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Saturday, May 17, 2025

CIP and CIM : Failure to Wean and Increase Risk Reintubation

CIP, CIM & Extubation Failure – Quick‑Reference

CIP, CIM & extubation failure – at a glance

1. Does critical‑illness polyneuropathy (CIP) make it hard for patients with secretions to stay off the ventilator?

Yes. CIP – and its sibling critical‑illness myopathy (CIM) – weaken the diaphragm, expiratory muscles and bulbar/pharyngeal musculature. Patients do not produce more secretions, but they lose the cough strength and airway‑protective reflexes required to clear them. Retained mucus  →  atelectasis  →  increased work of breathing  →  fatigue  →  re‑intubation.

Table 1. Mechanisms by which CIP/CIM promote ventilator dependence
Primary deficit Clinical consequence Impact on extubation
Loss of expiratory muscle power Peak cough flow often <60 L·min‑1 Inability to expel pooled secretions → clogging of larger airways
Diaphragmatic & phrenic‑nerve dysfunction ↓ Inspiratory capacity; ↑ WOB Even a modest secretion load tips the balance into fatigue & hypercapnia
Bulbar / pharyngeal weakness Blunted swallow & glottic closure; silent aspiration Further secretion burden & atelectasis after extubation
Global limb weakness (MRC <48) Correlates closely with ineffective cough 2‑ to 3‑fold increase in re‑intubation risk
Practical bedside rule: If peak cough flow <60 L·min‑1 or MRC sum <48 at planned extubation, treat as high‑risk: clear secretions, augment cough (e.g., mechanical insufflation–exsufflation), bridge with HFNC ± NIV.

2. How are CIP and CIM treated in the meantime?

No single drug reverses CIP/CIM. Management bundles target (1) preventable drivers, (2) early mobilisation & muscle‑specific therapies, (3) optimum nutrition, (4) respiratory support during recovery.

2.1 Modifiable drivers

Table 2. Stop or minimise the insults
Driver Bedside action Evidence highlight
Sepsis / systemic inflammation Source control, early ABx Strongest CIP risk factor
Hyperglycaemia Target 110‑180 mg/dL (6‑10 mmol/L) Tight but safe control ↓ ICU‑AW ≈40 %
Deep sedation & NMBAs Daily sedation breaks; keep NMBA <48 h Independent predictors of CIP/CIM
High corticosteroid dose Use lowest effective course Dose‑response link to CIM

2.2 Early mobilisation & muscle‑specific therapies

Table 3. Mobilise & stimulate
Strategy Practical application 2023‑25 evidence
Passive → active physiotherapy Begin <48 h after haemodynamic stability Earlier = less ICU‑AW, faster discharge
Neuromuscular electrical stimulation (NMES) 30‑60 min/day on quads & diaphragm Meta‑analysis: ↑ MRC, ↓ MV duration ≈1.7 d
Inspiratory‑muscle training (IMT) 30 breaths BID at 30‑50 % PImax 2024 RCTs: ↓ re‑intubation, faster weaning

2.3 Nutrition & metabolism

Target 1.3‑2.0 g protein·kg‑1·day‑1, start enteral feeds within 24‑48 h, avoid early full PN.

2.4 Respiratory support bundle

  • Secretion‑clearance: scheduled suction, mucolytics, cough‑assist.
  • Extubate when cough ≥60 L·min‑1; bridge with HFNC/NIV.
  • Early tracheostomy (≥10‑14 d failed weaning) for severe weakness.

3. How is the diagnosis made with EMG & nerve‑conduction studies (NCS)?

Electrophysiology separates neuropathy (CIP) from myopathy (CIM). The stepwise algorithm below is widely used.

Table 4. Signature electrophysiologic patterns
Parameter CIP CIM
Motor CMAP amplitude ↓ (<80 % LLN) ↓ (<80 % LLN)
Sensory SNAP amplitude Normal
CMAP duration Normal Prolonged (>10 ms)
Direct‑muscle stimulation (DMS) Preserved excitability Reduced excitability
Nerve : muscle CMAP ratio > 0.5 < 0.5
Typical conclusion Diffuse axonal sensorimotor neuropathy Primary myopathy

Low sensory amplitudes + preserved direct‑muscle response → CIP; Normal sensory amplitudes + muscle inexcitability → CIM.

