Spinal cord injuries are devastating not just for those who suffer from them but their loved ones, too. Depending on the spinal cord level and severity of the injury, it can impact all areas of life: the ability to be independent; to be mobile; to work; to not live with chronic pain; to have bowel and bladder control; and to participate in so many activities those without such injuries can take for granted.
Although spinal cords may be injured by direct trauma (such as from an automobile collision or surgical mishap), many spinal cord medical malpractice cases involve compression injuries. Often, such injuries are caused in two different settings, and with two different causes for the compression.1
First are spinal epidural abscess cases, typically arising from failures in medical services provided in an urgent care or emergency department setting. Second are compression cases caused by post-operative spinal epidural hematomas, typically in the hospital setting.
Both of these conditions involve masses impinging on the spinal cord which causes swelling, a cascade of inflammation, and eventual death of spinal cord tissue if the offending mass is not removed in time. Because of the devastating consequences of spinal cord tissue death, time is of the essence in diagnosing these high stakes conditions.
This article will describe negligence issues surrounding potential claims in both settings, and causation issues applicable to both.
Failure to Diagnose a Spinal Epidural Abscess (SEA)
An epidural abscess is a collection of pus between the vertebral bone and the covering of the spinal cord (dura) caused by an infection that has spread from the blood and seeded the space around the spinal cord. When it is of sufficient size, it can cause compression on the spinal cord and neurologic deficits. Often the initial infection that led to bacteria being in the blood is elusive. While an epidural abscess can occur in all types of people, certain patient populations such as diabetics and IV drug abusers are at increased risk.
Commonly, the diagnosis of SEA is missed on the patient’s first visit to the ER or urgent care when the only complaint may be back or neck pain. It is not until the second or third visit to a medical provider when more obvious symptoms develop such as fever, difficulty walking, or problems with bodily functions that the diagnosis is finally made.
Because of the frequency of narcotic pain medicine abuse, many doctors are reluctant to take a patient with back pain seriously, often chalking up the symptoms to malingering or drug seeking. However, since drug abusers who come to the ER complaining of pain are at high risk for a SEA, the situation of a drug abuser presenting to the ER with unrelenting back pain is the perfect set up for a missed diagnosis.
One of the most important diagnostic clues for the diagnosis of SEA is fever. Another is any new neurologic symptoms such as difficulty walking or leg weakness. In many malpractice cases, the physician missed or minimized a patient’s fever or failed to adequately pursue new neurologic findings. Because of the frequency with which back pain presents to the ER, a thorough neurologic exam is often not performed.
The diagnostic study of choice for diagnosing a SEA is an MRI of the spine. The problem is that an MRI is often delayed for the reasons noted above, and time is of the essence as even hours can make a difference in outcome. Treatment of a SEA is emergency surgical decompression by drainage of the abscess. The duration and extent of the compression, among other factors, will dictate the extent of permanent neurological damage.
One example in our office of a claim involving a SEA is that of a 44-year-old machinist with no significant medical history. He developed severe back pain at work without any inciting trauma. He went to a local ER where he was given a diagnosis of “mid-thoracic” back pain, and he was discharged with pain meds. Two days later, he returned to the ER in the morning with worsening pain, this time described as “low back.” Again, he was given paid meds and sent home.
Later that evening, he returned again to the same ER with worsening pain, and a lumbar MRI was read as normal. At this point he was using a cane to ambulate. The next day he returned to the same ER (visit #4) with leg weakness, tingling, numbness, urinary retention, and no bowel movement for five days. He was admitted to the hospital for further evaluation, and over the next three days he gradually became paralyzed.
He was finally transferred to a hospital where an MRI of the thoracic spine disclosed an epidural abscess. It was emergently drained, but by that time the damage was permanent. He was left a paraplegic with neurogenic bowel and bladder.
Failure to Diagnose a Post-Operative Epidural Hematoma
Spinal epidural hematomas (SEH) are caused by post-operative bleeding following spine surgery, usually when the surgeon has caused a dural puncture. Because the area between the spinal vertebrae and the spinal cord is a fixed space, any post-operative bleeding has the potential to cause spinal compression if not relieved.2 The result can be mechanical pressure on the cord, just as in the epidural abscess cases. The treatment is also the same: emergent surgical decompression of the spinal cord.
In SEH cases, the signs and symptoms are similar to SEA cases. Patients often complain of back pain that is greater than expected post-operatively.3 However, the hallmark sign is any change in neurologic status such as decreased strength, decreased sensation, or urinary retention. These early post-operative changes are often challenging to discover when the patient is coming out of sedation. However, given that such complications are well known in the post-operative setting, there should be regular (usually each half-hour) neuro checks in which extremity strength, sensation, and reflexes are thoroughly tested by nursing staff.
