple ways. He said a classic example may be somebody who has chronic viral hepatitis and drinks a lot of alcohol. He stated that in his opinion, Employee did have cirrhosis prior to seeking medical attention in 2004. He agreed that an overdose of acetaminophen, at once, can cause liver disease. He stated that most people would say an overdose is 250 milligrams, body weight, and in a person, there is some controversy, a little more, a little less.

Dr. Worman was asked if the amount of acetaminophen overdose average was not decreased for any condition. He answered that there was no data that it actually was or was not. He stated there are anecdotal reports in the literature that people who drink alcohol have had an acute liver injury when taking lower doses. He stated that the mechanism that causes acetaminophen to be harmful at the overdose level that is in most textbooks, and is believed by most people, is, most of it is metabolized and eliminated by conjugation. There is a small amount that is metabolized by the cytochrome P-450. Having a little bit of that around normally does not matter because it does not stick around as a toxic intermediate that is metabolized almost immediately with glutathione. When you take an overdose, you produce more of a toxic metabolite

than a glutathione can reduce, and that causes acute liver injury.

Dr. Worman agreed to a large extent that we do not know exactly how alcohol damages the liver. He thought there is very good epidemiological evidence that alcohol can damage the liver. There are hundreds or thousands of studies. When asked, "It's just that we can't say exactly how it's done?", he answered that he would say molecular mechanism. He acknowledged that the FDA requires an alcohol warning on Tylenol and other forms of acetaminophen as well as aspirin, ibuprofen, and many over-the-counter drugs. He agreed that Lortab is a combination of hydrocodone and acetaminophen. He was asked to read the label on Tylenol. He prefaced his answer by stating that Tylenol is a particular product sold over-the-counter, and Lortab as prescribed by doctors may not be applicable to a drug being prescribed by a physician. The label states: "Uses warning, alcohol warning, if you consume three or more alcoholic drinks a day ask your doctor whether you should take aspirin or other pain relievers or fever reducers, as acetaminophen may cause liver damage."

Dr. Worman acknowledged that the patients in the Kuffner study cited in his report did not receive any acetaminophen until the alcohol had been eliminated from the patient. He did not disclose in his report that the study was performed by those who received compensation from the makers of Tylenol. He said he was not sure he knew that. He acknowledged that the Temple study cited in his report did not utilize patients with known alcohol abuse problems. He acknowledged that he did not disclose that Dr. Temple was the vice president for the company of Tylenol. He said he did not disclose that because it was a scientific study and he did not always disclose where the author was from.

Judicial notice is taken of Division of Workers' Compensation's file in this case. It is noted that the original Claim for Compensation, dated June 7, 2005, was filed on June 10, 2005, prior to Employee's death on July 4, 2005. No deposition of Employee was offered in evidence. It is also noted that 21 CFR Section 201.322 (Exhibit H) provides that any OTC drug product, labeled for adult use, containing acetaminophen, "alone or in combination shall bear an alcohol warning statement on its labeling as follows:

(1) Acetaminophen. 'Alcohol Warning' [heading in boldface type]: 'If you consume 3 or more alcoholic drinks every day, ask your doctor whether you should take acetaminophen or other pain relievers/fever reducers. Acetaminophen may cause liver damage.'

1. Was Employee's death medically causally related to an accident or occupational disease that arose out of and in the course of his employment for Employer, resulting in Claimant being entitled to death benefits, including burial expenses?

The employee must establish a causal connection between the accident and the claimed injuries [9] or death.[10] Section 287.020.2, RSMo[11] requires that the injury be "clearly work related" for it to be compensable.[12] An injury is clearly work related, "if work was a substantial factor in the cause of the resulting medical condition or disability. An injury is not compensable merely because work was a triggering or precipitating factor."[13] Injuries that are triggered or precipitated by work may nevertheless be compensable if the work is found to be a "substantial factor" in causing the injury.[14] A substantial factor does not have to be the primary or most significant causative factor.[15] An accident may be both a triggering event and a substantial factor in causing an injury.[16] Further, there is no "bright-line test or minimum percentage set out in the Workers' Compensation Law defining 'substantial factor.'"[17] A claimant has the burden to prove all the essential elements of his or her case, and a claim will not be validated where some essential element is lacking.[18] Although all doubts should be resolved in favor of the employee and coverage in a workers' compensation proceeding, if an essential element of the claim is lacking, it must fail.[19] Section 287.240.1, RSMo provides for compensation "if the injury causes death."

The quantum of proof is reasonable probability.[20] "Probable means founded on reason and experience which inclines the mind to believe but leaves room to doubt."[21] Such proof is made only by competent and substantial evidence. It may not rest on speculation.[22] Expert testimony may be required where there are complicated medical issues.[23] "Medical causation of injuries which are not within common knowledge or experience, must be established by scientific or medical evidence showing the cause and effect relationship between the complained of condition and the asserted cause."[24] Compensation is appropriate as long the performance of usual and customary duties led to a breakdown or a change in pathology.[25]

Where there are conflicting medical opinions, the fact finder may reject all or part of one party's expert testimony which it does not consider credible and accept as true the contrary testimony given by the other litigant's expert.[26] The acceptance or rejection of medical evidence is for the Commission.[27] The testimony of the claimant or other lay witnesses as to facts within the realm of lay understanding can constitute substantial evidence of the nature, cause, and extent of disability when taken in connection with or where supported by some medical evidence.[28] The trier of facts may also disbelieve the testimony of a witness even if no contradictory or impeaching testimony appears.[29] The testimony of the employee may be believed or disbelieved even if uncontradicted.[30]