4. How do I calculate the Medical Research Council (MRC) sum score?

Score six muscle groups (bilaterally), grade 0–5, then add the 12 numbers (max 60).

Table 5. MRC Sum‑Score worksheet
Limb Muscle group Grade R Grade L
UpperShoulder abduction (deltoid)
Elbow flexion (biceps)
Wrist extension (ext. carpi)
LowerHip flexion (iliopsoas)
Knee extension (quadriceps)
Ankle dorsiflexion (tibialis ant.)
Subtotal each side
MRC sum score = R + L (max 60)
Table 6. MRC grading scale
GradeDescription
0No visible/palpable contraction
1Flicker/trace contraction, no movement
2Active movement with gravity eliminated
3Active movement against gravity
4Active movement against gravity + resistance
5Normal power

Interpretation: Sum < 48 = ICU‑AW likely; Sum < 36 = severe weakness → high risk of extubation failure & prolonged rehab.

Bottom line: CIP/CIM + heavy secretions = weak cough → retained mucus → atelectasis → fatigue → re‑intubation. Mitigate drivers early, mobilise daily, augment cough, and choose the right airway strategy.

OMI RCA versus Circumflex Coronary Artery Recognition by EKG

1. Right-Dominant Coronary Anatomy

Scenario: Posterior descending artery (PDA) arises from the RCA — standard anatomy (≈ 80 % of hearts). An inferior STEMI may be due to RCA or LCx occlusion; table below highlights distinguishing ECG / clinical clues.

ECG / Bedside clue RCA Culprit LCx Culprit
Inferior ST elevation pattern Lead III > Lead II (right-ward injury vector) Lead II ≈ III or II > III
Reciprocal ST depression in aVL Marked (≥ 1 mm) Milder or none
Lateral ST elevation (I, aVL, V5-6) Absent / minimal Present
Right-sided involvement (V1, V4R) ST ↑ common (RV infarct) Rare
Posterior clues (V7-9, mirror in V1-2) Minimal Tall R + ST ↓ in V1-3 or ST ↑ V7-9
Early AV block / brady-arrhythmia Frequent (AV-node branch) Less common
Haemodynamics RV-dependent hypotension; fluid responsive LV posterolateral failure; pulmonary congestion

Practical bedside memory aid: “III beats II with deep aVL = RCA; lateral or posterior lift = LCx.”


2. Left-Dominant Coronary Anatomy (Circumflex gives PDA)

Scenario: In ≈ 10-15 % of hearts the LCx supplies the PDA and most of the inferior wall. The pattern of inferior STEMI shifts accordingly; RCA infarcts are usually smaller and RV-centred.

ECG / Bedside clue Nondominant RCA Culprit Dominant LCx Culprit
Inferior ST elevation pattern Modest; III > II but smaller ΣST II ≈ III or II > III with larger amplitude
Reciprocal ST depression in aVL Often ≥ 1 mm Mild / neutralised by lateral ST ↑
Lateral ST elevation (I, aVL, V5-6) None or < 0.5 mm Concordant elevation common
Posterior involvement Uncommon ST ↑ V7-9 or tall R + ST ↓ V1-3
Right-sided ST elevation (V4R, V1) Possible (RV branch) Absent
AV-nodal block Can occur Less frequent
Haemodynamics RV preload sensitive Higher risk LV failure / cardiogenic shock

Practical bedside rule: “Inferior plus lateral or posterior lift → LCx dominant; isolated small inferior (III > II) or RV clues → RCA.”

Why it matters clinically

  • RCA occlusion—watch for high-grade AV block and RV infarction; preload-dependent, so give fluids cautiously but early.

  • LCx occlusion—greater posterolateral necrosis risk; may masquerade as a “normal” ECG if posterior only, so record V7-V9 when suspicion is high.

Practical bedside rule in left dominance

Inferior + lateral or posterior lift → think LCx.
Isolated smaller inferior (III > II) or RV signs → think RCA.


 Example RCA Infarct/OMI (2nd EKG right -sided leads)                                                                                                         




Another example of an Inferior Wall MI


What is the culprit vessel in this inferior wall STEMI?

Answer: Right coronary artery (RCA) is the most likely culprit.
The ECG demonstrates a classic right-dominant inferior MI pattern: larger ST elevation in lead III than II, conspicuous reciprocal depression in aVL, and no concordant lateral ST elevation.

