Surviving Statistics

I thought I would share a few statistical outliers from my own time out in the tail.

At Sparrow Bioacoustics, part of our work involves understanding the impact of early intervention in cardiac disease. That means we spend a lot of time staring at data: screening rates, risk factors, survival curves. We try to understand the early signals, those that often manifest before people experience obvious or specific symptoms.

But the more you live inside the numbers, the more you think about how unforgiving they can be. Most people live somewhere near the middle of the bell curve; where things make sense. But medicine doesn’t always stay there. Sometimes, life drags you out to the margins, where evidence is thin, outcomes are uncertain, and survival becomes an outlier event.

If you’ve ever landed on the wrong side of those statistics, you know it’s not just a clinical problem, it’s personal. It’s terrifying. It’s brutal for your care team, your family, and anyone trying to fight their way back through uncertainty.

In 2019, I experienced acute septic shock as a result of necrotizing fasciitis (NF).

…Twice

The odds say I should not be here, and I find that interesting. So I thought I would share a few statistical outliers from my own time out in the tail.

Necrotizing Fasciitis: The Idiopathic Variant

Necrotizing fasciitis (NF) is rare, affecting roughly 0.4 cases per 100,000 people annually in developed countries [1]. It’s most commonly associated with trauma, surgery, diabetes, cancer, immunosuppression, or injection drug use [2]. I had none of those. No underlying conditions, no wounds, no risk factors, just a modest bruise on the knee after a ski trip and a fever of 105.

That puts me in the idiopathic category, a subset that accounts for only 5–10% of NF cases [3]. In these, the infection likely enters through a microscopic skin break or transient bacteremia, with no clear source ever identified.

What makes this variant particularly dangerous is the delay in diagnosis and appropriate intervention. Without a visible injury, portal of entry, or other risk factors, NF can masquerade as a muscle strain, hematoma, or viral illness until the infection explodes beneath the fascia.

Necrotizing fasciitis carries a high baseline mortality rate, estimated at 20–30%, and as high as 70% when septic shock is involved [4]. A retrospective study by Hua et al. (2011) found that NF complicated by shock required vasopressors in over half of cases, with dramatically worsened prognosis. When compounded by multi-organ failure (like mine) mortality climbs to 70–90% depending on severity and ICU course [5].

According to the Sepsis-3 consensus definition (published in JAMA in 2016), septic shock is: A subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. Septic shock is what happens when an infection doesn’t just stay local, it hijacks the entire body. The immune system launches a chemical war so intense that it starts damaging the body’s own tissues. Blood vessels leak. Organs lose oxygen. Blood pressure collapses. The heart struggles to compensate. Left unchecked, it spirals into multi-organ failure and death. Once it starts, it’s also very hard to stop.

By the time I entered the hospital, I was already in septic shock. My labs showed lactic acidosis, elevated creatinine, and leukocytosis. I was also in respiratory failure. After a CT confirmed the infection, I was intubated, sedated, put on a massive course of broad-spectrum antibiotics, placed on vasopressors, and rushed into emergent surgery to debride the affected areas of my leg. Months later, I would lose that leg.

My kidneys had failed completely, requiring dialysis throughout my ICU stay and for weeks afterward. Liver function was also impaired and failing, but that took a back seat to my heart. After several days on life support, my heart began to weaken, a condition described as a "soft heart," shorthand for septic cardiomyopathy which is characterized by myocardial stunning, reduced ejection fraction, and circulatory collapse [6]. In my case, the heart couldn’t maintain perfusion on its own, and every other organ suffered. Somewhere in the chaos, my left lung also collapsed. It went unnoticed for a time, masked by the fact that I was already on a ventilator. Whether iatrogenic or spontaneous, it only worsened my respiratory compromise.

My blood pressure was often unrecordable without pharmacological support, meaning that, without continuous IV vasopressors, it was too low to measure with a cuff. Systolic BP < 60 mmHg with no palpable pulse, is the kind of hypotension that erases the line between life and death. Problematically when mean arterial pressure (MAP) drops below ~65 mmHg, cerebral blood flow becomes critically impaired. Prolonged hypotension like this can lead to diffuse cortical injury, neuronal death in the hippocampus, and long-term cognitive deficits.

Apparently I also soaked up 40 units of saline. With the kidney failure, most of it was retained in my tissues for weeks. The resulting edema was extreme, and every intervention became a high-stakes balance between keeping organs perfused and not drowning the rest of me.

I continued to decompensate for days. Cardiac decompensation during septic shock is particularly dangerous because it undermines the very measures, like fluids and vasopressors, meant to stabilize the patient. When the heart can no longer serve as a reliable engine, the rest of the body shuts down. Eventually, a combination of time, high-dose Linezolid, and IV immunoglobulin halted the downward spiral and I stabilized.

