Commentary:
Despite a rare complication leading to a poor patient outcome, the jury returned a verdict in favor of the defendant neurologist.
The Case:
The patient, a 49 YOWM (5’9”, 245 lbs.; BMI 36.2), saw his family medicine physician for complaints of neck pain, left arm weakness, and right arm numbness. The patient also complained his fingers occasionally “locking up.” He had a history of anxiety, diabetes, gout, and elevated cholesterol. The family medicine physician assessed cervical radiculopathy and ordered an MRI.
A week later, a C-spine MRI noted the patient had compression on the thecal sac at all cervical levels with bone spurs at some levels. The radiologist’s impression was “spinal stenosis and narrowing of the neural foramina over the cervical region.” Dorsal MRI findings showed degenerative changes but no significant bulging or herniated disc over the dorsal region. No significant stenosis was seen on the MRI, and the small herniated disc was again noted at C7-T1 and T12-L1. The defendant neurologist performed an EMG. The impression was the patient had very mild right C4 radiculopathy and mild right cervical radiculopathies that affected posterior rami only.The neurologist referred the patient to neurosurgery.
Four months later, the neurosurgeon performed a C2-Tl laminectomies and spinal cord decompression for cervical spondylotic myelopathy secondary to ossification of the posterior longitudinal ligament. Intraoperative complications included blood loss of 2000 ml. One unit of PRBCs was given. Post-operative orders included notifying the physician for BP less than 90/60 or greater than 150/90, and a temperature over 101°F. The patient’s stay in the PACU was uneventful, and he was stable upon transfer to the ICU.
The next day, the neurosurgeon performed a neurological exam on the patient; the results were normal. The patient was transferred to a regular unit. He was able to sit in a chair and walk short distances. Overnight, he began to experience discomfort. Early the next morning, his BP was 103/53. Pain Management evaluated the patient and started oral OxyContin® 10 mg BID to supplement his current pain medications. Three hours later, the patient’s BP was 158/62. Two hours later, the physical therapist noted the patient was "lethargic." The nurse noted the patient was sleepy but arousable at noon; occupational therapy documented the patient was alert, awake, and oriented x 3.
That afternoon, the defendant neurologist examined the patient at the request of the neurosurgeon, and noted the patient’s BP was 90/46. The patient was very sleepy but arousable. The defendant neurologist documented the somnolence was secondary to pain medications. He then asked the nurse to move the patient from the chair to the bed as a fall precaution.
About 30 minutes later, the nurse returned to the patient’s room to transfer him back to the bed, and noted he was unresponsive. The patient’s BP was 60/44; Narcan was given with little response. The rapid response team was called. Twenty-five minutes later, the patient’s BP was 67/37. Additional doses of Narcan were administered, but the patient’s BP remained low and the patient was unresponsive to sternal rub. IV fluid resuscitation was started. The patient was transferred to the CCU.
The next day, an MRI demonstrated fairly significant cervical cord edema. The patient remained hospitalized for over a month. The patient was subsequently transferred to a rehabilitation facility where he remained for the next four months. The patient currently has bilateral lower extremity and upper left extremity paralysis with limited use of his right upper extremity.
The plaintiff alleged the defendant neurologist failed to monitor, evaluate, and treat the patient; failed to notify the neurosurgeon of the patient’s condition change; and failed to order closer observation of the patient’s vital and neuro signs. The plaintiff’s experts stated the patient suffered a hypotensive event caused by a combination of inadequate blood volume (caused by hypovolemia and anemia), diabetes, and the narcotics he was given. The hypotensive event subsequently caused an ischemic spinal cord infarct.
The defense experts testified that the plaintiff’s theory of a spinal cord infarct caused by ischemia due to low BP was incorrect. The pattern in this case is not characteristic of ischemic damage. Experts stated the patient sustained a rare complication of decompression reperfusion injury sometimes seen in patients with diabetes and ossification of the posterior longitudinal ligament. They further testified that when chronic compression of the spinal cord is relieved, extensive venous engorgement occurs and the cord is unable to handle the sudden resumption of blood flow. The drop in BP was not the cause of the injury, but rather a result of the reperfusion injury to the spinal cord that interfered with the auto-regulation of the BP.
The jury agreed with the defense experts and returned a defense verdict. The plaintiff filed a motion for a new trial arguing the verdict was contrary to the manifest weight of the evidence. The presiding judge granted their motion. Appeals were denied. The case was re-tried and resulted in a defense verdict.
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