Although a member of the surgical team will do an initial post-op neurological assessment, most often nurses or other non-physicians, such as physical therapists or occupational therapists, are charged with noting any signs that may be the result of spinal cord compression. As with the epidural abscess cases, MRI is the definitive imaging study. It is critical that nursing staff immediately notify the surgeon of any post-operative neurologic deficits so that a stat MRI can be ordered. Identifying the exact time when a patient manifested signs and symptoms that mandated further work-up becomes essential in any spinal epidural hematoma legal case.
Treatment for neurologic deficits caused by epidural hematomas, just like epidural abscesses, will almost always be emergent decompression surgery.
One recent claim involved a failure of providers to alert the surgeon of worrisome post-operative symptoms. A 66-year- old woman had a long history of scoliosis with several major surgeries to place hardware. She developed pain because of movement of the hardware, and she underwent a major surgery to replace the hardware and fuse a number of vertebral levels.
The surgery was long but seemed to go well. There was bleeding in the epidural space, but it was controlled through cauterization. After the surgery, she was still intubated and sedated, and an initial neuro check found that her legs had 4/5 strength,4 which was expected. But the next morning, repeat neurologic checks by nurses found leg strength at two fifths,5 and by noon she had absent movement in her ankle.
This continued throughout the day without notification to the surgeon or other doctors. Early the next morning, the neurosurgeon did rounds and found the patient could not move her legs. An MRI showed an epidural hematoma, which led to emergent re-exploration and evacuation of the hematoma. Sadly, the patient is left with incomplete paraplegia requiring use of a wheelchair.
Causation in Spinal Cord Compression Cases
A plaintiff in any delay in diagnosis case has the burden to prove both negligence and that such negligence caused the harm complained of.6 Such testimony must not be based on speculation, but instead on the facts of the case, and any opinion must be held to a reasonable degree of medical probability or certainty.7
A major legal problem in both cord compression settings is proving causation.8 In many other types of cases (medical malpractice and other tort claims), the harm complained of may be clear, such as when an automobile collision results in a broken arm. However, in delay in diagnosis cases, causation may be less clear.
Typically, the underlying medical condition needing diagnosis and treatment was not caused by the providers. The burden is on the plaintiff to prove how much of the bad outcome was caused by the delay (as opposed to the underlying condition warranting intervention in the first place).
So often in these cases, one defense position will be that the plaintiff cannot bear the burden of quantifying the degree of harm caused by the delay. Without evidence in the form of a clinical picture and/or imaging at the time the plaintiff alleges intervention should have occurred, this can be a difficult hurdle to overcome.
It is therefore important to establish what the patient’s neurological status was at the time when the diagnosis should have been made. Fortunately, in such cases attorneys have, at a minimum, a hospital encounter that includes some data such as a physical exam (either an ER visit or hospital encounter), or a patient’s subjective complaints. Interviewing your client in detail about the events can help better understand the degree of weakness or sensory loss, and whether or not there was bowel or bladder involvement. This data, coupled with evidenced-based literature, can support an expert’s conclusion regarding a likely outcome had timely surgical intervention occurred.
As one might expect, there are no studies on humans where their spinal cords were compressed at various intervals, then decompressed, and data collected of the harm done. That would, of course, be incredibly unethical. There have been similarly designed animal studies,9 and there have also been retrospective studies, which look back at cases to extrapolate hypotheses about the likely outcome at different points in time.
This literature supports the general proposition that “the sooner the better”. Most intellectually honest expert witness surgeons will agree with this. Next, many conservative experts will concede that with timely intervention at least one keeps the function they have at the time of surgery. Some will even concede that most patients usually get a little better than immediately prior to the decompression surgery.10 After that, it turns into a fight between plaintiff experts with the burden of proof, and defense experts who can sit back and say: “There are no definitive studies that prove that the patient would have had a significantly better outcome.”
Fortunately, there is literature that supports the common-sense idea that earlier intervention likely results in quantifiably better outcomes. Generally speaking, the literature suggests that incomplete or very recent loss of function can be reversible, while complete loss of function is more often permanent.11
Faced with these problems, many experts rely on the basic theory that, once spinal cord decompression surgery occurs, the patient will at least be left with neurological function that they had just before the surgery and sometimes improve. Under this view, “causation” of the deficits is a function of how soon intervention occurs after the onset of neurologic symptoms, and what the neurological deficits were at various points in time when it can be shown that intervention should have occurred.12
Loss of function is often described in the literature with grading systems, which can lend themselves to the sort of quantification of difference in outcome that is necessary for a plaintiff to sustain her burden. One such system is the Frankel Grade classification system, which provides an assessment of spinal cord function.