The Second Shock: A System Already Primed to Fail

A few days later, while still in a coma, the team decided to take me in for a second debridement surgery. Shortly after I began bleeding massively and my blood pressure crashed below 60. This was a second round of septic shock, an event that further, dramatically, reduced my odds of survival.

In critical care, this kind of deterioration is known as a "second hit", a new physiological insult that occurs while the body is still reeling from the first. This secondary inflammatory cascade, marked by renewed cytokine storms and systemic endothelial damage, has been shown to double mortality risk in ICU patients [4]. A study by Luecke et al. (2005) found that surgical patients with secondary septic deterioration faced >70% mortality when combined with multi-organ dysfunction. Other analyses show that survival following recurrent septic shock within the same hospitalization can fall below 10% [5].

The severity and idiopathic nature of my case brought in specialists from across the hospital network. Mount Sinai West eventually presented a report based on my case at the CHEST 2019 Conference, documenting how NF can present without trauma or known immunosuppression, and how devastating delays in recognition can be [8].

Am I Still Me?

A few weeks into it, they brought me out of the coma and extubated me. Though I was awake and breathing on my own, I had profound amnesia. I couldn’t form new memories or retrieve old ones. Neurological injury due to prolonged hypotension was suspected. The hippocampus is especially vulnerable to ischemia. Neuronal death in this region is associated with short-term memory loss, confusion, spatial disorientation, and difficulty forming new memories. On top of that, being in a coma can (on its own) cause lasting cognitive impairment. Being in a coma is not the same as sleeping. Sedation doesn’t replicate REM or restorative brain activity. Your brain basically becomes damaged by prolonged sleep deprivation. Many ICU patients emerge from comas with fragmented sleep-wake cycles, impaired cognition, and something resembling PTSD. This kind of disruption is now known to be a major contributor to long-term cognitive impairment. A 2013 study published in The Lancet Respiratory Medicine found that over 50% of coma patients had cognitive scores equivalent to moderate traumatic brain injury or early Alzheimer’s one year after discharge. [7].

After a few days, I finally did actually sleep, and something suddenly reset. Memory began to return; I could focus and process my surroundings. Mentally, I was myself again.

The Statistical Tail

If you build a model from the data, my odds of surviving the acute phase were less than 5%. The odds of avoiding permanent dialysis, heart failure, a liver transplant, and returning to a neurological baseline with no lasting emotional or cognitive impairment, were likely less than 1%.

There’s no tidy moral here. No heroic arc. Just a shitty hand dealt by biology, and the extraordinary, coordinated response from clinicians, caregivers, and my wife who had to play that hand. My wife never stopped watching. My care team never stopped adjusting. Things went wrong, some even failed, but everyone adapted fast enough to save me.

Does knowing the odds help in the fight? Maybe not. But someone has to know them. Someone has to fight with clarity even when the numbers say you probably won't make it. Especially when you're way out in the tail, where medicine gets less certain, and survival stops being expected. They talk a lot about the bell curve in critical care. But what happens at the margins matters too. Because sometimes, even at the farthest edge of probability, someone survives.

And when they do, the tail talks back.

a few references

1. CDC. Necrotizing Fasciitis: A Rare Disease, Especially for the Healthy. https://www.cdc.gov/groupastrep/diseases-hcp/necrotizing-fasciitis.html

2. Stevens DL, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections. Clin Infect Dis. 2014;59(2):e10–e52.

3. Chelsom J, Halstensen A, Haga T. Necrotizing fasciitis: Rapid diagnosis and treatment is key to survival. BMJ. 1998;316(7145):654–655.

4. Gajic O, et al. Secondary sepsis and multiple organ failure in the intensive care unit: incidence and outcome. Intensive Care Med. 2003;29(10):1693–1700.

5. Luecke T, et al. Mortality and multiple organ failure after secondary surgical interventions in patients with severe abdominal sepsis. Br J Surg. 2005;92(3):380–386.

6. Vieillard-Baron A, et al. Myocardial dysfunction in sepsis: reversible myocardial depression. Intensive Care Med. 2008;34(1):9–16.

7. Pandharipande PP, et al. Long-term cognitive impairment after critical illness. N Engl J Med. 2013;369(14):1306–1316.

8. Rajeeve S, et al. NECROTIZING FASCIITIS TRIGGERED BY TRAUMA- BUT NOT TRAUMA: A Case Report. Presented at the CHEST Annual Meeting 2019; New Orleans, LA.