The hyperbaric oxygen therapy nurse’s communication challenge
The hyperbaric oxygen therapy nurse works at the intersection of basic physics, cellular biology, and a patient population that almost never expected to be inside a pressurized steel cylinder breathing pure oxygen. HBOT patients arrive with three diagnoses that at first glance have nothing in common: the diabetic foot wound that antibiotics have failed to heal, the carbon monoxide poisoning in a patient who “already recovered” in the emergency department, and the necrotizing fasciitis patient who has just survived a radical surgical debridement. What they share is a question: why do I need this?
The communication challenge in each case is mechanistic. The diabetic foot wound family cannot understand how breathing gas in a machine does anything to an infection in the foot. The CO poisoning family cannot understand why the chamber is needed when the oxygen given in the emergency department clearly worked — the level came down from 32 percent to 6 percent, and the patient is awake and talking. The necrotizing fasciitis family cannot understand why daily hyperbaric sessions are being added when surgeons already removed the infected tissue and three intravenous antibiotics are already targeting the bacteria.
In each case, the family’s logic is entirely coherent based on their model of how treatment works. The HBOT nurse’s job is to explain the mechanism that makes HBOT different — not a replacement for antibiotics or surgery, but an intervention that targets a biological problem those treatments cannot reach: the tissue hypoxia that disables the immune system, the lipid peroxidation cascade that causes delayed brain injury, and the anaerobic microenvironment that enables the most destructive wound pathogens to survive and spread.
Three conversations from the hyperbaric unit:
Scenario 1: Elena Gutiérrez-Flores — 58, retired bookkeeper from San Antonio, Texas
Elena Gutiérrez-Flores had been managing type 2 diabetes for twenty-two years. She had started with metformin in her mid-thirties, added glipizide in her forties, and been on insulin — long-acting glargine at night, rapid-acting aspart before meals — for the past seven years. Her HbA1c had run between 8.2 and 9.4 percent for most of that time; she was not an outlier in her clinic’s patient panel, but she was not controlled either. She had background diabetic retinopathy, early proteinuria, and the peripheral neuropathy that had cost her the protective sensation in her feet four years ago. She could not feel the bottom of her feet.
Eleven weeks earlier, she had noticed a small area of redness under her right heel. She had not felt it develop — she had only found it because her daughter Marisol, a 30-year-old dental hygienist who did her mother’s weekly foot inspection, had seen it during their Sunday dinner ritual. Marisol had photographed the heel, called the wound care clinic first thing Monday morning, and driven her mother in herself. The wound had been measured at 1.4 centimeters in diameter and less than 0.5 centimeters deep — a Wagner Grade 1 diabetic foot ulcer, clean base, minimal slough, no probe-to-bone. The tissue oxygen at the wound edge, measured by transcutaneous oxygen monitoring (TcPO2) with the patient breathing room air, was 18 millimeters of mercury.
Eleven weeks and three wound care visits per week later, the wound had not closed. The wound base was pale, non-granulating. The TcPO2 had not improved. The wound care team had optimized offloading with a total-contact cast, maximized insulin management in coordination with endocrinology (HbA1c now 8.3 percent), and debrided the wound weekly. The wound was clean, not infected. It just was not healing. At the multidisciplinary wound team meeting, the vascular surgeon had measured the ankle-brachial index at 0.62 — consistent with peripheral arterial disease of moderate severity that was not amenable to endovascular revascularization given the distribution. The wound care physician had recommended HBOT evaluation.
Elena and Marisol were sitting in the HBOT consultation room at University Hospital when registered nurse and HBOT coordinator Gabriela Espinoza-Herrera came in with the TcPO2 probe results from that morning’s pre-treatment testing. The probe had been placed at the wound edge with Elena breathing room air (TcPO2: 18 mmHg), then breathing 100 percent oxygen by face mask at normal pressure (TcPO2: 34 mmHg), and then — this was the number that mattered — while Elena sat in a portable pressure test breathing 100 percent oxygen at 2.4 atmospheres (TcPO2: 276 mmHg).
Marisol had driven her mother to every wound care appointment for eleven weeks. She was a careful, organized person, and she had googled “hyperbaric oxygen diabetic foot wound” the previous night. She had questions.
“Le entiendo la idea general, pero lo que no entiendo es cómo respirar oxígeno en una cámara le hace algo a una herida en el pie. Los antibióticos llegan a la herida por la sangre. El oxígeno que respira uno va a los pulmones. ¿Cómo llega a la herida?” (I understand the general idea, but what I don’t understand is how breathing oxygen in a chamber does anything to a wound in the foot. Antibiotics reach the wound through the blood. The oxygen one breathes goes to the lungs. How does it reach the wound?)
