Necrotizing Fasciitis

The diagnosis is tissue, and delay kills - No lab or imaging test should hold up surgery. CT is more sensitive than plain film and plain x-ray has no value; the definitive answer is what the surgeon finds when necrotic tissue gives way to finger dissection with little resistance. If someone wants to send the patient to the scanner, that is a conversation, not a foregone conclusion.

Use LRINEC to support, never to exclude - The Laboratory Risk Indicator for Necrotizing Infection scores CRP, white cell count, hemoglobin, sodium, creatinine, and glucose. A score of six carries a 92% positive predictive value and 96% negative predictive value; eight or above means a 75% risk. Those same six values are the labs you want anyway before induction.

Pain out of proportion, then no pain at all - Early on the pain far exceeds what the skin shows, with tenderness beyond the erythematous border, crepitus, subcutaneous emphysema, bullae, and ecchymosis. Later the area goes numb as vessels thrombose and superficial nerves are destroyed. A patient whose excruciating pain suddenly stopped is worse, not better.

Emergency airway with a full stomach - These patients arrive septic and unresuscitated, and any fasting interval is accidental. Plan an RSI with suction on the field, and choose induction drug and dose on the assumption that cardiac output is low and arm-to-brain time is long.

Resuscitate for capillary leak, not just for volume - The sepsis produces refractory hypotension and diffuse capillary leak, so crystalloid alone will not hold a pressure. Expect to need vasopressors and inotropes. Norepinephrine and phenylephrine can be run peripherally at high dose if central access would delay the incision. See the sepsis and septic shock entry for the resuscitation framework — this entry assumes it.

Neuraxial is usually contraindicated - Systemic infection and coagulopathy are exactly the contraindications to subarachnoid and epidural block, and this patient has both. Plan GETT.

The debridement is wide and it will be repeated - The operation removes all necrotic tissue, and anything of doubtful viability comes out too. Second-look surgery is common and some patients need daily returns to the OR. Plan for a series of anesthetics in a patient who never fully recovers between them, and place lines and access that will survive multiple trips.

Hemodynamics usually improve once the tissue is out - Stability is typically restored after the necrotic tissue and pus are removed, so the worst of the case is before and during debridement rather than at the end. Expect the vasopressor requirement to fall, but do not wean support ahead of the surgical progress.

Expect bleeding and plan for hemostasis - Wide debridement of inflamed, thrombosed tissue bleeds, and the surgical literature specifically calls for meticulous hemostasis in these cases. Have blood available and check hemoglobin serially through the case rather than once at the end.

Heat loss is the default - Large open wounds left packed with wet gauze, repeated exposure, and a long case make hypothermia the expected outcome. Forced-air warming, fluid warmers, and a warm room from the start, not as a rescue.

They stay intubated - The patient should remain intubated and go to critical care after debridement. Plan the transport and the handoff, not an OR extubation.

Perineal involvement adds an abdominal case - Many of these patients need a fecal diversion to keep the perineal wound from being contaminated. Ask the surgeon about the plan before you set up, because a soft tissue debridement and a colostomy are different anesthetics.

Know the comorbidity you are inducing - Most of these patients are diabetic, and alcohol use and cirrhosis are common. The LRINEC panel already hands you the glucose, sodium, creatinine, and hemoglobin; add LFTs and coagulation studies for the cirrhotic patient before you plan any invasive line.

Reconstruction is a separate later problem - Once granulation appears, closure usually requires muscle flaps or grafts. Hyperbaric oxygen is adjunctive only and never a substitute for debridement. Those cases arrive weeks later in a deconditioned, catabolic patient who has already had many anesthetics.

Necrotizing fasciitis is an aggressive skin and soft tissue infection that destroys muscle fascia and subcutaneous tissue. Bacteria enter through a break in the skin in roughly 80% of cases — most often Staphylococcus aureus or Streptococcus in single-source disease, or a mixed gram-negative and anaerobic flora — then track along the fascial plane, which has a poor blood supply and offers little resistance.

Small and medium vessels thrombose, producing vascular occlusion, ischemia, extensive fascial and fat necrosis, and destruction of the superficial nerves, all while the overlying skin still looks nearly normal. That mismatch is exactly why the diagnosis arrives late. Diabetes, alcohol use, and cirrhosis dominate the risk profile. Systemically it produces sepsis with refractory hypotension and diffuse capillary leak; mortality runs 20% to 80% and tracks directly with how fast the tissue comes out.