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Spinal epidural abscess cases

By Tyler Goldberg-Hoss

A spinal epidural abscess (SEA) is a neurosurgical emergency, since any delay in diagnosing SEA can lead to permanent neurologic deficits and death. Unfortunately, SEA is a notoriously difficult disease process to diagnose, and patients can make multiple trips to the ER or other health care providers before the diagnosis is made.

Delays and failures to diagnose SEA give rise to lawsuits against medical providers due to the unfortunate fact that many don’t consider it as a possible diagnosis until it’s too late, and when the catastrophic nature of injuries cannot be avoided. This article attempts to serve as a primer to attorneys considering handling these claims, and addresses a number of legal issues associated with prosecuting such a case.

Spinal epidural abscess

A SEA is an encapsulated collection of pus (or sometimes granulation tissue) that forms in the epidural space within the spinal column. SEAs are primarily bacterial infections, with staphylococcus aureus the most common cause. Within the spinal column, SEAs most often occur in the thoracic and lumbar spine. SEAs can occur three different ways: from hematogenous (within the blood stream) spread; by extension from nearby infected areas; and by iatrogenic means (typically by some previous surgery or epidural anesthetic procedure).

Some people are more at risk of developing SEA than others. Diabetics, alcoholics, people with underlying infections or who are otherwise immunocompromised, IV drug abusers, and people with a recent history of surgery, particularly spine surgery, are at greatest risk. Men suffer from SEA more than women, and the typical age range is between 31-70 years of age.

Although not completely understood (or at least to the degree a defense expert can attempt to muddy the waters), SEAs injure the spinal cord three different ways.

First, the compression of the cord creates a blockage of both arterial flow in and venous flow out of the spinal cord. Second, the compression itself causes the fibers in the spinal cord to not work properly. Third, and least understood, when the cord is in trouble from lack of oxygen due to the first two reasons, a person’s autoimmune system will send in cells called inflammatory mediators to “mediate” the damage. Unfortunately, these cells go in to digest the foreign material, and also end up digesting the cells of the spinal cord itself.


There are significant challenges to diagnosing SEA on the front lines. Originally, the literature described a “classic triad” of symptoms including fever, spine pain and neurologic deficits. But unfortunately, more recent studies have concluded that only between 8-13% of people who are eventually diagnosed with SEA have these three symptoms upon initial presentation.

SEA is now thought of as a progressive disease, albeit one with a time course that is highly variable. Generally speaking the literature discusses four stages. First, back pain at the level of the infected area and possibly fever. Second, nerve root pain radiating from the affected area. Third, motor weakness, sensory deficit, and bladder and bowel dysfunction. Fourth and finally, paralysis with neurogenic bowel and bladder.

Few patients who are eventually diagnosed with SEA initially present with neurologic findings, making diagnosis possible but difficult at stage one or two when outcomes are likely to be the best. The literature describes best practices as considering SEA in the setting of unexplained spinal tenderness together with any of the previously stated risk factors.

A careful neurologic exam, including percussing each level of the spine looking for focal tenderness, can help a provider zero in on the precise level if an abscess is suspected. Additionally, if there are neurologic symptoms, those can help a provider identify the level as well, depending on the distribution of nerve roots affected.

Often, neurologic exams are inadequate. Further complicating the picture are the patient’s complaints of pain. This is, in part, because the pain is coming not from the abscess pushing on the cord, but on the irritation it is creating on the paraspinal musculature lateral to the spine itself. When these paraspinal muscles are irritated they can spasm, creating feelings of pain in parts of the muscle that may not be at the precise level of the abscess.

In addition to a neurologic exam, lab tests that include inflammatory markers can help exclude SEA or conversely narrow the focus on SEA as a diagnosis. ESR (erythrocyte sedimentation rate) is a non-specific measure of inflammation in the body. While it is not diagnostic for SEA, it is a very good screening tool: in nearly all patients with SEA, their ESR level will be high.

Similarly, CRP (C-reactive protein) levels rise in response to inflammation. Either or both of these tests can help a provider determine whether further work up is warranted to rule out SEA. In a patient complaining of back pain, if either of these tests is elevated it should trigger an urgent request for MRI. This is particularly true if the patient has any of the above risk factors.

With a raised suspicion for SEA, MRI is the gold standard for diagnosis. Although it is prudent to start the MRI at the location where the tenderness is on the spine, if the MRI does not show an abscess, it is incumbent upon the provider to continue looking at the rest of the spine.


In the event that the SEA is caught early, some neurosurgeons, orthopedic surgeons, or infectious disease doctors – those providers who would likely treat SEA patients – advocate starting high doses of antibiotics in the hopes that they can avoid invasive surgery. It is vitally important, if such a decision is made, to pay careful attention to all neurologic symptoms. If the abscess isn’t adequately treated with antibiotics, and continues pressing on the cord, providers need to know this quickly so that decompression surgery can be performed.