Gabriela had answered this question hundreds of times in eleven years of HBOT nursing. She had learned that the best answer started not with the chamber but with why normal tissue oxygen delivery was failing.
“Primero me permita explicarle por qué la herida no está cerrando, aunque su mamá no tiene infección activa ahora mismo. La razón es que el tejido de la herida tiene muy poco oxígeno.” (First let me explain to you why the wound is not closing, even though your mother does not have an active infection right now. The reason is that the wound tissue has very little oxygen.)
She explained the two systems that normally deliver oxygen to a healing wound. The first is the hemoglobin system: red blood cells carry oxygen bound to hemoglobin molecules and release it in capillary beds as the hemoglobin encounters tissues with lower oxygen concentrations. The second, smaller, component is oxygen dissolved directly in plasma — at sea level breathing normal air, approximately 0.3 milliliters of oxygen per deciliter of blood. In a diabetic foot wound, the first system — the hemoglobin system — is impaired because the small vessels supplying the wound have narrowed and thickened from years of high glucose exposure. Elena’s ankle-brachial index of 0.62 meant that arterial pressure at the ankle was only 62 percent of what it was in the arm. The capillary beds in the wound bed were underperfused. The transcutaneous oxygen monitor confirmed it directly: 18 mmHg at the wound edge, compared to the 40 to 50 mmHg healthy wound tissue would have.
“Con dieciocho milímetros de mercurio de oxígeno en el tejido, dos cosas importantes no pueden funcionar bien. La primera: las células blancas de la sangre — los neutrófilos — son las que matan las bacterias en la herida. Los neutrófilos matan bacterias generando radicales de oxígeno, que son tóxicos para las bacterias. Para hacer esos radicales necesitan oxígeno. Por debajo de 30 milímetros de mercurio, su capacidad de matar bacterias cae alrededor de un 60 por ciento. Los antibióticos llegan a la herida, pero el sistema inmune que debería estar matándolas está trabajando con el 40 por ciento de su capacidad normal.” (With 18 millimeters of mercury of oxygen in the tissue, two important things cannot function well. The first: the white blood cells — the neutrophils — are the ones that kill bacteria in the wound. Neutrophils kill bacteria by generating oxygen radicals, which are toxic to bacteria. To make those radicals they need oxygen. Below 30 millimeters of mercury, their ability to kill bacteria falls by approximately 60 percent. Antibiotics arrive at the wound, but the immune system that should be killing the bacteria is working at 40 percent of its normal capacity.)
Marisol was leaning forward. “¿Y la segunda cosa?” (And the second thing?)
“Los fibroblastos. Son las células que construyen el tejido nuevo en una herida — producen colágeno, que es la estructura del tejido de cicatriz. La producción de colágeno requiere un paso químico que necesita oxígeno — la hidroxilación de prolina, que convierte la prolina en hidroxiprolina, el aminoácido que da al colágeno su estabilidad. Por debajo de 20 milímetros de mercurio de oxígeno, los fibroblastos no pueden producir colágeno de manera adecuada. El tejido nuevo no crece aunque no haya infección.” (The fibroblasts. They are the cells that build new tissue in a wound — they produce collagen, which is the structure of scar tissue. Collagen production requires a chemical step that needs oxygen — the hydroxylation of proline, which converts proline to hydroxyproline, the amino acid that gives collagen its stability. Below 20 millimeters of mercury of oxygen, fibroblasts cannot produce collagen adequately. New tissue does not grow even if there is no infection.)
Elena had been listening quietly. She understood what it meant for things not to work. “Entonces la herida no cierra porque le falta oxígeno.” (So the wound is not closing because it lacks oxygen.)
“Exactamente. Y ahora la pregunta que hizo Marisol: ¿cómo llega más oxígeno a la herida si los vasos pequeños están dañados? Aquí es donde entra la física de la cámara.” (Exactly. And now the question Marisol asked: how does more oxygen reach the wound if the small vessels are damaged? This is where the physics of the chamber comes in.)
Gabriela took the TcPO2 printout and placed the three numbers side by side: 18 (room air), 34 (100 percent oxygen at normal pressure), 276 (100 percent oxygen at 2.4 atmospheres in the chamber). She pointed at the middle number.
“Cuando su mamá respira oxígeno puro a presión normal — por máscara aquí en el cuarto — el oxígeno en la herida sube de 18 a 34 milímetros de mercurio. Eso es porque la hemoglobina ya está casi llena de oxígeno en condiciones normales — solo puede añadirse un poco más. La hemoglobina es como un taxi con casi todos los asientos ocupados: agregar un pasajero más no cambia mucho el número total de personas que llegan al destino.” (When your mother breathes pure oxygen at normal pressure — through a mask here in the room — the oxygen in the wound rises from 18 to 34 millimeters of mercury. That is because hemoglobin is already almost full of oxygen under normal conditions — only a little more can be added. Hemoglobin is like a taxi with almost all seats occupied: adding one more passenger does not change much the total number of people reaching the destination.)
