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Patients with distributive shock who are unresponsive to traditional vasopressors are commonly considered to have severe distributive shock and are at high mortality risk. Here, we assess the cost-effectiveness of adding angiotensin II to the standard of care (SOC) for severe distributive shock in the US critical care setting from a US payer perspective.
Short-term mortality outcomes were based on 28-day survival rates from the ATHOS-3 study. Long-term outcomes were extrapolated to lifetime survival using individually estimated life expectancies for survivors. Resource use and adverse event costs were drawn from the published literature. Health outcomes evaluated were lives saved, life-years gained, and quality-adjusted life-years (QALYs) gained using utility estimates for the US adult population weighted for sepsis mortality. Deterministic and probabilistic sensitivity analyses assessed uncertainty around results. We analyzed patients with severe distributive shock from the ATHOS-3 clinical trial.
The addition of angiotensin II to the SOC saved .08 lives at Day 28 compared to SOC alone. The cost per life saved was estimated to be $108,884. The addition of angiotensin II to the SOC was projected to result in a gain of .96 life-years and .66 QALYs. This resulted in an incremental cost-effectiveness ratio of $12,843 per QALY. The probability of angiotensin II being cost-effective at a threshold of $50,000 per QALY was 86 percent.
For treatment of severe distributive shock, angiotensin II is cost-effective at acceptable thresholds.
Background: Theories concerning the aetiology of functional neurological symptom disorder (FNSD; also known as conversion disorder) have historically inferred that psychological factors or dissociative states underlie patients’ symptoms. Current psychological models of functional neurological symptoms suggest that some type of ‘top-down’ representations/beliefs are activated automatically (without conscious awareness), leading to symptoms. It is assumed that these representations or beliefs are similar to the idea ‘I am neurologically damaged’, as in our clinical experience, almost all patients have some reason to doubt the integrity of their neurological system. Aims: It was hypothesized that FNSD arises from a belief of being neurologically damaged (via a mechanism akin to a nocebo response), and an interdisciplinary treatment protocol was developed consistent with this hypothesis, transparently sharing this theory with participants. Method: A retrospective consecutive case series design was utilized, measuring functional independence and symptom remission. Results: Of the 13 episodes of care, 12 resulted in complete or almost complete symptom remission. Length of stay in rehabilitation was also reduced compared with previous treatment attempts. Conclusions: It appears as if the treatment protocol may be very effective, and further controlled study appears warranted.
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