In most cases, though, and in nearly all cases where there are neurologic symptoms, emergent surgical decompression is necessary.


At the beginning of the 20th century, everyone with SEA died. Mortality has dropped since then to 34% in the 1950s and 15-20% beginning in the 1990s. Mortality today is usually the result of uncontrolled sepsis or other co-morbid conditions.

Patients who survive are left with varying degrees of neurologic deficit, from no deficits to paralysis with neurogenic bladder and bowel. General factors associated with better outcomes include patients younger than 50, less compression of the cord, and the location of the abscess (better outcome when it’s in the lumbar area and posterior in the spinal column).

The preoperative neurologic stage and duration of neurologic compromise are important predictors of the final neuro­logic outcome for any one patient. A conservative view on prognosis is that a patient at least keeps the neurologic function that he or she had prior to surgery. More consistent with the literature is that a patient keeps what he or she has, and likely gets a little better. The caveat is that a few patients do, in fact, get worse following decompression.

Put another way, there are two types of patients with SEA – those with incomplete deficits prior to surgery, and those with complete deficits (flaccid paraplegia). For those with incomplete deficits when decompression surgery occurs, the chances of good, functional recovery are very good. For those with SEAs caught in stage one or two, this means they will likely remain neurologically intact. Those in stage three can reasonably expect no weakness or a lesser degree of weakness after surgery than before.

For those in stage four and complete paralysis, if paralysis occurs less than 24-36 hours prior to decompression, they can expect to regain some neurologic function post-operatively. For those with paralysis greater than 24-36 hours, surgery is unlikely to reverse paralysis (although surgery might still be necessary to treat the infection and control sepsis). Within this 24-36 hour window of complete paralysis, the best chance at getting full or near full recovery is decompression within the first 4-6 hours. Chances of recovery decrease the longer the delay.

For patients in all stages, almost half are left with some neurologic deficits, including 15% with partial or complete paralysis. For those with motor deficits present at time of diagnosis (stages 3-4) almost 90% were left with at least some residual weakness.

The final result of the spinal cord injury isn’t known until 1-2 years later. Patients can continue to make progress and regain motor and sensory function during this time and even longer, particularly if they are showing consistent improvement and getting good quality health care.

Medical legal issues with delays in diagnosing SEA

SEA has been called the “great masquerader.” In one study, 75% of patients suffered from a diagnostic delay. It is often a missed diagnosis because it is rare and because there is no unifying set of symptoms.

The one symptom nearly every SEA patient does have – back pain – is such a common complaint it is easy to see why patients must often return to the ER over and over before diagnosis is eventually made. Further, in stage two of the disease progression there is nerve root irritation and radiating pain. Unfortunately, this is a common symptom of many people with lumbar stenosis or disc bulges – sciatica.

A patient’s presenting complaints may also confuse the picture. Perhaps she has suffered from back spasms in the past, and thinks this is another flare up of a musculoskeletal problem.

Furthermore, pain is subjective, and complaints of pain can ebb and flow depending in part on whether narcotics are given. As discussed above, the location of the pain can change based on paraspinal muscle spasms. And the presence of pain can lead to inconsistent motor and sensory testing results.

Bowel and bladder symptoms can be confusing too. Likely, a patient has already been to a health care provider (or two or three), and is already taking narcotic mediations for the pain. These narcotics can cause constipation, and can also cause urinary retention, although this is less common. Providers might be fooled into thinking the reason for the lack of bowel movement, or need for a catheter, is due to the opioid medications, and not entertain the idea of neurologic deficits.

Although constipation is a reasonable conclusion from narcotic use, sometimes urine retention is not: the amount can be high enough that a reasonable and prudent health care provider should think it might have a neurologic cause. A normal human male bladder can hold between 600-800 mls, with the urge to urinate occurring somewhere between 150-300 mls. If a patient has a catheter placed due to difficulty urinating, and has retained a large volume of urine, the standard of care may be to consider that something other than narcotics is causing the retention.

It is difficult to fault a provider for failing to have SEA on his or her differential when the only presenting complaint is back pain. However, when there is back pain plus some neurologic dysfunction (either motor, sensory, bowel or bladder), or the patient has returned a number of times due to the severity of the pain, cord compression of some kind must be on the differential.

If a provider has cord compression on his or her differential, whether it be from a tumor, from an abscess, or from some other disease process, it is so dangerous that it needs to be ruled out quickly. The standard of care in such a situation is to perform a full and complete neurologic exam, refer the patient emergently to a specialist (a neurologist, neurosurgeon, orthopedist or physiatrist) for such an exam, or skip the exam and send the patient for imaging directly.

