Are Ethical Considerations Being Forgotten in ICU care : A Case Example

What is the 6-month post-hospital average life expectancy of critically ill patients with polymicrobial bacteremia and septic shock, complicated by severe metabolic acidosis that required mechanical ventilation and IV bicarbonate after an esophageal perforation?

Six-Month Post-Hospital Survival After Septic Shock from Esophageal Perforation

Quick answer: Only about 15 – 25 % of patients who suffer polymicrobial bacteremia, septic shock, severe metabolic acidosis, and require mechanical ventilation + IV bicarbonate following an esophageal perforation are still alive six months after hospital discharge. For the whole cohort, average post-discharge survival is measured in weeks to (at most) a few months.

Why the number is so low — key prognostic contributors

Major prognostic factor	Representative contemporary data	Typical mortality reported
Esophageal perforation (all comers)	Meta-analysis of 45 series (1999–2019)	Immediate/30-day mortality ≈ 10 % in early-treated cases, but 40–60 % when perforation is septic or treatment delayed
Mechanical ventilation at presentation	27-year Canadian cohort (n = 119)	Ventilation raised odds of death >>30-fold vs. non-ventilated peers
Septic shock (vasopressors ± ventilation)	Large single-centre series (n = 543)	In-hospital mortality ≈ 45 %
Severe metabolic acidosis (pH < 7.20)	Prospective multi-ICU study (n = 155)	ICU mortality ≈ 57 %
Polymicrobial bacteremia (≥ 2 organisms)	Systematic reviews & modern cohorts	Six-month mortality 36–63 % (vs. 15–30 % in monomicrobial cases)

• Composite estimate: Hospital mortality stacks to roughly 60–70 % in patients who experience all of the above insults.
• Among hospital survivors, a further 35–40 % die before month 6.

Resulting six-month picture: Out of 100 comparable patients, only about 15–25 remain alive at six months.

Average life-expectancy once discharged: Because most deaths cluster early, mean post-discharge survival for the whole group averages just 90–120 days.

---

Quality of Life in Six-Month Survivors & Their One-Year Outlook

Among the 15–25 % of the original cohort who do reach six months:

Domain (6-month survivors)	What the evidence shows	Practical takeaway
Physical functioning	30–40 % report moderate-to-extreme mobility limits (EQ-5D); 37 % have Barthel Index ≤ 90	Most need a walking aid or daily help with basic ADLs
Cognitive & mental health	15–20 % screen positive for significant cognitive decline; anxiety/depression in 20–25 %	“Brain-fog” and mood symptoms are common; can limit return to work
Overall HR-QoL	Mean EQ-5D index 0.55–0.65 (population norm ≈ 0.85); SF-36 physical score ≈ 35 (norm = 50)	Quality of life sits roughly one SD below age-matched community norms
Post-Intensive-Care Syndrome (PICS)	≈ 60 % meet ≥ 1 PICS criterion; 24 % have ≥ 2 domains affected	Multidisciplinary rehab (PT, OT, neuro-psych) is almost always needed
Social / occupational recovery	Only 40–45 % of working-age survivors are back at their previous job by 12 months	Expect staggered return-to-work and high readmission rates (30–40 %)

One-Year Mortality Once the Six-Month Mark Is Reached

• Additional attrition between months 6 and 12 is 30–40 % of six-month survivors.
• Net result: Only about 10–15 % of the original cohort are still alive at one year.

One-year survival once a patient has made it to 6 months

• Baseline: We already estimated that only 15-25 % of the original cohort are alive at 6 months.

• Additional attrition between 6 and 12 months:

  • Large multicentre sepsis series with > 60 % mechanically ventilated show mortality rising from 23 % at discharge to 37 % at 12 months—an absolute 14-point loss, which translates to ~25–30 % mortality among discharge survivors. 

  • Population-level bloodstream-infection data (many polymicrobial) report 46 % one-year case-fatality, implying a ~30 % drop between 30 days and one year. 

  • ARDS/septic-ventilation cohorts show a similar ~17-20 % additional loss after hospital discharge.

Putting those pieces together:

Of every 100 index patients

• 15–25 reach the 6-month mark.