“Pero cuando la presión sube a 2.4 veces la presión normal dentro de la cámara, el oxígeno empieza a disolverse directamente en el plasma — la parte líquida de la sangre — en cantidades mucho mayores. Es la ley de Henry: a mayor presión, más gas se disuelve en líquido. En condiciones normales, el plasma lleva 0.3 mililitros de oxígeno por decilitro. Dentro de la cámara a 2.4 atmósferas, el plasma lleva aproximadamente 6 mililitros de oxígeno por decilitro. Ese oxígeno disuelto en el plasma no necesita hemoglobina ni vasos pequeños funcionales para llegar al tejido. Difunde directamente del plasma hacia el tejido de la herida, siguiendo el gradiente de concentración.” (But when the pressure rises to 2.4 times normal pressure inside the chamber, oxygen begins to dissolve directly in the plasma — the liquid part of the blood — in much larger quantities. It is Henry’s Law: at higher pressure, more gas dissolves in liquid. Under normal conditions, plasma carries 0.3 milliliters of oxygen per deciliter. Inside the chamber at 2.4 atmospheres, plasma carries approximately 6 milliliters of oxygen per deciliter. That oxygen dissolved in plasma does not need hemoglobin or functional small vessels to reach the tissue. It diffuses directly from plasma into the wound tissue, following the concentration gradient.)
Marisol looked at the number 276 on the printout. “Y eso es suficiente para que funcionen los fibroblastos y los neutrófilos.” (And that is enough for fibroblasts and neutrophils to function.)
“Más que suficiente. A 276 milímetros de mercurio en el tejido, los neutrófilos funcionan con su capacidad completa. Los fibroblastos producen colágeno normalmente. Y una cosa más: el oxígeno alto estimula a las células del vaso sanguíneo en la herida a producir una proteína llamada VEGF — factor de crecimiento vascular endotelial — que hace crecer vasos sanguíneos nuevos en la herida. Con el tiempo, esos vasos nuevos mejoran la circulación permanentemente.” (More than enough. At 276 millimeters of mercury in the tissue, neutrophils function at full capacity. Fibroblasts produce collagen normally. And one more thing: the high oxygen stimulates the blood vessel cells in the wound to produce a protein called VEGF — vascular endothelial growth factor — which causes new blood vessels to grow in the wound. Over time, those new vessels permanently improve circulation.)
Elena was looking at the number on the printout — 276 — and comparing it to 18. “¿Y el antibiótico qué hace entonces?” (And what does the antibiotic do then?)
“El antibiótico hace lo que hace bien: mata bacterias por mecanismos químicos — bloquea su pared celular, interrumpe su metabolismo. No puede cambiar el nivel de oxígeno en el tejido. El oxígeno hiperbárico no puede llegar a una bacteria que está dentro de tejido sin circulación. Los dos hacen cosas diferentes y juntos funcionan mejor que cada uno solo.” (The antibiotic does what it does well: it kills bacteria through chemical mechanisms — blocks their cell wall, disrupts their metabolism. It cannot change the oxygen level in the tissue. Hyperbaric oxygen cannot reach bacteria inside tissue without circulation. The two do different things and together work better than either one alone.)
Marisol looked at her mother. “El antibiótico mata las bacterias que ya están ahí. El oxígeno hiperbárico cambia el ambiente para que el cuerpo pueda cerrar la herida.” (The antibiotic kills the bacteria already there. The hyperbaric oxygen changes the environment so the body can close the wound.)
“Exactamente. Y cambia el ambiente para que las bacterias que viven sin oxígeno no puedan sobrevivir.” (Exactly. And it changes the environment so that bacteria that live without oxygen cannot survive.)
Elena nodded. “¿Cuántas sesiones necesito?” (How many sessions do I need?)
“El protocolo para heridas diabéticas es típicamente treinta sesiones a lo largo de seis semanas — cinco días a la semana. Cada sesión dura noventa minutos dentro de la cámara. Los estudios muestran que las heridas diabéticas tratadas con oxígeno hiperbárico tienen una tasa de cierre un 60 por ciento mayor que las tratadas solo con cuidado estándar de heridas en pacientes con TcPO2 que responde a la presión como el de usted.” (The protocol for diabetic wounds is typically thirty sessions over six weeks — five days per week. Each session lasts ninety minutes inside the chamber. Studies show that diabetic wounds treated with hyperbaric oxygen have a 60 percent higher closure rate than those treated with standard wound care alone in patients with TcPO2 that responds to pressure like yours.)