If an exam is done, it must include, at a minimum, motor and sensory evaluation of the lower extremities and a sphincter tone test. If neurologic deficits are present on exam, the standard of care requires imaging the spine or immediate neurosurgical consultation. Once the abscess is found it is a neurosurgical emergency, and it must be decompressed as quickly as possible.

One other point about the standard of care is to consider whether it makes sense to allege that a number of physicians were negligent in failing to diagnose the SEA. Often these cases involve patients who come to the ER numerous times, or are even admitted to the care of one or more hospitalists. On one hand, it may be hard to single out one provider as negligent, when others saw the patient too. On the other, it may be difficult to argue that five doctors were all negligent, one right after the other.


As discussed above, it’s difficult to fault an ER provider for failing to diagnose SEA in a patient with back pain but no neurologic deficits, or only the presence of sciatic pain. So unfortunately, at the point where the standard of care requires action to rule out some form of cord compression, causation becomes the major issue. With all delayed diagnosis cases, as the delay gets longer, arguments for standard of care violations get stronger, while arguments that intervention would have made a difference get weaker. The key is to hit that spot where a violation is clear, and the outcome would be demonstrably better.

Defending these cases on causation grounds can include a number of arguments, mostly focusing on making the medicine and the patient’s symptoms seem confusing. To the extent the records and symptoms are unclear or inconsistent, defense experts can highlight this muddiness. This can include whether or not symptoms are neurologic deficits or consequences of narcotic drugs, or patients’ unwillingness or inability to perform adequately in neurologic testing.

Today’s world of electronic medical records contribute to this confusion. Neurologic exams on two separate days might look oddly similar, as if the physician merely populated over the previous day’s chart. It may be unclear when a particular note was entered and accessible to subsequent a provider. And the printed record attorneys receive can be missing key information that is available to the providers at the time of the care in question, including drop down menu choices.

Defense causation experts can also highlight inconsistencies and differences of opinion in the scientific community, whether or not such inconsistencies exist. This can include testifying that they do not know – and no one can know – what the outcome would have been had early intervention occurred, or whether or not an earlier MRI would have shown the abscess. They can rely on the unknown nature of the mechanism of injury, as between mechanical, vascular, inflammatory mediators or some combination. They can argue that even after decompression, the inflammatory mediators can continue to damage the spinal cord. In addition, causation experts will often push back the time of intervention: an MRI takes three hours, then transferring the patient to a neurosurgical unit takes another two hours, then surgery itself doesn’t start until yet some other, later time. Each hour is critical to a patient’s hypothetical, cause-in-fact prognosis.

Blaming the patient

Defendants may also place blame on the victim, alleging that the patient misled his or her providers, or failed to inform the defendant’s employee doctors with information. For example, a patient might have had a dental procedure done in the recent past, and fail to alert his providers when asked if he had any recent surgery.


Patients who suffer serious cord compression and subsequent deficits to their lower extremities, bladder and bowel are left with a lifetime of challenges. Leaving aside the obvious inability to stand or walk, they are at increased risk for infections due to the need for catheterization, pressure ulcers, cardiac problems, osteoporosis, and myriad other complications.

Having a primary care doctor who can coordinate all of the specialty care is vital to the patient’s well being. For purposes of proving damages, a spine specialist – a neurologist, neurosurgeon, orthopedic surgeon or physiatrist with a spine specialty – will be necessary to fully articulate the patient’s current and future challenges, and work with a life care planner to explain the costs of medical care.

Sometimes, but not always, a neuropsychological evaluation can help explain a patient’s emotional distress. Often patients can be diagnosed with Adjustment disorder and depression. However, depending on the patient, it may be unnecessary.

An economist may also be useful describing any wage loss. Although the defense may argue that the patient can be retrained to do similar-paying work, it is likely that a wheelchair-bound patient would suffer from a number of barriers to successful employment, including tiring easily, spasticity that limits the number of hours one can spend in a wheelchair, and pain that necessitates narcotics, which can cloud thinking. More likely, a patient seeking to continue in the work force might need to consider self-employment, or other employment with flexible schedules, such as the ability to work from home.


Spinal epidural abscess cases can be difficult and expensive to litigate. But when a provider has the necessary information to have cord compression or SEA on the differential, and fails to rule it out quickly, the catastrophic consequences to a patient often justifies the effort.

Tyler Goldberg-Hoss, WSAJ EAGLE member, is chair of WSAJ’s New Member Committee. He is a partner with the Seattle firm Chemnick|Moen|Greenstreet, which limits its practice to representing those injured by medical malpractice.

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