• Another 30–40 % of those die before 12 months (≈ 5–10 patients).

• ≈ 10–15 % of the original cohort are still alive at one year.

Clinically: If you are counselling families, it is reasonable to say that roughly one in three of the 6-month survivors will not survive the first anniversary, and that the remainder often live with significant physical or cognitive disability.

Key Follow-Up Priorities for Survivors

• Early, structured rehabilitation (mobility + ADL retraining + swallow therapy).
• PICS screening at 3 and 6 months; proactive mental-health support.
• Optimised infection control & nutrition to mitigate late deaths from relapse and sarcopenia.
• Readmission planning: nearly half will require rehospitalisation during year 1.

Disclaimer: Figures are synthesized from overlapping modern studies; individual prognosis varies with the speed of source control, burden of comorbidity, and intensity of post-ICU rehabilitation.

How Does Being 68 Years Old Change the Prognosis in Polymicrobial Sepsis After Esophageal Perforation?

In short: Age ≥ 65 worsens both mortality and disability. For a 68-year-old who develops polymicrobial bacteremia, septic shock, severe metabolic acidosis, and requires prolonged ventilation after an esophageal perforation, only ≈ 8 – 15 % are still alive six months after hospital discharge, and just ≈ 5 – 10 % survive to one year. Fewer than 3 % of the original cohort regain full independence.

Numbers at a Glance

Outcome	“Average” adult (all ages)	68-year-old	Key evidence*
Alive at 6 months after discharge	15 – 25 %	≈ 8 – 15 %	Elderly ventilated sepsis series: 60–70 % 6-mo mortality vs ≈ 45 % in younger adults
Alive at 12 months (from ICU admission)	10 – 15 %	≈ 5 – 10 %	Age ≥ 67 doubles 1-yr mortality (FROG-ICU; geriatric BSI cohorts)
Regain independent ADLs at 1 yr	35 – 40 % of survivors	≈ 20 – 25 % of survivors (< 3 % of the original cohort)	MONITOR-IC & systematic QoL reviews in elderly ICU survivors

^*Composite of modern sepsis, bloodstream-infection, and ICU survivorship studies (FROG-ICU, MONITOR-IC, multiple geriatric BSI cohorts).

Translated to people: start with 100 similar 68-year-olds. About 90 will die before 6 months, another 30–40 % of the few who remain alive will die before the first anniversary, and only two or three will be living independently at one year.

---

Why Age Magnifies Risk

• Immunosenescence & frailty → weaker pathogen clearance, but stronger inflammatory injury.
• Higher comorbidity load → cardiovascular, renal, and cognitive diseases synergise with sepsis-induced organ failure.
• Reduced ventilation tolerance → stiffer lungs and weaker diaphragm extend ventilator days and raise VAP/delirium rates.
• Bacteremia-specific data → Odds of 6-mo death rise ≈ 1.1–1.2× per decade; one geriatric BSI study showed 57 % 6-mo mortality despite source control.

---

Practical Counselling Points for a 68-Year-Old With This Illness

• Survival ≠ Survivorship. Getting out of the ICU and getting back to one’s life are very different hurdles.
• Functional trajectory. Even among the ~10 % who reach one year, most need mobility aids, home-health support, or long-term care.
• Goals-of-care talks & time-limited trials. Early, explicit discussion is crucial; the chance that ongoing maximal therapy will yield a life the patient values falls sharply with age.
• Aggressive rehabilitation still matters. Begin within 48 h of awakening and continue post-discharge to maximise any recovery potential.

---

Bottom Line

Adding the patient’s age (68 years) shifts an already dire outlook from roughly one-in-five survival at six months to about one-in-ten. Among those rare survivors, the odds of meaningful independence are halved. These sobering figures reinforce the ethical imperative to place long-term prognosis front-and-centre during initial decision-making conversations with patients and families.

The Tension Between Life-Saving Instincts and Long-Term Outcomes in Critical Care

Critical care culture has been forged around an unwavering rescue mindset: if modern organ-support technology can keep a patient alive today, that mission eclipses almost every other consideration. The impulse is understandable—ICU teams are trained and rewarded for reversing shock, oxygenating blood, and correcting acidosis hour-by-hour—but the same momentum can make it dangerously easy to overlook what survival will look like months later, or whether today’s treatments truly align with a patient’s values.