Elena, who had driven herself to three wound care visits per week for eleven weeks with a wound that had not budged, did not hesitate. “Empieza el lunes.” (We start Monday.)
Scenario 2: Roberto Sánchez-Medina — 44, high school history teacher from Houston, Texas
Roberto Sánchez-Medina had been found by his wife Patricia at 7:15 in the morning, unconscious on the floor of their attached garage with a 2019 Honda Accord running. The garage door had been closed. She had pulled him into the driveway and called 911. Paramedics had arrived in seven minutes and found him with a Glasgow Coma Scale of 8 — responsive to painful stimuli but not to verbal commands — and a pulse oximeter reading of 98 percent, which was misleadingly normal because pulse oximetry cannot distinguish oxyhemoglobin from carboxyhemoglobin. A co-oximeter blood draw confirmed what the paramedics suspected: carboxyhemoglobin 32 percent.
He had been brought to Memorial Hermann by paramedics on 100 percent oxygen by non-rebreather mask. By the time the emergency department physician ordered the HBOT consultation ninety minutes later, Roberto was awake, oriented to person, place, and date, answering questions coherently, and walking to the bathroom unassisted. His repeat co-oximeter reading was COHb 6 percent — a drop of 26 percentage points in ninety minutes of normobaric oxygen. The emergency medicine attending had documented his neurological examination as intact and had noted the HBOT referral as indicated given the initial COHb level.
Patricia Sánchez — a 42-year-old high school principal who had spent the previous three hours in the emergency department waiting room oscillating between terror and relief — had watched her husband walk out of the bay holding a cup of coffee and joking with the nurse about missing his third-period class. She was sitting next to him in the consultation bay when HBOT nurse David Castillo-Reyes walked in with the consent form.
“Entiendo que me dijeron que necesita la cámara, pero ¿puede explicarme por qué? El nivel de CO ya bajó de 32 a 6. Está despierto, está hablando, está caminando. Parece que el oxígeno del hospital ya lo curó.” (I understand they told me he needs the chamber, but can you explain why? The CO level already went from 32 to 6. He is awake, he is talking, he is walking. It seems like the hospital oxygen already cured him.)
David had been an HBOT nurse for nine years and had done this consultation dozens of times. He knew that the family’s logic was entirely coherent — the patient appeared recovered — and that the explanation required two separate concepts that needed to be presented in the right order.
“Tiene razón en que el oxígeno del hospital funcionó para lo más urgente. El monóxido de carbono que estaba pegado a la hemoglobina bajó de 32 a 6 por ciento — eso es una mejora enorme. Roberto está consciente y orientándose porque ese CO ya se desprendió. Pero hay dos razones por las que la cámara todavía está indicada, y quiero explicarle las dos.” (You are right that the hospital oxygen did its job for the most urgent issue. The carbon monoxide that was attached to the hemoglobin dropped from 32 to 6 percent — that is an enormous improvement. Roberto is conscious and oriented because that CO has already detached. But there are two reasons why the chamber is still indicated, and I want to explain both to you.)
He began with the kinetics.
“La primera es la velocidad. El nivel de CO todavía no es cero — está en 6 por ciento. Para bajar a cero, el CO que queda tiene que desprenderse de la hemoglobina a su propio ritmo. Ese ritmo depende de la presión del oxígeno que Roberto está respirando. En aire normal, la mitad del CO restante tarda entre 4 y 5 horas en salir. Con oxígeno puro a presión normal — la máscara que le están dando aquí — la mitad del CO restante sale en 60 a 90 minutos. Dentro de la cámara a 2.4 atmósferas, la mitad del CO restante sale en 15 a 30 minutos. Una sesión de 90 minutos en la cámara saca el CO a cero más rápido que varias horas más de oxígeno por máscara.” (The first is speed. The CO level is still not zero — it is at 6 percent. For it to get to zero, the remaining CO has to detach from hemoglobin at its own rate. That rate depends on the pressure of the oxygen Roberto is breathing. In normal air, half of the remaining CO takes 4 to 5 hours to leave. With pure oxygen at normal pressure — the mask they are giving him here — half of the remaining CO leaves in 60 to 90 minutes. Inside the chamber at 2.4 atmospheres, half of the remaining CO leaves in 15 to 30 minutes. A 90-minute session in the chamber removes the CO to zero faster than several more hours of mask oxygen.)