Where an employee sustains an injury arising out of and in the course of his employment, every natural consequence that flows from the injury, including a distinct disability in another area of the body, is compensable as a direct and natural result of the primary or original injury.[31] Every natural consequence that flows from the injury likewise arises out of employment, unless it is the result of an independent intervening cause attributable to the employee's own intentional conduct.[32] So, if the resultant disability is directly traceable to the original accident, the intervention of other causes by which the disability is increased will not bar recovery.[33]

I find that Claimant was married to Employee at the time of his death on July 4, 2005, and that she is Employee's sole dependent under the Missouri Workers' Compensation Law. I find that Employee had an accident that arose out of and in the course of his employment for Employer when he fell while working for Employer on July 12, 2004, and that he injured his low back as a result of that accident. The treatment records recite that history. Those records document extended treatment of Employee's back injury for several months. The treatment included the use of pain relievers containing acetaminophen. Employer provided authorized medical care, including back surgery, and paid temporary total disability benefits. Claimant's testimony was consistent with Employee going to work on July 12, 2004, and calling her to take him to the doctor that day because of a back injury he sustained at work that day. However, for the reasons discussed hereafter, I find that Claimant failed to prove that Employee's work injury was a substantial factor in causing his death.

Claimant asserts Employee's liver failed due to the acetaminophen he took for back pain, while Employer's position is that the liver failure was due entirely to alcohol consumption. Each side presented expert testimony, but I find one doctor to be much more credible than the other.

Dr. Worman concluded that to the highest degree of medical certainty, Employee died from complications of cirrhosis, which developed as a result of many years of excessive alcohol consumption. He noted that the natural history of Employee's liver disease was typical for someone with alcoholic hepatitis and cirrhosis. He further concluded, "Based on the available medical records, there

were no factors other than excessive consumption of alcohol that contributed to his developing end stage liver disease or that led to his death."

Dr. Parmet testified that Employee's chronic intake of prescribed acetaminophen was a very substantial factor of Employee's death and an accelerator of his liver failure. He thought the damage was synergistic with continuing alcohol use and that acetaminophen is synergistic with alcohol.

I find Dr. Worman's conclusions more credible than Dr. Parmet's on the issue of the cause of Employee's death. I find that Employee died from liver failure which was secondary to alcoholic cirrhosis. I find that Dr. Worman is better qualified than Dr. Parmet to express opinions regarding the cause of Employee's liver disease. Dr. Worman is a highly qualified specialist in the liver and liver disease. He teaches liver disease to medical students at Columbia University. He has been active in the American Association for the Study of Liver Diseases and has been on the editorial board of their journal Hepatology for many years. He directs care for patients, and most of his inpatient care is liver disease, including end stage liver disease and acute or sudden liver failure cases. Dr. Parmet is not a specialist in liver disease and had not had specific training in hepatology.

Dr. Worman noted that in April 2005, Employee had alcoholic cirrhosis and alcoholic hepatitis, and that the alcoholic cirrhosis was the result of many years of heavy drinking. He noted that Employee reported drinking six to eight and sometimes ten to twelve beers a day. Dr. Worman noted that Employee had a low BUN on December 28, 2004, and that one of the few causes, if not the only cause, of a low BUN concentration is severe liver disease. The alcohol noted in Employee's blood demonstrated he was actively drinking. Dr. Worman credibly identified and explained several factors that supported that Employee had long-standing cirrhosis in March 2005. Ultrasound and CT imaging both showed a small liver. He had a significantly low blood albumin concentration which usually becomes so low with long-standing liver dysfunction. He also had muscle wasting and abnormal connections between the veins draining the gut and the veins draining the skin, both of which occur in long-standing cirrhosis.

Dr. Worman noted that there was no evidence that chronic use of acetaminophen, especially at recommended doses as prescribed to Employee, causes or contributes to chronic liver disease. He stated that there are no studies demonstrating that chronic intake of acetaminophen, or any of the other medications Employee received, contributes to the development of end stage liver disease in an individual with another chronic liver disease, such as alcoholic cirrhosis.

Dr. Parmet stated that people do not go down the tubes this fast. Yet, he acknowledged that he did not have specific training in hepatology, and stated that most of his personal work had not been looking at acute doses. Dr. Parmet stated he had completed the course work for a Ph.D. in toxicology. However, he was not a practicing toxicologist. Dr. Parmet agreed that Employee was felt to have alcoholic cirrhosis when he appeared in the emergency room on April 18, 2005. He agreed that alcoholic cirrhosis comes from many years to decades of heavy drinking rather than just a year's period of time. By definition, alcoholic cirrhosis is due to chronic alcohol use. He thought that Employee's cirrhosis probably was long-standing. He stated there was no other way to explain his demise except that he had cirrhosis for a very long time.

Dr. Parmet's opinion, standing alone, fails to support Claimant's case because it is not supported by the evidence of record. Dr. Parmet stated that he was aware of numerous reports demonstrating that ingestion of acetaminophen by alcoholics causes and precipitates liver failure, but he did not cite any in his report. His report stated that the acute lethal dose of acetaminophen falls to 4 g in individuals who consume alcohol. He stated that it was impossible to say to what extent acetaminophen contributed to the end stage liver disease versus the alcohol. He stated that he could not offer within a reasonable degree of medical certainty to what extent the ingestion of Lortab combined with the alcohol would have led to the end stage liver disease, or accelerated the end stage liver disease. He stated that it would be difficult to know one way or another whether Employee was taking the prescribed dosages of acetaminophen. He said he did not see evidence of Employee running out early and going in for refills. Dr. Parmet agreed that there was no evidence to suggest that Employee was taking an amount of acetaminophen in excess of what was prescribed.

