ERIC G. COMSTOCK, M.D., P.A.
Medical toxicology consultation concerning the above-captioned patient is requested by (Attorney). I am asked to review the materials provided and determine whether the documented events in the medical records support an allegation that the treating physician provided services that fall below the acceptable standard of care to a degree of reasonable medical probability.
Under letter of February 2, 2004, I am provided, and have reviewed medical records from
(Physician, M.D).; medical records from a hospital; and medical records from (Healthcare Center), as documented in the attached Summary of Medical Records by identified healthcare providers and covering an interval from October 2, 2001, to the terminal hospitalization on January 29, 2003. Also provided is the post mortem examination and the report of the Medical Examiner, and a death certificate.
I am advised by counsel that particular concern focuses upon the use of opiate narcotic drugs during the course of treatment of this patient.
The first narcotic prescription was provided on July 1, 2002, for Lortabs 5/500, one to be taken three to four times daily as necessary, with 40 ordered plus two refills. At that time, the patient was being treated for herpes zoster, degenerative joint disease, chronic obstructive pulmonary disease, probable mild cerebrovascular accident, decreased memory, gastroesophageal reflux disease, back pain, and upper respiratory infection.
The next opiate prescription was January 3, 2003, for Lortabs 7.5/500, one to two every six hours, with instructions to dispense 30, with two refills. At that time, the patient reported having had a fall and complained of lumbosacral pain. An x-ray of the lumbar spine was reported as no acute abnormal findings.
On January 13, 2003, Duragesic patch 25 micrograms (dispense 5) was ordered, with one patch to be applied every third day. Methadone 10 mg (one to be taken each morning) and hydrocodone/APAP (one every six hours) were also prescribed for pain uncontrolled by Lortabs described above.
On January 18, 2003, the patient was examined by (Physician 2) in the emergency department of the hospital for complaint of persistent back pain that has increased in severity and not controlled by the treatment regimen prescribed by (Physician 1).
On admission, pupils were reactive to light, bowel sounds were normal, and absence of respiratory distress was noted, and breath sounds were reported as normal. In the emergency department, the patient received intramuscular injection of Demerol 50 mg and Phenergan 12.5 mg, resulting in good pain relief. The patient was admitted to the hospital with diagnoses of dehydration, anorexia and back pain.
On January 19, 2003, a Duragesic patch was applied at 1:50 a.m.; Vicodin 7.5 mg, one capsule, was given at 3:50 a.m.; Lortab 7.5 mg, one capsule at 11:00 a.m.; and Lortab 7.5 mg, one capsule, at 6:25 p.m..
On January 20, 2003, a bone scan confirmed the presence of a compression fracture of lumbar vertebra, L3. This was not identified on the routine lumbar spine series performed on January 6, 2003, subsequent to the accidental fall on January 3, 2003.
On January 20, 2003, opiate drug administration consisted of Lortab 7.5 mg at 7:50 a.m.; Methadone 10 mg at 9:30 a.m.; and Methadone 10 mg at 3:00 p.m..
I do not identify any additional opiates having been given on January 21, 2003.
On January 22, 2003, Methadone 20 mg was given at 6:00 a.m.; Methadone 10 mg was given at 2:00 p.m.; and Duragesic patch was applied at 9:00 p.m..
During the above hospitalization, the pattern and frequency of opiate drug administration is consistent with the usual clinical care, considering the patient’s condition, and in reasonable medical probability, does not exceed the standard of care for opiate administration in this patient. In addition, during this hospitalization, his lungs remained clear, and were clear when examined by (Physician 1) on the morning of January 23, 2003, prior to the patient’s discharge to (Healthcare Center), with instructions to continue Methadone as necessary, 10 to 20 mg per day, on a schedule of 7:00 a.m., 2:00 p.m., and before bedtime, to be decreased if the patient appeared sedated.
The absence of respiratory distress as well as the presence of pupillary reaction and normal bowel sounds on admission to the hospital on January 18, 2003, are physical signs supportive of the absence of opiate excess. There is a notation on January 18, 2003, that “patient had recent constipation, probably aggravated by pain medications.” Constipation caused by opiate excess is accompanied by diminished or absent bowel sounds.
Under the circumstances prevailing in this patient of inactivity and poor dietary intake, rather than opiate excess, are factors that likely contributed to or accounted for constipation. There is, in reasonable medical probability, no evidence supporting excess opiate drug administration during the interval from January 18th through January 23rd of 2003.
The patient was transferred to (Healthcare Center) on January 23, 2003, at which time he was noted to have wheezing and congestion in the chest, labored respiration, and episodes of apnea of eight to 12-second duration. While these findings caused consideration of opiate overdose, which led to the discontinuation of opiates and the administration of Narcan (an opiate antagonist), the note that there were active bowel sounds present reduces the probability that opiate excess was the primary causative factor in this episode of respiratory congestion and hypoventilation.