Patricia nodded slowly. “Eso tiene sentido. Pero si ya está en 6, ¿es realmente tan importante la diferencia entre sacar el 6 en media hora versus en dos o tres horas?” (That makes sense. But if it is already at 6, is the difference between removing the 6 in half an hour versus two or three hours really that important?)
David had been expecting this question. “En sí mismo, no. Un nivel de 6 por ciento no es el mismo riesgo que 32. La segunda razón es más importante, y es la que más le quiero explicar.” (In itself, no. A level of 6 percent is not the same risk as 32. The second reason is more important, and it is the one I most want to explain to you.)
He explained that carbon monoxide does not only bind hemoglobin. CO is a small molecule that diffuses across cell membranes and enters mitochondria, where it binds to cytochrome c oxidase — the last enzyme in the mitochondrial respiratory chain, the protein complex that uses oxygen to generate the proton gradient that drives ATP synthesis. When CO blocks cytochrome c oxidase, cells cannot use oxygen even if it is available. This is why CO poisoning is so dangerous even for patients whose blood oxygen saturation appears normal by standard pulse oximetry: the hemoglobin may be carrying oxygen, but the cells cannot use it.
“Durante el tiempo que Roberto estuvo inconsciente en el garage — que fueron probablemente varias horas antes de que usted lo encontrara — las células de su cerebro, especialmente en dos regiones llamadas globo pálido e hipocampo, no podían producir energía normalmente. Eso genera radicales de oxígeno que dañan las membranas de las neuronas en un proceso llamado peroxidación lipídica.” (During the time Roberto was unconscious in the garage — which was probably several hours before you found him — the cells of his brain, especially in two regions called the globus pallidus and hippocampus, could not produce energy normally. That generates oxygen radicals that damage the membranes of neurons in a process called lipid peroxidation.)
“¿Y eso ya no está pasando porque ya bajó el CO?” (And that is no longer happening because the CO has already come down?)
“El CO en la sangre ya no está bloqueando el nuevo oxígeno. Pero el daño que ocurrió durante las horas de exposición puede seguir desarrollándose. El problema que preocupa a los médicos se llama secuelas neurológicas tardías. Entre un 30 y un 50 por ciento de los pacientes con intoxicación grave por CO que no reciben tratamiento en la cámara hiperbárica desarrollan, entre 2 y 40 días después de parecer recuperados, problemas neurológicos: cambios de personalidad, dificultades de memoria, problemas de atención y concentración, y a veces síntomas similares al Parkinson por daño en el globo pálido. Muchos de estos pacientes pasan por un exámen neurológico normal en urgencias — igual que Roberto ahorita — y presentan estos síntomas semanas después.” (The CO in the blood is no longer blocking new oxygen. But the damage that occurred during the hours of exposure may continue developing. The problem the doctors are concerned about is called delayed neurological sequelae. Between 30 and 50 percent of patients with serious CO poisoning who do not receive treatment in the hyperbaric chamber develop, between 2 and 40 days after appearing to recover, neurological problems: personality changes, memory difficulties, attention and concentration problems, and sometimes symptoms similar to Parkinson’s from damage to the globus pallidus. Many of these patients have a normal neurological examination in the emergency department — just like Roberto right now — and develop these symptoms weeks later.)
Patricia had been very still. “¿Y cuántos de cada 10 que sí reciben la cámara presentan esos síntomas?” (And how many out of 10 who do receive the chamber develop those symptoms?)
“Hay un estudio aleatorio controlado publicado en el New England Journal of Medicine en 2002 — el estudio Weaver — que comparó el oxígeno hiperbárico con el oxígeno normobarico en pacientes con intoxicación por CO. Los que recibieron tres sesiones en la cámara hiperbárica tuvieron una tasa de secuelas neurológicas tardías de aproximadamente 25 por ciento a las seis semanas. Los que recibieron solo oxígeno a presión normal tuvieron una tasa de aproximadamente 46 por ciento. Es una reducción relativa del 46 por ciento en el riesgo.” (There is a randomized controlled trial published in the New England Journal of Medicine in 2002 — the Weaver study — that compared hyperbaric oxygen with normobaric oxygen in patients with CO poisoning. Those who received three sessions in the hyperbaric chamber had a rate of delayed neurological sequelae of approximately 25 percent at six weeks. Those who received only oxygen at normal pressure had a rate of approximately 46 percent. That is a relative reduction of 46 percent in risk.)
Patricia did the arithmetic. “De cada diez sin cámara, casi cinco tienen problemas. De cada diez con cámara, dos o tres tienen problemas.” (Out of every ten without the chamber, almost five have problems. Out of every ten with the chamber, two or three have problems.)
“Aproximadamente, sí.”
Roberto had been listening. He was a history teacher. He understood evidence. “¿Tres sesiones?” (Three sessions?)