Key ECG / Bedside clue Finding on the provided tracing Interpretation
ST height: lead III vs II ST ↑ in III > II Injury vector points right-inferior → favors RCA occlusion
Reciprocal change in aVL Clear ≥ 1 mm ST depression Classic RCA signature (deep aVL depression)
Lateral leads (I, aVL, V5-6) No concordant ST elevation Absence of lateral lift argues against LCx culprit
Posterior / right-sided clues Posterior leads not shown; V1-3 lack tall R / ST ↓; right-sided leads pending RCA can still involve RV → record V4R to confirm
Rhythm / conduction Sinus rhythm; no high-grade AV block yet RCA supplies AV node in ≈ 90 % → monitor for late block

Practical bedside rule to remember
“III beats II with deep aVL depression → think RCA. Lateral or posterior lift → think LCx.”

Example typical left circumflex infarct:




Friday, May 16, 2025

Bicarbonate therapy in DKA: A Practical Approach

Bicarbonate Use in Diabetic Ketoacidosis

Venous / Arterial pH Bicarbonate dose How to mix (dilution + electrolytes) Infusion rate When to reassess / repeat
< 6.9 100 mmol NaHCO3
(two 50-mL amps of 8.4 %)
Dilute in 400 mL 0.45 % NaCl
+ 20 mmol KCl → ~250 mOsm L-1
200 mL h-1 (2 h total) Check VBG/ABG q 2 h; repeat same dose if pH < 7.0
6.9 – 7.0 50 mmol NaHCO3
(one 50-mL amp)
Dilute in 200 mL 0.45 % NaCl
± 10 mmol KCl
200 mL h-1 (1 h total) Re-check pH at end of infusion; rarely needs second dose
> 7.0 No bicarbonate indicated Insulin + fluids will close the gap

Practical bedside recipe (pH < 6.9 example)

1. Draw 2 amps (100 mL) of 8.4 % NaHCO3.
2. Add to a 500-mL bag of 0.45 % saline after discarding 100 mL (final volume = 400 mL).
3. Add 20 mmol KCl (e.g., 10 mL of 2 mEq mL-1) unless K+ > 5.5 mEq L-1.
4. Label “Sodium bicarbonate 100 mmol + KCl 20 mmol in 400 mL”; infuse at 200 mL h-1.
5. Repeat VBG and electrolytes in 2 h; if pH < 7.0, mix and run the same bag again.

Key reminders

  • Use venous blood gas for trending; pH difference from ABG is < 0.03.
  • Stop bicarbonate once pH ≥ 7.0 or HCO3- > 18 mEq L-1; overshooting delays anion-gap closure.
  • Bicarbonate adds the same millimoles of Na+; monitor sodium balance and osmolality.
  • Insulin and volume resuscitation correct keto-acid production—the NaHCO3 drip is only a bridge while pH is critically low.

Bottom line

When venous/arterial pH in DKA falls below 6.9, give 100 mmol (two amps) of 8.4 % sodium bicarbonate only after diluting to 400 mL with 0.45 % saline and adding potassium. Infuse over 2 hours, then reassess; repeat only if pH remains < 7.0. For pH > 7.0, bicarbonate therapy offers no benefit and may be harmful.

Grading AS on Echocardiography

Parameter Mild AS Moderate AS Severe AS
Aortic Valve Area (AVA) > 1.5 cm² 1.0 – 1.5 cm² < 1.0 cm²
Indexed AVA (AVA/BSA) > 0.85 cm²/m² 0.6 – 0.85 cm²/m² < 0.6 cm²/m²
Peak Aortic Jet Velocity < 3.0 m/s 3.0 – 4.0 m/s ≥ 4.0 m/s
Mean Transvalvular Gradient < 20 mmHg 20 – 40 mmHg ≥ 40 mmHg
Dimensionless Index (DI) > 0.50 0.25 – 0.50 < 0.25
Aortic Valve VTI Ratio > 0.50 0.25 – 0.50 < 0.25
Clinical Symptoms Usually absent May be present Often present (dyspnea, angina, syncope)

Note: Always interpret AS severity in the context of flow status, LV function, and patient symptoms. Consider dobutamine stress echocardiography or CT calcium scoring in low-flow, low-gradient cases.