Dr. Olson's last prescription for pain medication containing acetaminophen for Employee noted in the records was in the December 28, 2004 Heartland Discharge Summary. That record referred to Hydrocodone 7.5 mg acetaminophen 500 milligrams one po every 4-6 hours PRD pain \# 60, no refills. If Employee took one pill

every four hours, he would take six in a day, or 3 g per day for ten days. But Employee was prescribed medication that contained acetaminophen "prn", or "as needed." The record does not establish how many pills Employee took. Claimant said Employee did not take more Lortab than was prescribed. He may have taken less. The treatment records referred to Employee taking Lortab, a pain medication that contained acetaminophen, but the records do not clearly disclose the number of times Lortab was prescribed for Employee. Some entries in the table in footnote 8 referred to Lortab without identifying a new prescription for it. The records do not clearly reflect if and when Lortab prescriptions were filled. Further, because Employee did not testify, and his pharmacy records were not in evidence, it is not known how many times Employee's prescriptions for Lortab were filled or refilled, and how many pills were contained in the prescriptions. There was no evidence of how many Lortab pills Employee took each day, or of how many days he took medication containing acetaminophen.

Claimant did not offer Employee's pharmacy records into evidence. Those records may have shown what prescriptions were filled and when they were filled. Those records may have provided a more definite indication of how much acetaminophen Employee had taken at various times between July 12, 2004 and the time of his death. Claimant failed to prove how much acetaminophen Employee consumed during that period. Dr. Parmet's conclusions regarding the effect of Employee taking acetaminophen are based on speculation because of the lack of documented evidence of the amount of acetaminophen taken by Employee. Dr. Parmet presumed that Employee continued to take the Lortab at the prescribed dose, but there is no definite evidence of the amount of Lortab Employee actually consumed.

I find that Employee's July 12, 2004 work accident, and his taking medications, including acetaminophen, to treat the resulting injury was not a substantial factor in causing his death. Further, I find that Employee suffered serious liver disease caused by his chronic consumption of alcohol over several years, and that his death was caused by his chronic alcohol use, and not by his consumption of the acetaminophen he took to treat the accidental injury. Claimant's claim for death benefits, including burial benefits, is denied.

1. What is Employer/Insurer's liability, if any, for permanent partial disability benefits?

When seeking disability benefits with respect to a work-related injury, the claimant has the burden of proof to show that a disability resulted and the extent of such disability.[34] Claimant must prove the nature and extent of any disability by a reasonable degree of certainty.[35] Missouri courts require that the permanent nature of an injury be shown to a reasonable certainty, and such proof may not rest on surmise and speculation.[36] "Under Missouri law, a Workers' Compensation claimant alleging permanent disability must adduce medical evidence demonstrating with reasonable certainty that the disability is in fact permanent."[37] "The phrase 'permanently disabled' is not to be narrowly construed, but means a condition that appears to be reasonably certain or likely to continue permanently or indefinitely."[38] A disability is "permanent" if "shown to be of indefinite duration in recovery or substantial improvement is not expected."[39]

The determination of the degree of disability sustained by an injured employee is not strictly a medical question.[40] While the nature of the injury and its severity and permanence are medical questions, the impact that the injury has upon the employee's ability to work involves factors, which are both medical and nonmedical. Accordingly, the Courts have repeatedly held that the extent and percentage of disability sustained by an injured employee is a finding of fact within the special province of the Commission.[41] Where there are several events, only one being compensable, contribute to the alleged disability, Claimant has the burden to prove the nature and extent of disability attributable to the job-related injury.[42] The employee must also prove the extent of pre-existing disability. Failure to do so bars the recovery of permanent partial disability.[43]

The fact-finding body is not bound by or restricted to the specific percentages of disability suggested or

stated by the medical experts.[44] It may also consider the testimony of the employee and other lay witnesses and draw reasonable inferences in arriving at the percentage of disability.[45] The finding of disability may exceed the percentage testified to by the medical experts.[46] The Commission "is free to find a disability rating higher or lower than that expressed in medical testimony."[47] The Court in Sellers noted that " $[t]$ his is due to the fact that determination of the degree of disability is not solely a medical question. The nature and permanence of the injury is a medical question, however, 'the impact of that injury upon the employee's ability to work involves considerations which are not exclusively medical in nature.'"[48] The uncontradicted testimony of a medical expert concerning the extent of disability may even be disbelieved.[49]

"If it appears that the injury has caused a partial loss of bodily function, which impairs the efficiency of the employee in the ordinary pursuits of life, recovery may be had under $\S 287.190$ for permanent partial disability, notwithstanding the fact that the employee injured has suffered no loss of time from work and no immediate loss of earning power."[50] "Thus, even if an employee is working at the same wage, he is entitled to compensation if, from a consideration of the whole record, he sustained an injury that caused a partial loss of bodily function which impairs the efficiency of the person in the ordinary pursuits of life."[51]

Section 287.230.1, RSMo provides:

The death of the injured employee shall not affect the liability of the employer to furnish compensation as in this chapter provided, so far as the liability has accrued and become payable at the time of the death, and any accrued and unpaid compensation due the employee shall be paid to his dependents without administration, or if there are no dependents, to his personal representative or other persons entitled thereto, but the death shall be deemed to be the termination of the disability.

1. Where an employee is entitled to compensation under this chapter for an injury received and death ensues for any cause not resulting from the injury for which he was entitled to compensation, payments of the unpaid accrued compensation shall be paid, but payments of the unpaid unaccrued balance for the injury shall cease and all liability therefor shall terminate unless there are surviving dependents at the time of death.