“El protocolo estándar para intoxicación grave por CO es tres sesiones en las primeras 24 horas. La primera lo más pronto posible. Cada sesión dura 90 minutos. Si Roberto empieza en la próxima hora, podría terminar las tres sesiones esta noche.” (The standard protocol for severe CO poisoning is three sessions in the first 24 hours. The first as soon as possible. Each session lasts 90 minutes. If Roberto starts in the next hour, he could finish all three sessions tonight.)
Patricia reached across and took Roberto’s hand. “No es que el oxígeno del hospital no sirvió,” she said to him. “Sí sirvió. La cámara sirve para algo diferente: para proteger tu cerebro de un daño que puede aparecer semanas después.” (It is not that the hospital oxygen did not work. It did work. The chamber serves a different purpose: to protect your brain from damage that can appear weeks later.)
Roberto looked at David. “¿Por qué funciona la cámara si el CO ya salió de la hemoglobina?” (Why does the chamber work if the CO has already left the hemoglobin?)
“Dos mecanismos. El primero: dentro de la cámara, el oxígeno disuelto directamente en el plasma llega a los tejidos sin necesitar hemoglobina. El CO que todavía está bloqueando algunas moléculas de citocromo c oxidasa en las mitocondrias — la enzima que las células necesitan para usar el oxígeno — es desplazado por la alta presión de oxígeno más rápidamente. El segundo: el oxígeno a alta presión interrumpe el proceso de peroxidación lipídica que ya empezó en las neuronas, reduciendo el daño acumulado durante las horas de exposición.” (Two mechanisms. The first: inside the chamber, oxygen dissolved directly in plasma reaches tissues without needing hemoglobin. The CO that is still blocking some cytochrome c oxidase molecules in the mitochondria — the enzyme cells need to use oxygen — is displaced by the high oxygen pressure more quickly. The second: oxygen at high pressure interrupts the lipid peroxidation process that has already started in the neurons, reducing the accumulated damage from the hours of exposure.)
Roberto nodded slowly. He was a person who needed the mechanism, not just the recommendation. “Como sofocar un incendio desde adentro antes de que se extienda.” (Like smothering a fire from inside before it spreads.)
“Exactamente como eso.”
Scenario 3: Carlos Delgado-Vega — 51, landscape contractor from Miami, Florida
Carlos Delgado-Vega had not felt the small puncture wound on his left lower leg until it had turned red. He had been working in a client’s garden in Coral Gables three days earlier when something — a garden stake, he thought, or possibly a rusted fence wire — had broken his skin just below the calf. He had cleaned it with water, applied antibiotic ointment from his truck’s first-aid kit, and covered it with a bandage. By that evening, the lower leg was red and swollen. By midnight, the redness had spread six inches up the calf and he had a fever of 39.1. His wife Carmen — a 48-year-old preschool director — had driven him to Jackson Memorial Hospital at 2 in the morning.
The emergency department CT had showed gas in the fascial planes of the left lower leg, extending from the ankle to the mid-calf. The diagnosis had been made before the culture results: necrotizing fasciitis. Carlos had been in the operating room by 5 a.m. The trauma surgeon had performed radical debridement of the left lower leg — removing approximately 30 percent of the calf musculature, all of the infected fascia, and the overlying skin, leaving a large open wound that had been dressed with a wound VAC. He had gone back to the OR the following day for a second-look procedure and additional debridement of two small areas of tissue that had appeared equivocal at the first operation.
He was now in the surgical ICU on his third post-operative day. Blood cultures had grown Bacteroides fragilis and Clostridium perfringens; the wound cultures had additionally grown Peptostreptococcus anaerobius. He was on piperacillin-tazobactam, vancomycin, and metronidazole. His fever had resolved. His white count was trending down from 22 to 18 to 15. He was awake, talking, and looking at the wound VAC attached to the stump of what had been a calf with a combination of grief and the focused attention of someone who was determined to survive this.
Carmen Delgado had been in the ICU waiting room for three days. She was an organized woman — a preschool director who had been managing a 24-child school for eleven years — and she had been using every hour in the waiting room to research exactly what was happening to her husband. She had read about necrotizing fasciitis. She had read about Bacteroides and Clostridium. She had read about HBOT. When HBOT nurse Anaís Vega-Torrealba came to explain the adjunctive HBOT plan, Carmen had specific questions.
“Le agradezco que venga a explicarme. Lo que me genera duda es esto: Carlos ya tuvo dos cirugías que sacaron todo el tejido infectado. Está en tres antibióticos distintos. Sus números están mejorando. ¿Por qué agregar la cámara ahora, cuando lo que más necesita es descansar y recuperarse?” (Thank you for coming to explain to me. What generates doubt for me is this: Carlos has already had two surgeries that removed all the infected tissue. He is on three different antibiotics. His numbers are improving. Why add the chamber now, when what he most needs is rest and recovery?)
