Spine Infection After Surgery

A surgical site infection of the spine is, by definition, an infection introduced into or seeded around the operated tissues at or after the time of surgery. It is conventionally divided by depth. A superficial infection lies above the deep fascia, the tough sheet that covers the spinal muscles, and involves the skin and the fatty layer beneath it. A deep infection lies below that fascia and involves the muscle, the bone, the disc space and, where present, the implanted metalwork. This distinction by depth runs through the whole subject, because depth largely determines how serious the infection is.

Postoperative discitis, sometimes called postoperative spondylodiscitis, is a particular form of deep infection in which the organism takes hold within a disc space that has been operated upon, typically after a discectomy. From the disc it can spread to the adjacent vertebral bone. It is recognised as a distinct entity precisely because it occurs in a disc that surgery has already disturbed.

What sets postoperative spinal infection apart is that it must be carefully distinguished from several look-alikes while at the same time never being dismissed too readily. It can resemble a simple non-infected wound problem such as a seroma or a haematoma; it can be confused with spontaneous, blood-borne infections of the spine; and, when it is low-grade, it can masquerade as one of the purely mechanical reasons that pain sometimes returns after spinal surgery.

After spinal surgery, fluid can collect beneath the healing wound. A seroma is a collection of clear, straw-coloured tissue fluid; a haematoma is a collection of blood. Both can cause the wound to swell, feel tense and sometimes leak, and both can be uncomfortable. In their early stages they can look very much like an infection, and this overlap is one of the central difficulties of the postoperative period. The difficulty is compounded by imaging: a scan performed soon after surgery shows swelling, fluid and tissue reaction as a matter of course, and these expected changes are not reliably separated from infection by imaging alone.

A further subtlety is the difference between colonisation and true infection. A wound or fluid collection may grow bacteria on culture and yet not be truly infected; what marks a genuine infection is the presence of pus and of inflammatory white cells, rather than simply a positive culture. The practical consequence is that separating a non-infected wound problem from a true infection often rests on the overall clinical picture and on the examination of fluid or tissue, rather than on any single test.

The spine can also become infected without any operation at all. In spontaneous, or haematogenous, vertebral osteomyelitis and discitis, bacteria travel through the bloodstream from a distant source and settle in the spine, seeding the disc and the bordering bone. Postoperative infection differs from this in its origin and therefore in its whole context. Here the organism is introduced in relation to the surgery rather than carried in by the blood from elsewhere, the operated tissues and any metalwork form the setting in which it develops, and the imaging is complicated by the changes that surgery itself produces.

Pain that returns or persists after spinal surgery has many possible explanations that have nothing to do with infection: pseudarthrosis or non-union, loosening or breakage of the metalwork, symptomatic adjacent segment disease, or a recurrent disc herniation. The complication is that a low-grade, smouldering infection can imitate these mechanical problems closely. When an infection is caused by a low-virulence organism, especially one that forms a film on the surface of metalwork, it may produce little more than gradually worsening pain, without fever, redness or obvious wound trouble. Loosening of the implants seen on a scan, which might at first be read as a purely mechanical failure, can in some cases be the only outward sign of an indolent infection.

The reason all these distinctions are drawn so carefully is the asymmetry of the stakes. On one side lie the benign mimics — a seroma, a haematoma, a colonised but not truly infected wound, an ordinary mechanical cause of pain. On the other side lies a missed deep infection. A deep infection around an instrumented fusion threatens two things at once. It threatens the construct, because infection can interfere with the bone healing that the metalwork is there to support, and can ultimately loosen the fixation before fusion is achieved. And it threatens the neural elements, because infection in the spinal canal can form a collection that presses on the spinal cord or nerve roots.

Across a broad systematic review and meta-analysis, the pooled rate of infection after spine surgery was in the region of three per cent overall, but this single figure conceals a wide spread. The presence of metalwork raises the rate: infection in around four to four and a half per cent of instrumented operations, compared with roughly one and a half per cent of operations without instrumentation. Simple, clean procedures such as a lumbar discectomy carry among the lowest rates, often well under one per cent. The approach also matters: minimally invasive surgery has been associated with lower infection rates than equivalent open surgery, on the order of one and a half per cent against close to four per cent. The risk rises with longer and more complex operations, longer instrumented constructs, deformity correction and revision surgery.

Early, or acute, infection typically declares itself within the first few weeks, commonly cited as up to around six weeks. It tends to behave in a recognisable way, with features such as fever, redness or warmth around the wound, prolonged or pus-like wound drainage, and increasing pain. Delayed, or late, infection appears later, sometimes many months or even years after the operation, and behaves very differently. It is almost always deep, and it is characteristically quiet. Rather than fever and an angry wound, it may present only as gradually worsening pain, or as loosening of the metalwork on a scan. Infections caused by the slow-growing organism Cutibacterium acnes are a notable example, with the interval between the first symptoms and the diagnosis often measured in months rather than weeks.