Although there are conflicting opinions as to Employee's work related diagnosis and prognosis prior to his death, the evidence does establish the need for ongoing back treatment. Dr. Finley noted in March 2005 that a March 21, 2005 MRI of the lumbar spine noted a soft tissue defect within the spinal canal and a broad based component that may be touching nerve. The MRI noted that Employee needed to follow up with the surgeon. Dr. Zarr examined Employee on April 4, 2005 and noted that Employee complained of low back pain that radiated down his left lower extremity. Dr. Zarr noted the MRI scan showed a residual disc fragment in the spinal canal at the L4-5 level which may be touching on the nerve root. He recommended that Employee be reevaluated by Dr. Olson to see if any further surgery was indicated, and if not, he recommended a series of lumbar steroid epidural injections followed by a work hardening program and a functional capacity evaluation. Employee was hospitalized at Heartland in April 2005 for treatment of liver disease. His back was not treated or evaluated during that hospitalization.

Dr. Olson saw Employee on May 9, 2005 for the last time and noted Employee continued to have the same pain he had pre-operatively in the back and his leg roughly in the L5 distribution. He noted that Employee had not had any clinical improvement at all since his surgery. He thought that the repeat MRI showed excellent anatomical results, and that there did not appear to be any entrapment of the nerve root or any remaining compression. He suspected that Employee had injury to the sciatic nerve in the location of his sciatic notch, but he did not explain the basis of his suspicion. He assessed persistent radiculopathy, but he offered no further evaluation, surgery, or other treatment to Employee on May 9, 2005. Dr. Olson did not perform a second back surgery or provide additional treatment for Employee's back after May 9, 2005. Employee died on July 4, 2005.

The March 21, 2005 MRI report was not consistent with Dr. Olson's reading of the report. Dr. Olson thought that the repeat MRI showed excellent anatomical results, and that there did not appear to be any entrapment of the nerve root or any remaining compression. The MRI report noted, however, that a residual soft tissue defect was seen within the spinal canal in the antero left portion which was displacing the thecal sac posteriorly. The report noted that there was also a broad based component which extended into the neural foramen and narrowed it mildly, and that it may be touching the nerve. The Impression was postoperative changes at L4-5 on the left with probable residual or recurrent disc material in the antero left bony canal. Dr. Finley noted in March 2005 that a March 21, 2005 MRI of the lumbar spine noted a soft tissue defect within the spinal canal and a broad based component that may be touching nerve. Dr. Zarr noted the MRI scan showed a residual disc fragment in the spinal canal at the L4-5 level which may be touching on the nerve root. While Dr. Olson did not offer any further surgery, Employee may have had a second opinion surgical evaluation by another doctor in light of his continued radiculopathy complaints and the MRI results.

Dr. Zarr did not treat Employee after April 4, 2005. Employee did not receive lumbar steroid epidural injections, a work hardening program, or a functional capacity evaluation. The suspected injury to the sciatic nerve identified by Dr. Olson on May 9, 2005 was not evaluated further or treated. Employee did not testify in this case. No ratings of permanent partial disability other than Dr. Parmet's were offered in evidence.

No Missouri case has been cited or found that allows benefits for permanent partial disability when an employee dies from causes unrelated to the employment before he or she reaches maximum medical improvement or completes the healing period. The Court of Appeals in Sanders[52] affirmed the Labor and Industrial Commissions denial of permanent partial disability benefits to a widow based on failure to prove the nature and extent of disability. The employee in Sanders was injured while working for employer, and had two surgeries, including a laminectomy and discectomy, after a herniated L4-5 disc, fracture of the back, and degenerative disc disease had been diagnosed. The employee later died from cancer. After the employee's death, a doctor specializing in occupational medicine reviewed employee's medical records, employee's deposition, and a treating doctor's deposition. She did not personally examine the employee. When asked if she had "an estimation" about the permanent partial disability "would have suffered concerning his low back and low back injuries, had he lived," she said he had sustained "an approximate 30 to 35 percent permanent partial impairment of the total body. The ALJ found that the employee's expected residual disability was 30 % of the body as a whole.[53]

The Court noted that the Commission denied permanent partial disability benefits based on the failure to prove the nature and extent of such disability, rather than as a matter of law based on a conclusion that, under section 287.230.2, maximum medical improvement must have been reached prior to death. The Court stated that the Commission noted that permanent partial disability means a disability which is permanent in nature and partial in degree, citing section 287.190.6. The Court also stated that the Commission correctly noted that Missouri courts have routinely required that the permanent nature of an injury be shown to a reasonable certainty, and that such proof may not rest on surmise and speculation. The Commission noted that one doctor gave no opinion about permanency, another doctor testified that employee had not reached maximum medical improvement and gave no opinion about residual disability, and the occupational doctor's opinion was based on an assumption of improvement if employee had not suffered from cancer. The Court of Appeals affirmed the Commission, and noted that the denial of benefits to claimant was based on a lack of requisite proof of a permanent partial disability.[54]

The Commission's final award in Sanders[55] noted that the Administrative Law Judge relied on the treatise by Professor Larson, Workman's Compensation Law, section 58.45, in reaching her conclusion.[56] The Commission noted that Professor Larson stated that the proper procedure in this circumstance is to make the best possible medical estimate of the probable residual disability which would have remained had the employee lived to complete his healing period. The Commission stated that Professor Larson's approach presented a major difficulty in the Sanders case. It noted that the occupational doctor's posthumous

disability rating necessarily rested on mere assumptions. The Commission noted that Missouri appellate courts have repeatedly held proof of permanency of an injury requires reasonable certainty, and their decision can not rest on surmise or speculation. The Commission further noted that in order to receive permanent partial disability it must appear the employee's disability "is permanent in nature and partial in degree." The Commission noted that those facts had not been shown in the Sanders case.