🔎 Notes:

  • DI is especially useful when LVOT diameter is unreliable or in low-flow states (e.g., preserved EF but small stroke volume).

  • Low-flow, low-gradient severe AS may have:

    • AVA < 1.0 cm²

    • DI < 0.25

    • But mean gradient < 40 mmHg due to low output — requires dobutamine stress echo or CT calcium scoring for confirmation.

  • Always interpret in context with symptoms and LV function.

Wednesday, May 14, 2025

Airway strategies for extubated patient with abundant , think secretions and weak cough at risk for reintubation

Strategy How to Implement Typical Dose / Setting Key Pearls & Cautions
Heated-humidified HFNC Large-bore nasal cannula connected to heated humidifier (37 °C) 30–60 L min-1; FiO2 to keep SpO2 > 92 % Restores 100 % RH, thins mucus & adds mild PEEP; watch for gastric distention
Systemic hydration IV balanced crystalloids or encourage PO fluids if safe Maintain euvolemia; avoid over-hydration in HF/ARDS Dehydration is the easiest reversible “mucolytic”
Nebulised saline In-line or mouthpiece nebuliser 3–5 mL 0.9 % q4–6 h; step up to 3 % if secretions remain viscous Hypertonic draws water into ASL; pre-treat with albuterol in reactive airways
N-acetylcysteine (N-AC) Jet neb via mask or mouthpiece 3 mL 10 % (or 1–2 mL 20 %) q4–6 h Bronchospasm risk → give albuterol first; avoid in frank hemoptysis
Hypertonic saline 7 % Nebulise as alternative/adjunct to N-AC 3 mL q6–8 h Monitor serum Na+ with frequent doses
Dornase alfa Mouthpiece neb (off-label outside CF) 2.5 mg q24 h Consider for lobar collapse or DNA-rich sputum; expensive
Mechanical insufflation-exsufflation (MI-E / “Cough-Assist”) Face-mask or mouthpiece interface +40 / −40 cm H2O, 3–5 cycles × 3–6 sets q4–6 h Continuous SpO2/ECG; stop if SpO2 < 90 % or haemodynamic drop
OPEP devices (Acapella®, Aerobika®) Active exhalations through device followed by huff-cough 10–20 breaths × 4–6 sessions day-1 Small, patient-controlled; contraindicated if unable to form good seal
Manual/air-stack cough Caregiver timed abdominal thrust or air-stack via resuscitation bag 3–5 assisted coughs per session; repeat q4 h Simple for neuromuscular disease; watch for rib fracture in frail pts
Chest physiotherapy (CPT) Postural drainage, percussion & vibration Each lung segment 3–5 min q2 h Combine with turns/early sitting for best effect
Deep oropharyngeal suction Yankauer or large-bore suction catheter PRN & at least q2 h; set suction 80–120 mm Hg Avoid mucosal trauma; pre-oxygenate if severe hypoxaemia
Early mobilisation Bed-to-chair, ambulation as tolerated N/A Enhances cephalad mucus movement & prevents atelectasis
NIV/BiPAP “boost” sessions Full-face mask between clearance sessions IPAP 10–14 / EPAP 5–6 cm H2O Helpful for hypercapnia or lobar collapse; monitor gastric insufflation
Flexible bronchoscopy Diagnostic & therapeutic lavage/suction As indicated if clearance fails within 6–12 h Low threshold in lobar opacity or hypoxaemia; requires procedural sedation
Analgesia / lighter sedation Limit opioids; use multimodal pain control N/A Excess sedation blunts cough; pain inhibits deep breaths
Head-of-bed ≥ 30° Maintain semi-Fowler position; side-to-side rotation N/A Reduces aspiration & promotes drainage
Culture-directed antibiotics Obtain sputum culture if purulent; start/adjust antibiotics accordingly Per culture & local guidelines Treats bronchitis/pneumonia driving secretion load

Tip — Combine 2–3 complementary strategies (e.g., HFNC + N-AC + MI-E) and reassess work of breathing and chest imaging every 6–12 h. Escalate to bronchoscopy or NIV if lobar collapse or CO2 retention persists.

Tuesday, May 13, 2025

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.

Sunday, May 11, 2025

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

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

Pathogens of Concern

GroupTypical PathogensNotes
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

SettingPreferred 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.

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