Staphylococcus aureus, including the meticillin-resistant form, is the single most common organism, followed by the coagulase-negative staphylococci such as Staphylococcus epidermidis, by Cutibacterium acnes, and by various Gram-negative bacteria. Early infections are more often caused by the more aggressive organisms; delayed infections more often by the quieter, low-virulence organisms that provoke little reaction and are easily overlooked.

Central to the behaviour of infection on metalwork is the phenomenon of biofilm. Bacteria that reach the surface of an implant can attach to it and surround themselves with a protective slime layer, switching from a free-floating, active state to a dormant, shielded one. Within this biofilm they are far less exposed to the body's defences and to antibiotics, and they provoke little inflammation. Once a mature biofilm has formed, clearing the infection by cleaning the tissues alone, without addressing the implant, is difficult, and the chance of the infection returning is high if established biofilm on the metal is left in place.

Recognised risk factors fall into two groups. Patient factors include diabetes, obesity, smoking, long-term steroid or other immune-suppressing treatment, rheumatoid disease, poor nutrition, older age, a previous surgical site infection and a generally higher burden of illness. Several act through similar mechanisms: diabetes and smoking impair the small blood vessels and starve the healing tissues of oxygen, while obesity creates a thick, poorly supplied layer of fat that heals less readily. Operative factors include a longer operating time (often cited as three hours or more), greater blood loss, instrumentation, longer fusions, deformity surgery and revision procedures.

C-reactive protein and the erythrocyte sedimentation rate follow a predictable course after uncomplicated surgery: C-reactive protein rises sharply, peaks within a day or two and usually settles within one to two weeks, while the sedimentation rate falls more slowly. A marker that fails to fall, or that rises again after starting to settle, draws attention. C-reactive protein is the most useful single marker, both for raising suspicion and for following the response to treatment.

Magnetic resonance imaging with contrast is the imaging test of choice for deep infection and postoperative discitis. Its difficulty is twofold. First, the operated level normally shows swelling and enhancement as part of healing, so distinguishing expected post-surgical change from infection is genuinely hard. Second, metalwork distorts the image; specialised metal-reduction scanning techniques, and computed tomography for the bone and the implants, are used to work around this. Because imaging often cannot give a definitive answer, sampling of deep tissue for culture holds a central place. Tissue taken at operation is regarded as the most reliable way to identify the responsible organism. Several deep samples are usually taken, and cultures may be held for a prolonged period to detect slow-growing Cutibacterium acnes.

Superficial infections are often described as manageable with local wound care and a course of antibiotics, sometimes with a minor procedure to clean the wound. Deep infections are generally addressed by surgical debridement and irrigation — a thorough cleaning of the infected tissues with copious washout — sometimes repeated, and sometimes combined with negative-pressure dressings.

Around this sits the central question of what to do with the metalwork. In early or acute deep infection, the prevailing principle is implant retention: the metalwork is still needed to hold the spine while the bone fuses, so the described approach is debridement and irrigation with the implants left in place, combined with a prolonged course of antibiotics. Several large series report that retaining the implants in this way is effective in the majority of acute cases presenting within around three months, provided the metalwork is stable.

In late or chronic infection, by contrast, removal of the metalwork is more often required, particularly once the spine has fused and the implants are no longer mechanically essential. The reason is biofilm: a mature film on the metal cannot reliably be cleared while the metal remains, and the literature reports a high rate of recurrence — up to around half of cases in some reports — when established late infection is treated with the implants retained. Antibiotics are described as prolonged, commonly six weeks and often twelve weeks or longer where implants are retained, and ideally chosen to be active against organisms growing within biofilm; combinations including rifampicin for staphylococcal infection on retained metal are reported to improve outcomes.

Superficial infections, recognised and treated, generally resolve well and without lasting consequence. Deep infections are more demanding, but the literature is broadly encouraging about acute deep infection treated promptly with debridement, implant retention and prolonged antibiotics, with the majority of such cases controlled and the construct preserved while the bone fuses. The more difficult situations are the delayed, low-grade infections, where the diagnosis may have been slow to emerge and where established biofilm on the metalwork often dictates a more involved course. Even here, the literature describes good rates of eventual control, particularly once fusion has been achieved.

This page is general medical education and is not a substitute for individual advice. Fever, increasing wound pain or discharge, new neurological symptoms, saddle numbness or any disturbance of bladder or bowel control after spinal surgery requires urgent assessment.

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This information is for general patient education and is not a substitute for an individual consultation. Always seek personalised advice from a qualified spinal specialist.