This case is similar to Sanders. In both cases, the employee died before reaching maximum medical improvement. In the case at hand, Employee had not had recommended injections, work hardening, or a functional capacity evaluation at the time of his death. Other treatment may have been recommended depending on the results of his treatment and evaluation. The nature and extent of improvement that Employee might have had from additional medical treatment is uncertain and unknown.

In the case at hand, Dr. Parmet's rating is also based on assumption. Dr. Parmet did not examine Employee. He said that had Employee's ongoing pain and limitations clinically remained stabilized and not improved, Employee would have had a residual permanent partial disability of twenty to thirty percent of the body as a whole. His estimate of Employee's permanent partial disability was based on Employee's condition at the time of his death, and not on Employee's probable residual disability that would have remained if he had lived to complete the healing period. Dr. Parmet's rating assumed that Employee's condition would not improve. But he noted that Employee was not fully evaluated and treated at the time of his death. He acknowledged that Employee could improve with additional treatment and that further treatment was warranted. He stated that additional treatment could potentially decrease the level of Employee's disability. He also stated that it was conceivable that with further treatment, Employee would have been much less disabled, but he said he "would be speculating beyond reasonable certainty to assign a value to an ultimate outcome."

I find that Claimant failed to sustain her burden to prove with reasonable medical certainty the nature and extent of any permanent partial disability sustained by Employee as a result of his July 12, 2004 accident.[57] I find that she failed to satisfactorily prove the permanency of Employee's condition with reasonable medical certainty. Employee was not released from treatment of his back injury at the time of his death. Claimant failed to prove Employee's condition that was reasonably certain or likely to continue permanently or indefinitely. She failed to show that Employee's disability was of indefinite duration in recovery or that substantial improvement was not expected. Employee's treating doctors did not provide any opinions of what Employee's condition would have been when he completed treatment. His treating doctors did not provide any ratings of permanent disability. The medical treatment records did not note any permanent specific physical limitations or restrictions for Employee, such as lifting, bending, stooping, carrying, sitting, or standing. Claimant did not prove what impact Employee's injury had upon his ability to work.

I do not conclude that Claimant's claim for permanent partial disability benefits necessarily fails because Employee had not reached maximum medical improvement. Rather, I find that based on the evidence presented in this case, Claimant failed to prove the nature and extent of Employee's permanent partial disability by a reasonable degree of certainty. I find that Dr. Parmet's opinion rested on surmise and speculation, and that it does not support an award of permanent partial disability. I also find that the record does not permit the determination, based upon a reasonable certainty, of the best possible medical estimate of the probable residual disability that would have remained if Employee had lived to complete the healing period. Any award of permanent disability is inappropriate for lack of requisite proof. Claimant's claim for permanent partial disability benefits is denied.

1. What is Employer/Insurer's liability, if any, for past medical bills?

Section 287.140, RSMo requires that the employer/insurer provide "such medical, surgical, chiropractic, and hospital treatment ... as may reasonably be required ... to cure and relieve [the employee] from the effects of

the injury." The employee must prove that the medical care provided by the physician selected by the employee was reasonably necessary to cure and relieve the employee of the effects of the injury.[58] The employee may establish the causal relationship through the testimony of a physician or through the medical records in evidence that relate to the services provided.[59] The medical bills in Martin were shown by the medical records in evidence to relate to the professional services rendered for treatment of the product of the employee's injury.[60]

Claimant seeks an award for payment of the medical bills relating to Employee's hospitalization at Heartland from April 18, 2005 to April 25, 2005, itemized in Exhibit G.[61] The record demonstrates that Employee's hospitalization from April 18, 2005 to April 25, 2005 at Heartland was for treatment of his liver disease, not his back. I have previously found that Claimant failed to prove that Employee's accidental injury to his back on July 12, 2004 was a substantial factor in causing his liver disease and death. I find that Claimant failed to prove that the treatment Employee received for his hospitalization at Heartland from April 18, 2005 to April 25, 2005 was reasonably necessary to cure and relieve Employee of the effects of his back injury. Claimant's request for an award for payment of the medical bills relating to the hospitalization from April 18, 2005 to April 25, 2005, itemized in Exhibit G, is therefore denied.

In conclusion, based upon substantial and competent evidence and the application of The Missouri Workers' Compensation Law, I find in favor of the Employer and Insurer and deny Claimant's entire claim for benefits, including death benefits, permanent partial disability benefits, and past medical benefits.

I find that Claimant failed to prove that Employee's death was clearly work related and failed to show that work was a substantial factor in the cause of Employee's death. I further find that Claimant failed to prove with reasonable medical certainty the nature and extent of any permanent partial disability sustained by Employee as a result of his July 12, 2004 accident. I also find that Claimant failed to prove the treatment Employee received for his hospitalization at Heartland from April 18, 2005 to April 25, 2005 was reasonably necessary to cure and relieve Employee of the effects of his back injury. Claimant's entire claim is denied.

Date: July 24, 2007

Made by: $\qquad$ Robert B. Miner

Robert B. Miner

Administrative Law Judge

Division of Workers' Compensation

A true copy: Attest:

/s/ Jeffrey W. Buker

Jeffrey W. Buker, Acting Division Director

Division of Workers' Compensation

[1] The Report of Injury dated August 13, 2004 states that Employee was hired by Employer on June 29, 2004 as a carpenter.