Anaís sat down across from Carmen. She had been an HBOT nurse for seven years and had worked with many necrotizing fasciitis families. The explanation she had developed over those seven years started with the biology of the specific organisms in Carlos’s wound.
“Me permite que le explique por qué las bacterias que tienen a Carlos son especialmente peligrosas y por qué los antibióticos solos no son suficientes para el ambiente en que están.” (Allow me to explain why the bacteria that Carlos has are especially dangerous and why antibiotics alone are not sufficient for the environment they are in.)
She explained the category of obligate anaerobes. Bacteroides fragilis, Clostridium perfringens, and Peptostreptococcus anaerobius are organisms that evolved in environments with no oxygen — the anaerobic depths of the human gut, the soil, dead tissue. Over millions of years, aerobic and facultative organisms developed enzymes — catalase, superoxide dismutase — that neutralize the reactive oxygen species generated by exposure to oxygen. Obligate anaerobes never developed these enzymes. When oxygen partial pressures rise above approximately 50 millimeters of mercury in their environment, these organisms cannot neutralize the superoxide and hydrogen peroxide that accumulate inside their cells. The reactive oxygen species attack cell membranes, denature proteins, and break DNA strands. The organisms die.
“En tejido sano, bien perfundido, la presión de oxígeno es alrededor de 40 a 50 milímetros de mercurio. Eso está justo en el umbral — los anaerobios obligados a duras penas pueden sobrevivir en tejido normal. Pero la infección de fasciitis necrotizante consume el oxígeno en las capas fasciales que rodean la infección, bajando la presión de oxígeno en esa zona a entre 5 y 15 milímetros de mercurio. Eso crea el ambiente ideal para que los anaerobios sobrevivan, se reproduzcan, y produzcan sus toxinas. Es un círculo que se refuerza solo: las bacterias consumen el oxígeno, el ambiente se vuelve más anaerobio, y las bacterias crecen más fácil.” (In healthy, well-perfused tissue, the oxygen pressure is around 40 to 50 millimeters of mercury. That is right at the threshold — obligate anaerobes can barely survive in normal tissue. But the necrotizing fasciitis infection consumes the oxygen in the fascial planes surrounding the infection, lowering the oxygen pressure in that zone to between 5 and 15 millimeters of mercury. That creates the ideal environment for anaerobes to survive, reproduce, and produce their toxins. It is a self-reinforcing cycle: bacteria consume the oxygen, the environment becomes more anaerobic, and bacteria grow more easily.)
Carmen’s expression had sharpened. “Y los antibióticos llegan a un lugar donde las bacterias están en su ambiente ideal.” (And the antibiotics arrive at a place where the bacteria are in their ideal environment.)
“Exactamente. Y hay algo más. Los neutrófilos — las células del sistema inmune que matan bacterias — necesitan oxígeno para su mecanismo principal de matar. Generan radicales de oxígeno que son tóxicos para las bacterias — se llama explosión oxidativa. A menos de 30 milímetros de mercurio de oxígeno en el tejido, esa capacidad se reduce aproximadamente un 60 por ciento. Entonces en la zona alrededor de la herida de Carlos, el sistema inmune está trabajando al 40 por ciento de su capacidad porque no tiene suficiente oxígeno.” (Exactly. And there is something else. Neutrophils — the immune system cells that kill bacteria — need oxygen for their primary killing mechanism. They generate oxygen radicals that are toxic to bacteria — it is called oxidative burst. At less than 30 millimeters of mercury of oxygen in the tissue, that capacity is reduced by approximately 60 percent. So in the zone around Carlos’s wound, the immune system is working at 40 percent of its capacity because it does not have enough oxygen.)
“¿Y el Clostridium perfringens — el más preocupante de los que tiene Carlos — tiene algo especial?” (And Clostridium perfringens — the most worrying of the ones Carlos has — is there something special about it?)
“Sí. El Clostridium perfringens produce una toxina llamada alfa-toxina — químicamente es una fosfolipasa C, una enzima que destruye las membranas de las células musculares y los glóbulos rojos. Es esa toxina la que causa la gangrena gaseosa — el gas en las fascias que vió en la tomografía, la destrucción rápida del tejido, la formación de ampollas negras. Los estudios muestran que el oxígeno hiperbárico inhibe la producción de alfa-toxina por el Clostridium perfringens. Incluso si el organismo sobrevive al borde de la herida, produce menos de la toxina que causa la destrucción tisular.” (Yes. Clostridium perfringens produces a toxin called alpha-toxin — chemically it is a phospholipase C, an enzyme that destroys the membranes of muscle cells and red blood cells. It is that toxin that causes gas gangrene — the gas in the fascia you saw on the CT scan, the rapid tissue destruction, the formation of black blisters. Studies show that hyperbaric oxygen inhibits alpha-toxin production by Clostridium perfringens. Even if the organism survives at the wound edge, it produces less of the toxin that causes tissue destruction.)