The notation that the patient appeared to be drowsy on the morning of January 23, 2003, well may have been the consequence of opiate drugs since this observation accompanies the hypnotic and analgesic effect of opiates. Also, the records documenting administration of Narcan with some apparent improvement is consistent with some opiate effect. It is unreasonable, however, to presume that a questionable response to Narcan administration is evidence sufficient to attribute the entire respiratory compromise to opiate drugs. The patient is recorded to have had congestion and wheezing even after administration of the second dose of Narcan, at a time when an x-ray of the chest was clear, supporting alternative causes for the acute respiratory episode.
It is also noted in the records that the patient had had emesis (vomiting), which must be considered in the differential diagnosis of the pulmonary compromise sustained on January 23, 2003. As indicated in the medical records, opiate drugs and other drugs with the potential for central nervous system depression were discontinued during the treatment of this pulmonary episode.
In the early morning of January 24, 2003, the patient continued to be lethargic at
2:00 a.m., and bilateral lung congestion minimally labored respiration were still present at 7:00 a.m.. His lungs were noted to be clear on examination at 3:00 p.m., with no cough or shortness of breath. The patient was reported to be on oxygen at that time. Bowel sounds were also present. At 6:15 p.m., one dose of Methadone 10 mg by mouth was administered. Lungs remained clear at 11:00 p.m..
On January 24th and 25th, there were no signs or symptoms consistent with opiate excess, with a single dose of Methadone administered on the evening of January 24th. No opiates were administered on January 25th or January 26th.
On January 27, 2003, orders for Methadone 10 mg, one to three doses per day as necessary for pain were received. The only opiate recorded as being administered to the patient was a single dose of Methadone 10 mg, given at 4:00 a.m.. No further opiate drug appears to have been administered between January 27, 2003, and the onset of the patient’s terminal episode on January 29, 2003.
The overall picture of pulmonary congestion and respiratory compromise occurring on the day of transfer to the nursing home is inconsistent with a significant contribution of analgesic drugs including opiate administration, and is more consistent with acute compromise associated with gastroesophageal reflux and some degree of aspiration. At 3:00 p.m. on January 28th, respiration was unlabored, bowel sounds were present in all four quadrants, and lungs were clear with no shortness of breath, and there was no pedal edema.
At or about midnight and into the early morning hours of January 29th, the patient sustained onset of rapid respiration, temperature elevation for which he received two tablets of Tylenol 650 mg, and respiratory distress. By 8:00 a.m., his temperature had decreased to 96.8, respiration was even and unlabored, and bowel sounds were present.
On the afternoon of January 29th, he sustained another episode of respiratory distress, at which time his respirations increased to 28 and oxygen saturation was down to 93%. At 5:00 p.m., he experienced a third episode of respiratory impairment, with his respiratory rate increasing to 38, and the patient was transferred to the hospital.
On arrival at the hospital, the patient was found to have an oxygen saturation of 74% and unresponsive, and was intubated. He sustained cardiac irregularity, severe cyanosis, dyspnea and decreased pulses. His lungs, however, remained clear to auscultation. Laboratory evaluation revealed a BUN of 58 and creatinine of 2.4, suggestive of impaired kidney function. White blood count was elevated to 29.6, with 88% neutrophils and 5% bands, consistent with an infectious process. Myoglobin was elevated to greater than 500, consistent with rhabdomyolysis probably resulting from impaired perfusion of muscle. Portable chest x-ray at the time, however, revealed minimal infiltrate in the left lung base and lungs were otherwise clear.
The clinical observations reported on January 28th and 29th are inconsistent with compromise associated with a single dose of Methadone 10 mg at 4:00 a.m. on
January 27, 2003, nor is the final episode of multisystem failure consistent with an opiate effect or with the pattern of opiate administration.
The death certificate identifies a diagnosis of septic shock complicated by chronic obstructive pulmonary disease and spinal fracture.
The post mortem examination found no anatomical cause of death, with no evidence of deep vein thrombosis or large vessel pulmonary embolus, and no significant pericardial, pulmonary or perineal fluid, but did identify bilateral emphysematous changes with adhesions. Microscopic examination is consistent with a process of bronchopneumonia, interstitial pneumonitis involving both right and left upper lungs. Old myocardial infarction/scarring was noted in the left ventricle without evidence of acute myocardial infarction. The clinical course of rapid decline, hypotension and multisystem failure are consistent with septic shock.
The concentration of Methadone identified at post mortem was 0.13 mg/L, with a stated normal range of 0.01 to 1.10 mg/L. The concentration of Methadone is not in the order of magnitude such as to support any contribution of methadone to the terminal episode and death of this patient. Post mortem redistribution of Methadone probably caused some post mortem elevation of this substance.
It is my opinion in reasonable medical probability that the pattern of opiate drug administration in this patient does not deviate from the accepted standard of care with regard to the utilization of opiate drugs.
It is my opinion in reasonable medical probability that the clinical course documented in this patient’s medical records and summarized in the attached record summary fails to support the presence of opiate-induced compromise of vital function occurring over the period of time this patient sustained treatment. The post mortem examination fails to support opiate drugs as the causative factor in the terminal episode.
This opinion is based on more than 10,000 patient years of opiate drug administration and clinical experience as documented in my curriculum vitae (attached). Further, it is my opinion that a malpractice claim against the treating physician is not supported by the available material.