[2] Lortab is a prescription pain medication that contains acetaminophen.

[3] Stedman's Medical Dictionary (28th Ed. 2006), App p. 24, describes the following common abbreviations used in medication orders: "mg"--"milligram," "q"-- "each, every,"" "PO"--"by mouth."

[4] Stedman's Medical Dictionary (28th Ed. 2006), App p. 24, describes the following common abbreviations used in medication orders: "prn"--"needed, according to necessity," and "bid"-- "twice a day."

[5] “Ascites” is defined as “accumulation of serous fluid in the peritoneal cavity.” *Stedman’s Medical Dictionary* (28th Ed. 2006), p. 165.

[6] “Hyponatremia” is defined as “abnormally low concentrations of sodium ions in circulating blood.” *Stedman’s Medical Dictionary* (28th Ed. 2006), p. 934.

[7] “Hypokalemia” is defined as “the presence of abnormally low concentration of potassium ions in the circulating blood. . . .” *Stedman’s Medical Dictionary* (28th Ed. 2006), p. 934.

[8] The following table summarizes Lortab notations in Employee’s treatment records:

[9] Thorsen v. Sachs Electric Company, 52 S.W.3d 611, 618 (Mo.App. 2001), overruled in part on other grounds by Hampton v. Big Boy Steel Erection, 121 S.W.3d 220, 225 (Mo. 2003); Williams v. DePaul Ctr, 996 S.W.2d 619, 625 (Mo.App. 1999), overruled in part on other grounds by Hampton, 121 S.W.3d at 226; Fisher v. Archdiocese of St. Louis, 793 S.W.2d 195, 198 (Mo. App. 1990), overruled in part on other grounds by Hampton, 121 S.W.3d at 230. [10] Martin v. City of Independence, 625 S.W.2d 940, 942 (Mo.App. 1981); Cowick v. Gibbs Beauty Supplies, 430 S.W.2d 626, 630 (Mo.App. 1968).

[11] All statutory references are to the Revised Statutes of Missouri 2000, unless otherwise noted. See Lawson v. Ford Motor Co., --S.W.3d--, 2007 WL 817268 (Mo.App. 2007) where the Eastern District Court of Appeals held that the 2005 amendments to Sections 287.020, RSMo do not apply retroactively.

[12] Section 287.020, RSMo provides: "2. The word "accident" as used in this chapter shall, unless a different meaning is clearly indicated by the context, be construed to mean an unexpected or unforeseen identifiable event or series of events happening suddenly and violently, with or without human fault, and producing at the time objective symptoms of an injury. An injury is compensable if it is clearly work related. An injury is clearly work related if work was a substantial factor in the cause of the resulting medical condition or disability. An injury is not compensable merely because work was a triggering or precipitating factor. "3. (1) In this chapter the term "injury" is hereby defined to be an injury which has arisen out of and in the course of employment. The injury must be incidental to and not independent of the relation of employer and employee. Ordinary, gradual deterioration or progressive degeneration of the body caused by aging shall not be compensable, except where the deterioration or degeneration follows as an incident of employment. "(2) An injury shall be deemed to arise out of and in the course of the employment only if:

"(a) It is reasonably apparent, upon consideration of all the circumstances, that the employment is a substantial factor in causing the injury; and

"(b) It can be seen to have followed as a natural incident of the work; and "(c) It can be fairly traced to the employment as a proximate cause; and "(d) It does not come from a hazard or risk unrelated to the employment to which workers would have been equally exposed outside of and unrelated to the employment in normal nonemployment life."

[13] Kasl v. Bristol Care, Inc., 984 S.W.2d 852 (Mo. 1999).

[14] Kasl, 984 S.W.2d at 853; Cahall v. Cahall, 963 S.W.2d 368, 372 (Mo. App. 1998), overruled in part on other grounds by Hampton, 121 S.W.3d at 226.

[15] Bloss v. Plastic Enterprises, 32 S.W.3d 666, 671 (Mo. App. 2000), overruled in part on other grounds by Hampton, 121 S.W.3d at 225; Cahall, 963 S.W.2d at 372.

[16] Bloss, 32 S.W.3d at 671.

[17] Cahall, 963 S.W.2d at 372.

[18]Thorsen v. Sachs Electric Company, 52 S.W.3d 611, 618 (Mo.App. 2001), overruled in part on other grounds by Hampton v. Big Boy Steel Erection, 121 S.W.3d 220, 225 (Mo. 2003); Cook v. Sunnen Products Corp., 937 S.W.2d 221, 223 (Mo. App. 1996).

[19] Thorsen, 52 S.W.3d at 618; Sanders v. St. Clair Corporation, 943 S.W.2d 12, 17 (Mo.App. 1997), overruled in part on other grounds by Hampton, 121 S.W.3d at 226; White v. Henderson Implement Co., 879 S.W.2d 575, 579 (Mo.App. 1994), overruled in part on other grounds by Hampton, 121 S.W.3d at 228.

[20] Thorsen, 52 S.W.3d at 620; Downing v. Willamette Industries, Inc., 895 S.W.2d 650, 655 (Mo. App. 1995), overruled in part on other grounds by Hampton, 121 S.W.3d at 227; Fischer v. Archdiocese of St. Louis, 793 S.W.2d 195, 199 (Mo.App. 1990), overruled in part on other grounds by Hampton, 121 S.W.3d at 230.

[21] Thorsen, 52 S.W.3d at 620; Tate v. Southwestern Bell Telephone Co., 715 S.W.2d 326, 329 (Mo. App. 1986); Fischer, 793 S.W.2d at 198.