---

The Numbers We Under-Recognise

• Late mortality despite “successful” ICU discharge. In the prospective FROG-ICU cohort of 1,570 European ICU survivors, 21 % died within the first year after leaving hospital.
• Sepsis amplifies the penalty. Modern sepsis cohorts confirm that survivors face excess disability, cognitive impairment, and rehospitalisation that extend well beyond the initial crisis.
• Prognostic conversations lag behind reality. From the landmark SUPPORT trial to recent audio-record studies across U.S. ICUs, researchers consistently find wide variability in whether and how clinicians discuss long-term outlook with families.

When prognostic information is withheld—or presented only as percentages about in-unit survival—families frequently assume that “getting through the ICU” equals recovery, even though the data say otherwise. The result is a drift toward treatments unlikely to achieve goals the patient would have chosen if fully informed—what ethicists call potentially futile or non-beneficial care.

---

Ethical Dimensions

1. Autonomy & Informed Consent. If we know that patients with polymicrobial sepsis requiring prolonged ventilation have only a 10–15 % chance of living independently at one year, failing to share that reality undermines informed decision-making.
2. Beneficence versus Non-Maleficence. Continuing aggressive therapy that merely prolongs dying can expose patients to pain and indignity (maleficence) without delivering a life they would find acceptable (beneficence).
3. Justice & Resource Stewardship. ICU beds, dialysis cartridges, and ECMO circuits are finite. Employing them for care a patient would decline if fully informed also harms others waiting for those resources.

---

What the Literature Suggests We Should Do

• Introduce prognosis early—and revisit it often. A February 2025 multicentre RCT that added personalised one-year quality-of-life predictions to the first family meeting reduced depressive symptoms in relatives and improved clinician–family collaboration.
• Normalise time-limited trials (TLTs). Despite professional-society endorsement, an observational 2024 study found that only 20 % of ventilated ARDS patients were managed with a formal TLT.
• Measure and communicate long-term outcomes. Prognostic models such as FROG-ICU or MONITOR-IC can translate severity scores into one-year survival & functional predictions—data that should sit alongside lactate trends on rounds.
• Embed palliative-care principles inside the ICU. Early palliative co-management curbs non-beneficial treatment and reduces staff burnout; it is not a sign of “giving up.”

---

Closing Reflection

Keeping someone alive through the night will always be an essential, honourable part of critical care. But if we end the story there, we risk committing patients to months of profound disability—or to deaths their families later describe as “too much suffering.” Modern outcome data show that a significant proportion of ICU survivors either die within a year or live with severe limitations. Ethically, that obliges us to place prognostic numbers on the table—early, clearly, and compassionately—so patients and families can decide whether tomorrow’s life is one they wish to fight for today.

By shifting our default from “save at all costs” to “pursue goal-concordant care,” we honour both the science of outcomes and the humanity of the people we serve.

Question of the Week

Community Acquired Pneumonia NEJM 2023

Key Clinical Take-Home Points

• Diagnosis requires compatible symptoms plus a new infiltrate on chest imaging.
• Outpatients with mild disease can be treated empirically; however, test for SARS-CoV-2 and influenza.
• Hospitalized patients benefit from a broad, front-loaded microbiology work-up to guide pathogen-directed therapy.
• Initial antibiotic choice hinges on disease severity, comorbidities, and local resistance patterns.
• CAP is now viewed as a multi-system illness with important long-term sequelae (cardiac, pulmonary, neurologic).

