Osteomyelitis

Repeat anesthetics, not one - Debridement of all diseased bone is the treatment, because antibiotics penetrate abscess and necrotic bone poorly, and the pathology report from each washout decides whether another is needed. Expect a series of cases in the same patient over weeks. Carry the airway grade, access, and analgesic requirement forward from the last one instead of rediscovering them.

Vancomycin potentiates your relaxant - Vancomycin enhances the effect of neuromuscular blocking agents and piperacillin does the same to vecuronium. Six weeks into that combination, dose relaxant to the TOF rather than to weight and confirm reversal before extubation.

Aminoglycosides - what the label actually says - The gentamicin boxed warning is nephrotoxicity, worse with impaired renal function, high dose, or prolonged therapy, and neurotoxicity in the form of vestibular and auditory ototoxicity that is usually irreversible. The label asks for renal and eighth cranial nerve monitoring, peaks kept off prolonged levels above 12 mcg/mL and troughs below 2 mcg/mL, and flags dehydration and prior ototoxic exposure as added risk. Concomitant cephalosporins increase the nephrotoxicity.

Aminoglycoside blockade is a labeled precaution - The label says to consider neuromuscular blockade and respiratory paralysis whenever an aminoglycoside is given by any route to a patient receiving anesthetics or neuromuscular blocking agents such as succinylcholine, or after massive transfusion of citrate-anticoagulated blood - and that calcium salts may reverse it. Use caution in myasthenia gravis or parkinsonism, where the curare-like effect at the junction aggravates the weakness.

Irrigation counts as a dose - Neurotoxic and nephrotoxic antibiotics are almost completely absorbed from body surfaces after local irrigation or topical application during surgery. On a debridement where the field is washed with an aminoglycoside, expect the same blockade, respiratory paralysis, and oto- and nephrotoxicity you would from giving it intravenously.

Long courses move the electrolytes - Paresthesias, tetany, positive Chvostek and Trousseau signs, and mental confusion have been described during and after gentamicin therapy in patients with hypomagnesemia, hypocalcemia, and hypokalemia; in infants it presents as tetany and muscle weakness. Send magnesium and calcium with the creatinine, not instead of it.

Don't run the vancomycin in fast - Rapid infusion of a large dose causes the vancomycin infusion reaction (formerly called red man syndrome) with flushing, rash, and hypotension, and rarely severe hypotension and cardiovascular collapse. Give it over at least an hour; if a rash appears on face, neck, or trunk, slow to 1.5 to 2 hours and increase the dilution volume.

Renal function before every return - Check the creatinine and the vancomycin trough or AUC before you dose renally cleared drugs. Nephrotoxicity risk climbs with troughs above 15 mg/L, AUC above 650 mg·h/L, therapy beyond seven days, and any concurrent nephrotoxin - piperacillin-tazobactam, aminoglycosides, loop diuretics, amphotericin. Keeping the patient well hydrated reduces aminoglycoside nephrotoxicity, so don't let them sit dry through a long fast on a dosing day.

Check the CBC, not just the chemistry - Prolonged vancomycin causes neutropenia after about a week and immune thrombocytopenia typically one to two weeks in; piperacillin-tazobactam causes leukopenia, thrombocytopenia, and platelet dysfunction after 10 to 15 days. Both change the decision about a block or a neuraxial.

Host compromise is the anesthetic problem - Chronic osteomyelitis persists because the host is compromised. Systemically that means malnutrition, renal or hepatic failure, diabetes, chronic hypoxia, neoplasm, or immunodeficiency; locally it means peripheral vascular disease, arteritis, lymphedema, venous stasis, neuropathy, and tobacco. Work that list before you call it a routine washout.

Diabetic foot source - The commonest contiguous route is a neuropathic foot ulcer. Check the glucose trend and document the existing sensory deficit on exam before a popliteal or ankle block, because the neuropathy predates you. Revascularization often has to precede debridement, and failure of both ends in amputation.

Vertebral osteomyelitis and the needle - Infection tracks from the disc into the adjacent endplates and on into the paraspinal and epidural space, so don't pass a neuraxial needle through or near an involved level. ESR and CRP are the sensitive markers, 94% to 100%; the white count is normal in up to 40% and will falsely reassure you. MRI defines the extent, with accuracy of 90% or better.

Document the neurology first - A third of patients with vertebral osteomyelitis already have sensory loss, weakness, or radiculopathy when they present, and at least 15% end with a permanent deficit. Record the exam before you touch them.

You are one of the seeding routes - Vertebral osteomyelitis follows spinal surgery, facet injections, and epidural injections, with coagulase-negative staphylococci and Cutibacterium (Propionibacterium) acnes when hardware is present. Full sterile technique on every neuraxial and interventional pain procedure is the prevention.

Sickle cell overlap - Hematogenous osteomyelitis in sickle cell disease is Salmonella or S. aureus. That patient brings the sickle plan with them: the hydration, warming, and oxygenation targets don't lapse because the case is only a washout.

Osteomyelitis is infection of bone and marrow, seeded hematogenously, by contiguous spread from nearby soft tissue, or by direct inoculation through trauma or surgery. Bone is poorly vascularized and most antibiotics penetrate it badly, so the infection is hard to clear. As pus strips the periosteum the blood supply fails and bone dies; the dead fragment, a sequestrum, walls itself off inside reactive new bone called involucrum and drains through a cloaca and sinus tract. Once necrotic bone exists the disease is chronic and antibiotics alone will not cure it. Staphylococcus aureus dominates, with Salmonella and S. aureus in sickle cell disease. That is why these patients come back to the room repeatedly for debridement, weeks deep into intravenous antibiotics, still carrying the host compromise that let the infection take hold.