[22] Griggs v. A. B. Chance Company, 503 S.W.2d 697, 703 (Mo.App. 1974).

[23] Goleman v. MCI Transporters, 844 S.W.2d 463, 466 (Mo.App. 1992), overruled in part on other grounds by Hampton, 121 S.W.3d at 229.

[24] Thorsen, 52 S.W.3d at 618; Brundige v. Boehringer Ingelheim, 812 S.W.2d 200, 202 (Mo. App. 1991).

[25] Bennett v. Columbia Health Care, 134 S.W.3d 84, 87 (Mo.App. 2004).

[26] Kelley v. Banta \& Stude Constr. Co. Inc., 1 S.W.3d 43, 48 (Mo.App. 1999); Webber v. Chrysler Corp., 826 S.W.2d 51, 54 (Mo.App. 1992), overruled in part on other grounds by Hampton, 121 S.W.3d at 229; Hutchinson v. Tri-State Motor Transit Co., 721 S.W.2d 158, 162 (Mo.App. 1986), overruled in part on other grounds by Hampton, 121 S.W.3d at 231.

[27] Smith v. Donco Const., 182 S.W.3d 693 (Mo.App. 2006); Bowers v. Hiland Dairy Co., 132 S.W.3d 260, 263 (Mo.App. 2004).

[28] Pruteanu v. Electro Core, Inc., 847 S.W.2d 203, 206 (Mo.App. 1993), overruled in part on other grounds by Hampton, 121 S.W.3d at 229; Reiner v. Treasurer of State of Mo., 837 S.W.2d 363, 367 (Mo. App. 1992); Fischer, 793 S.W.2d at 199.

[29] Hutchinson, 721 S.W.2d at 161-2; Barrett v. Bentzinger Brothers, Inc., 595 S.W.2d 441, 443 (Mo.App. 1980), overruled in part on other grounds by Hampton, 121 S.W.3d at 231.

[30] Weeks v. Maple Lawn Nursing Home, 848 S.W.2d 515, 516 (Mo.App. 1993), overruled in part on other grounds by Hampton, 121 S.W.3d at 229.

[31] Cahall v. Riddle Trucking, Inc, 956 S.W.2d 315, 322 (Mo.App. 1997); Lahue v. Missouri State Treasurer, 820 S.W.2d 561, 563 (Mo.App. 1991). See also Second Injury Fund v. Arctic Bowl, 928 P.2d 590, 593 (Alaska 1996), where the Court notes: "SIF convincingly, and uncontroversially, demonstrates that harm suffered during medical treatment of a compensable injury is considered a consequence of the original injury, as opposed to a new, separate injury. [FN4] FN4. See, e.g., Sanders v. General Motors Corp., 137 Mich.App. 456, 358 N.W.2d 611 (1984); Lahue v. Missouri State Treasurer, 820 S.W.2d 561 (Mo.App.1991). Though harm caused by medical treatment for a compensable injury is not considered a separate work-related injury, it is compensable as a consequence of the original injury. 1 Arthur Larson, The Law of Workmen's Compensation Law § 13.21(a) (1993) ('It is now uniformly held that aggravation of the primary injury by medical or surgical treatment is compensable.'). See also Ribar v. H \& S Earthmovers, 618 P.2d 582, 584 (Alaska 1980) ('[T]he general rule is that the consequences of medical negligence committed while treating a compensable injury are themselves compensable.')."

[32] Cahall, 956 S.W.2d at 322, citing Wilson v. Emery Bird Thayer Company, 403 S.W.2d 953, 958 (Mo.App.1966).

[33] Cahall, 956 S.W.2d at 322, citing Manley v. American Packing Co., 363 Mo. 744, 253 S.W.2d 165, 169 (1952)

[34] Moriarty v. Treasurer of State of Missouri, 141 S.W.3d 69, 73 (Mo. App. 2004); Sanders, 943 S.W.2d at17.

[35] Elrod v. Treasurer of Missouri as Custodian of Second Injury Fund, 138 S.W.3d 714, 717 (Mo. banc 2004).

[36] Sanders, 943 S.W.2d at 16; Griggs, 503 S.W.2d at 703.

[37] Smith v. Richardson Bros. Roofing, 32 S.W.3d 568, 573 (Mo.App. 2000), overruled in part on other

grounds by Hampton, 121 S.W.3d at 225, citing Cochran v. Industrial Fuels \& Res., 995 S.W.2d 489, 497 (Mo.App. 1999).

[38] Johnson v. W. M. Grace Const. Co., Inc., 535 S.W.2d 555, 557 (Mo.App. 1976).

[39] Tiller v. 166 Auto Auction, 941 S.W.2d 863, 865 (Mo.App. 1997).

[40] Landers v. Chrysler Corp., 963 S.W.2d 275, 284 (Mo. App. 1997); Sellers v. Trans World Airlines, Inc., 776 S.W.2d 502, 505 (Mo.App. 1989), overruled in part on other grounds by Hampton, 121 S.W.3d at 230.

[41] Sharp v. New Mac Elec. Co-op, 92 S.W.3d 351, 354 (Mo. App. 2003); Elliott v. Kansas City, Mo., School District, 71 S.W.3d 652, 656 (Mo.App. 2002), overruled in part on other grounds by Hampton, 121 S.W.3d at 225; Sellers, 776 S.W.2d at 505; Quinlan v. Incarnate Word Hospital, 714 S.W.2d 237, 238 (Mo.App. 1986); Banner Iron Works v. Mordis, 663 S.W.2d 770, 773 (Mo.App. 1983); Barrett, 595 S.W.2d at 443; McAdams v. Seven-Up Bottling Works, 429 S.W.2d 284, 289 (Mo.App. 1968).