Carmen was quiet for a moment. She had the focused stillness of a person who was processing information that was both technical and deeply personal. “¿Y la cirugía sacó todo el tejido muerto?” (And the surgery removed all the dead tissue?)
“La cirugía sacó el tejido que no tiene circulación — el tejido necrótico donde los antibióticos y el oxígeno no pueden llegar porque no hay riego sanguíneo. Ese tejido debe salir quirúrgicamente y no hay alternativa. Los antibióticos eliminan las bacterias por mecanismos químicos — bloquean su pared celular, rompen su ADN. El oxígeno hiperbárico hace algo distinto a los dos: sube la presión de oxígeno en el tejido vivo alrededor de la herida por encima del umbral letal para los anaerobios, restaura la capacidad del sistema inmune de Carlos, y suprime la producción de alfa-toxina. Los tres trabajan en el mismo paciente por mecanismos completamente distintos.” (Surgery removed the tissue that has no circulation — the necrotic tissue where antibiotics and oxygen cannot reach because there is no blood flow. That tissue must be removed surgically and there is no alternative. Antibiotics eliminate bacteria through chemical mechanisms — block their cell wall, break their DNA. Hyperbaric oxygen does something different from both: it raises the oxygen pressure in the living tissue around the wound above the lethal threshold for anaerobes, restores Carlos’s immune system capacity, and suppresses alpha-toxin production. The three work in the same patient through completely different mechanisms.)
“¿Y el transporte del ICU a la cámara no lo va a cansar?” (And transporting him from the ICU to the chamber is not going to tire him out?)
“El protocolo de transporte para pacientes de UCI es seguro — Carlos puede ir en camilla con monitorización continua. La sesión en sí es de 90 minutos a dos horas, recostado dentro de la cámara. Para la mayoría de los pacientes, la sesión es tranquila. Muchos duermen. Y los estudios en fasciitis necrotizante muestran que los pacientes que reciben HBOT ademá de la cirugía y antibióticos tienen menor mortalidad y necesitan menos reoperaciones que los que reciben solo cirugía y antibióticos.” (The transport protocol for ICU patients is safe — Carlos can go by stretcher with continuous monitoring. The session itself is 90 minutes to two hours, lying down inside the chamber. For most patients, the session is calm. Many sleep. And studies in necrotizing fasciitis show that patients who receive HBOT in addition to surgery and antibiotics have lower mortality and need fewer reoperations than those who receive surgery and antibiotics alone.)
Carmen had one more question. “¿Cuántas sesiones?” (How many sessions?)
“El protocolo típico para fasciitis necrotizante es entre 20 y 30 sesiones — dos o tres sesiones por día al principio mientras la infección está activa, luego una vez al día. La primera fase del tratamiento intensivo corresponde al período de mayor riesgo de extensión de la infección. La segunda fase — una vez que la infección está bajo control — se enfoca en promover la cicatrización del tejido y preparar la herida para el injerto de piel que necesitará Carlos.” (The typical protocol for necrotizing fasciitis is between 20 and 30 sessions — two or three sessions per day initially while the infection is active, then once per day. The first intensive treatment phase corresponds to the period of highest risk of infection spread. The second phase — once the infection is under control — focuses on promoting tissue healing and preparing the wound for the skin graft Carlos will need.)
Carmen thought about the timeline. She thought about Carlos in the OR for five hours. She thought about what she had read about mortality in necrotizing fasciitis without adequate treatment. Then she thought about the three mechanisms Anaís had explained: surgery, antibiotics, oxygen. Each addressing something the others could not.
“El oxígeno hiperbárico no reemplaza la cirugía ni los antibióticos,” she said. “Los tres trabajan juntos: la cirugía saca el tejido muerto, los antibióticos atacan las bacterias que quedan, y el oxígeno crea un ambiente donde esas bacterias no pueden sobrevivir y donde el sistema inmune de Carlos puede funcionar.” (Hyperbaric oxygen does not replace surgery or antibiotics. The three work together: surgery removes the dead tissue, antibiotics attack the remaining bacteria, and oxygen creates an environment where those bacteria cannot survive and where Carlos’s immune system can function.)
Anaís met her eyes. “Exactamente eso.”