Incidence & Risk Factors

Metric	Data
US hospitalizations/yr	≈1.5 million (650/100,000 adults)
High-risk groups	Age >65, COPD/asthma, CHF/CAD, diabetes, malnutrition, immunocompromise, smoking, excess alcohol

Pathogens of Concern

Group	Typical Pathogens	Notes
Core bacteria	Streptococcus pneumoniae MSSA H. influenzae Atypicals: Mycoplasma, Chlamydophila, Legionella	Cause majority of ambulatory & ward cases
Respiratory viruses	SARS-CoV-2, Influenza A/B, RSV, Parainfluenza, hMPV, Rhinovirus	Rapid PCR panels recommended on admission
Uncommon / MDR	MRSA, Pseudomonas, ESBL-Enterobacteriaceae, fungi (e.g., Pneumocystis), MERS-CoV	Consider with structural lung disease, prior IV antibiotics, immunosuppression

Severity Assessment

• CURB-65 ≤1 ➔ treat as outpatient.
• CURB-65 = 2 ➔ short stay/observation.
• CURB-65 ≥3 or any ATS/IDSA major criterion (invasive ventilation or vasopressor-requiring shock) ➔ ICU level care.

Initial Empiric Therapy

Setting	Preferred Regimens
Healthy outpatient, no antibiotics <3 mo	Amoxicillin 1 g TID or Doxycycline 100 mg BID
Comorbidities / recent antibiotics	Amox-clav 875 mg BID + macrolide (azithro) or doxycycline Alt: Levofloxacin 750 mg daily
Ward (no MRSA/PSA risk)	Ceftriaxone 1–2 g daily + Azithro 500 mg daily or Levofloxacin 750 mg daily monotherapy
ICU / severe CAP	If MRSA risk ➔ add Vancomycin 15–20 mg/kg q8–12 h or Linezolid 600 mg BID If PSA risk ➔ use anti-pseudomonal β-lactam (Pip-Tazo 4.5 g q6 h or Cefepime 2 g q8 h) + Azithro

Antibiotic Stewardship

• Obtain sputum Gram stain/culture, blood cultures, urine Ag tests (Strep. pneumoniae, Legionella) and multiplex viral PCR on admission.
• De-escalate or stop antibiotics when:
  • Viral pathogen identified and no evidence of bacterial coinfection (low WBC, CRP <150 mg/L, procalcitonin <0.25 ng/mL).
  • MRSA nasal PCR negative ➔ stop anti-MRSA agent.
• Typical duration: 5 days (≥48 h afebrile & clinically stable). Certain pathogens/complications require longer courses.

Adjunctive & Supportive Measures

• Early glucocorticoids (e.g., Hydrocortisone 200 mg/day IV taper) improve survival in severe, non-viral CAP; avoid in influenza or aspergillosis.
• Vaccinate for influenza, Covid-19, and pneumococcus; counsel on smoking cessation & alcohol moderation.
• Arrange primary-care follow-up within 1 week; routine follow-up CXR only if high risk for malignancy or persistent symptoms.

Long-Term Sequelae (“Post-Acute CAP”)

• 30-day mortality: ~10–15% of hospitalized cases; 1-yr mortality rises to 30–35%, especially with ICU admission.
• Increased risk of MI, stroke, arrhythmia, chronic lung dysfunction, cognitive decline, and rehospitalization.

Source: File TM Jr, Ramirez JA. “Community-Acquired Pneumonia.” NEJM 2023;389:632-41.

Risk factors for MRSA/MSSA and Pseudomonas Aeruginosa in CAP

Pathogen	Established Community-Acquired Risk Factors*
Staphylococcus aureus (incl. CA-MRSA)	Recent (< 2 weeks) influenza or other viral respiratory infection Cavitary or necrotizing pneumonia on imaging Severe CAP requiring ICU admission or septic shock History of colonization or infection with MRSA Chronic skin/soft-tissue infection, abscesses, or active I.V. drug use Hemodialysis or chronic kidney disease (esp. end-stage) Diabetes mellitus or structural lung disease (COPD, bronchiectasis, cystic fibrosis) Immunosuppression or prolonged corticosteroid therapy Residence in crowded settings (long-term care, prisons, athletic facilities, military)
Pseudomonas aeruginosa	Structural lung disease (bronchiectasis, severe COPD FEV1 < 50%, cystic fibrosis) Prior colonization or documented infection with P. aeruginosa Frequent or recent (< 90 days) broad-spectrum antibiotics or systemic corticosteroids Recent hospitalization ≥ 48 h, mechanical ventilation, or tracheostomy Immunosuppression (HIV, neutropenia, solid-organ or stem-cell transplant) Malnutrition or low body-mass index Recurrent COPD exacerbations requiring oral steroids/antibiotics Chronic home oxygen therapy or nebulizer use

^*Adapted from IDSA/ATS Community-Acquired Pneumonia Guidelines (2019) and contemporary literature reviews on multidrug-resistant organisms in CAP.