[42] Bruflat v. Mister Guy, Inc., 933 S.W.2d 829, 835 (Mo.App. 1996), overruled in part on other grounds by Hampton, 121 S.W.3d at 227; Bersett v. National Super Markets, 808 S.W.2d 34, 36 (Mo.App. 1991).

[43] Plaster v. Dayco, 760 S.W.2d 911, 913 (Mo. App. 1988).

[44] Lane v. G \& M Statuary, Inc., 156 S.W.3d 498, 505 (Mo.App. 2005); Sharp, 92 S.W.3d at 354; Sullivan v. Masters Jackson Paving Co., 35 S.W.3d 879, 885 (Mo.App. 2001), overruled in part on other grounds by Hampton, 121 S.W.3d at 225; Landers, 963 S.W.2d at 284; Sellers, 776 S.W.2d at 505; Quinlan, 714 S.W.2d at 238; Banner, 663 S.W.2d at 773.

[45] Fogelsong v. Banquet Foods Corporation, 526 S.W.2d 886, 892 (Mo.App. 1975).

[46] Quinlan, 714 S.W.2d at 238; McAdams, 429 S.W.2d at 289.

[47] Jones v. Jefferson City School Dist., 801 S.W.2d 486, 490 (Mo.App. 1990); Sellers, 776 S.W.2d at 505.

[48] Sellers, 776 S.W.2d at 505.

[49] Gilley v. Raskas Dairy, 903 S.W.2d 656, 658 (Mo.App. 1995); Jones, 801 S.W.2d at 490.

[50] Sapienza v. Deaconess Hosp. 738 S.W.2d 149, 151 (Mo.App. 1987); Komosa v. Monsanto Chemical Co. 317 S.W.2d 396, 400 (Mo.1958).

[51] Sapienza, 738 S.W.2d at 151; Gordon v. Chevrolet-Shell Division of Gen. M. Corp., 269 S.W.2d 163, 170 (Mo.App. 1954); Betz v. Columbia Tel. Co., 224 Mo.App. 1004, 24 S.W.2d 224 (1930).

[52] Sanders v. St. Clair Corporation, 943 S.W.2d 12 (Mo.App. 1997)

[53] Id. at 15 .

[54] Id. at 17 .

[55] 1995 WL 765290 (Mo.Lab.Ind.Rel.Com.)

[56] 4 Larson's Workers' Compensation Law §89.06D (2005) provides:

Since awards for permanent partial disability are normally to be made only after the healing period has been

completed and the injury has become stabilized so that the degree of permanent impairment can be appraised, if the injured employee dies before stabilization has taken place, the degree of impairment should not be taken as that in effect at the moment of death. The proper procedure is to make the best possible medical estimate of the probable residual disability that would have remained if the employee had lived to complete the healing period.

No Missouri appellate case has been found that adopts this procedure set forth in Larson's.

[57] I also find that Employee had no pre-existing disability relating to his back before the July 12, 2004 accident. The medical records document his treatment on two occasions in June 2004 to treat a back injury from a lifting incident. The record does not establish that Employee sustained any permanent partial disability as a result of the lifting incident. The Report of Injury in this case dated August 13, 2004 states that Employee was hired by Employer on June 29, 2004 as a carpenter.

[58] Chambliss v. Lutheran Medical Center, 822 S.W.2d 926 (Mo.App. 1991), overruled in part on other grounds by Hampton, 121 S.W.3d at 229; Jones v. Jefferson City School District, 801 S.W.2d 486, 490-91 (Mo.App. 1990), overruled in part on other grounds by Hampton, 121 S.W.3d at 230; Roberts v. Consumers Market, 725 S.W.2d 652, 653 (Mo.App. 1987); Brueggemann v. Permaneer Door Corporation, 527 S.W.2d 718, 722 (Mo.App. 1975)

[59] Martin v. Mid-America Farm Lines, Inc., 769 S.W.2d 105 (Mo. 1989); Meyer v. Superior Insulating Tape, 882 S.W.2d 735, 738 (Mo.App. 1994), overruled in part on other grounds by Hampton, 121 S.W.3d at 228; Lenzini v. Columbia Foods, 829 S.W.2d 482, 484 (Mo.App. 1992), overruled in part on other grounds by Hampton, 121 S.W.3d at 229; Wood v. Dierbergs Market, 843 S.W.2d 396, 399 (Mo.App. 1992), overruled in part on other grounds by Hampton, 121 S.W.3d at 229.

[60] Martin, 769 S.W.2d at 111.

[61] Exhibit G contains medical bills relating to Employee's treatment at Heartland in September, October, and December 2004, and in April and May 2005. The bills for September, October and December 2004 note "Workers Compensation Allowanc" (sic) and "Insurance Paid" amounts, and show zero balances. The bills relating to treatment in April 2005 note Medicaid payments of $\ 1,007.65 and $\ 6,159.44, Medicaid discounts of $\ 3,460.98 and $\ 8,590.99, financial assistance of $\ 679.39, and a zero balance. Bills totaling $\ 212.00 for treatment on May 9, 2005 (the date Employee saw Dr. Olson of Heartland Neurosurgery) were shown paid by insurance, and no balance was shown owed for the May 9, 2005 treatment. The parties stipulated that medical aid had been furnished by Employer in this case in the amount of $\ 16,504.17. The Court determines that the only Heartland bills for which Claimant seeks an award in this case are the bills relating to the April 2005 treatment at Heartland.