Scores range from worse to better, with Grade A being no motor or sensory function detected below the level of the cord compression (i.e. the level of spinal disc where the compression occurred), and Grade E being normal motor function, although some abnormal reflexes may persist. In a major study of surgical outcomes in spinal cord hematoma cases, the findings were encouraging for better outcomes than simply the neurologic function the patient had just prior to the intervention:
Surgical evacuation of the hematoma was performed in all patients; 26 of these improved; four remained unchanged, and no patients worsened (mean follow up 11 months). Complete recovery (Frankel Grade E) was observed in 43% of the patients and functional recovery (Frankel Grades D or E) was observed in 87%. Preoperative neurological status correlated with outcome; 83% of Frankel Grade D patients recovered completely compared to 25% of Frankel Grade A patients. The rapidity of surgical intervention also correlated with outcome; greater neurological recovery occurred as the interval from symptom onset to surgery decreased.13
When dividing groups of patients into those treated within 12 hours of onset of neurologic symptoms, those treated between 12-24 hours from onset, and those treated 24-36 hours after onset, 52%, 25%, and 23% patients enjoyed complete motor recovery, respectively.14
SEA and SEH cases are quite similar from a causation perspective. In both, surgery is the necessary intervention.15 In both, outcomes are principally based on the extent and duration of the patient’s preoperative neurologic deficits.16 Further, timing is also described in similar fashion based on the time between neurologic deficits and surgery: generally speaking, the sooner the better.17 And in both, the principle suspected cause of injury is compression, which can lead to permanent ischemia if unrelieved.
The big difference involves the underlying disease with SEA – some infectious process that may be limited to a pocket of pus in the epidural space, but also might be causing systemic problems, including sepsis and death.18 A patient may therefore be less healthy overall than a patient recovering from spinal surgery and developing a SEH. This is consistent with literature that suggests that diabetes (itself a risk factor for SEA but not of SEH) is a “predictor of poor neurologic outcomes” in cases involving paraparesis following surgery for SEA evacuation.19
EAGLE Tyler Goldberg-Hoss is a partner at CMG Law (formerly Chemnick Moen Greenstreet) in Seattle, where he limits his practice to representing victims of medical malpractice.
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1 Although certainly related, this article will not discuss cases involving cauda equina syndrome since the causation issues and literature are somewhat different.
2 Although chemical prophylaxis to prevent blood clotting is not common in spine surgeries, when it is done there is a greater risk of late-onset bleeding that can result in an epidural hematoma.
3 It is important to note that pain may be absent during the early post-op period because of sedation or residual effects of anesthesia.
4 Movement against some resistance but weaker than normal.
5 No movement against gravity, or cannot pick the foot off the bed.
6 Reese v. Stroh, 128 Wn. 2d 300, 308, 907 P.2d 282, 286 (1995) (“the general rule in Washington is that expert medical testimony on the issue of proximate cause is required in medical malpractice cases.”)
7 Hill v. Sacred Heart Med. Ctr., 143 Wn. App. 438, 448, 177 P.3d 1152, 1157 (2008).
8 As you will see below, due to the underlying infectious disease process, SEA cases can involve causation issues other than simply compression.
9 See generally Tarlov, IM, et. al., Acute spinal cord compression paralysis, JNS 1972 Jan;36(1):10-20 (evaluating recovery of neurological function in dogs after spinal cord compression with epidural balloons at various forces and durations). Tarlov et. al found that large forces of compression were tolerated for up to one minute, whereas smaller forces were tolerated up to two hours. Anything more resolved in a less than full recovery.
10 Of course, the plaintiff is often another matter. It is common for defense causation experts to identify particular characteristics of the plaintiff’s particular spinal cord compression that may either be inconsistent with or unaccounted for in the medical literature.
12 Id.
13 Id (emphasis added).
14 Id.
15 Reihsaus, et. al., Spinal epidural abscess: a meta-analysis of 915 patients, Neurosurg Rev. 2000 Dec;23(4):175-204 (“an operation is the method of choice, according to the surgical motto ‘ubi pus, ibi evacua’” (“where there is pus, evacuate it”)).
16 Id. see also Curry et. al., Spinal Epidural Abscess: clinical presentation, management, and outcome, Surg Neurol. 2005 Apr;63(4):364-71; Bond and Manian, Spinal Epidural Abscess: A Review with Special Emphasis on Earlier Diagnosis, Biomed Res Int. 2016;2016:1614328.
17 But, consider Ghobrial GM et. al., Timing in the Surgical Evacuation of Spinal Epidural Abscesses, Neurosurg Focus. 2014 Aug;37(2):E1, which was a retrospective reviewed of 87 patients, who were divided based on a 24 hour cutoff. The paper found no different in outcome as between those decompressed within 24 hours versus those after 24 hours, at least as of the time of hospital discharge.
18 Gossman W, Knorr TL, Mesfin FB. Spinal Epidural Abscess. [Updated 2020 Jan 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan. This paper also notes “bacterial toxins” as a possible cause of injury to the cord.
Publication Date: May 2020
Volume: 55-9
Author: Tyler Goldberg-Hoss
Categories: Medical Negligence, Emergency Medicine, Medical Issues, Quadriplegia/Paraplegia