Rapid Sedation Non-Intubated ICU Patient

Guiding principles before you reach for a drug

• Rule-out and treat correctable drivers (pain, hypoxia, hypoglycaemia, urinary retention, withdrawal, severe delirium, etc.).
• Use the Richmond Agitation–Sedation Scale (RASS) or CAM-ICU to titrate to light, cooperative sedation (target RASS 0 to −2).
• Start with the lowest effective dose, give it IV whenever rapid control is essential, and re-assess every 5–10 min; repeat or escalate only as needed.
• Continuously monitor SpO₂, end-tidal CO₂ (if available), ECG (QTc) and haemodynamics.

Rapid-acting agents that keep the airway reflexes intact

Class / agent (typical ICU dose)	Onset (min)	Key advantages	Main cautions
Ketamine 0.5–1 mg kg-1 IV push (or 3–5 mg kg-1 IM)	1–2 IV; 3–5 IM	Very fast tranquilisation, preserves airway tone & respiratory drive, bronchodilator	Emergence reaction, ↑BP/HR, laryngospasm (rare)
Dexmedetomidine 0.5 µg kg-1 over 10 min (optional) → infusion 0.2–0.7 µg kg-1 h-1	5–10	“Co-operative” sedation, minimal resp. depression, useful to bridge into the night	Bradycardia / hypotension (avoid rapid bolus in unstable patients)
Droperidol 2.5–5 mg IV/IM (may repeat q15 min to 10 mg total)	5–10	Faster than haloperidol, short half-life, good for delirium	QTc prolongation → baseline ECG & Mg/K repletion
Haloperidol 2.5–5 mg IV/IM (q15–30 min up to 10–20 mg)	10–20	Familiar, little resp. depression, can combine with 0.5 mg benztropine to ↓EPS	QTc ↑ (less than droperidol), dystonia, akathisia
Second-generation antipsychotics • Olanzapine 10 mg IM • Ziprasidone 10–20 mg IM	15–30	Similar efficacy, less EPS than haloperidol	Post-injection somnolence, QTc ↑, avoid with IM benzodiazepines within 1 h
Small-dose benzodiazepine (e.g., Midazolam 1 mg IV every 2–3 min only if withdrawal or stimulant-driven agitation)	2–3	Synergistic with antipsychotics when a single agent fails	Respiratory depression—titrate in tiny aliquots, avoid large bolus

Practical bedside algorithm

1. First 2 minutes – verbal & environmental measures
   Family presence, low lighting, correct sensory deficits, treat pain.
2. If immediate chemical control is required
   • Choose ketamine for violent or stimulant-intoxicated patients where seconds matter.
   • Choose droperidol or haloperidol when delirium is the likely driver and you can wait 10 min.
   • Start a dexmedetomidine infusion early if agitation is expected to persist overnight or if the patient is at high risk for delirium.
3. Re-check RASS at 5 min
   • If still ≥ +2, repeat previous dose or add a different class (e.g., haloperidol + low-dose midazolam).
   • Stop escalating once RASS ≤ 0.
4. Ongoing care
   • Daily ECG if antipsychotics > 24 h or combined QT-prolonging drugs.
   • Maintain daytime wakefulness / night-time light to reduce delirium.
   • De-escalate and discontinue agents as soon as agitation resolves.

Pearls & pitfalls

• Avoid propofol or large benzodiazepine doses in the unconstrained airway—both cause dose-dependent apnoea.
• Correct electrolytes (K⁺, Mg²⁺) before or during antipsychotic therapy to minimise torsades risk.
• Consider low-dose clonidine (0.1–0.2 mg PO/NG) for milder agitation or sympathetic over-activity, but onset is ≥30 min.
• Always search for unmet physiologic needs—sedation should never replace treating hypoxia, sepsis, or painful invasive devices.