The Critical Care Practitioner

Tom, one of my colleagues from the Critical Care Outreach Team and I discuss this paper and its findings reaching our own conclusions.

Deferring Arterial Catheterisation in Patients with Septic Shock.

We return to our 48-year-old patient: jaundiced, hypotensive, drowsy, and bleeding. In decompensated cirrhosis, every treatment targets a disrupted system — splanchnic vasodilation, portal hypertension, toxin accumulation, and renal hypoperfusion.

Although these patients look fluid overloaded, they are effectively hypovolaemic. Start with small aliquots of balanced crystalloid, avoiding 0.9% saline. In hepatorenal syndrome or tense ascites, 20% albumin is key — not just for volume expansion, but for circulatory and anti-inflammatory support.

Once volume is optimised, flow must be redirected. Terlipressin reverses splanchnic vasodilation, reduces portal pressure, and improves renal perfusion. If contraindicated, noradrenaline targeting a MAP ≥65 mmHg is an effective alternative.

Variceal bleeding reflects portal hypertension, not missing clotting factors. Use restrictive transfusion, correct platelets and fibrinogen selectively, start antibiotics early, and proceed to endoscopic banding once haemodynamically stable. Avoid blanket correction of INR — treat bleeding, not numbers.

Hepatic encephalopathy management focuses on reversing precipitants and reducing ammonia with lactulose and rifaximin, while protecting the airway in advanced grades. Infection screening is essential — SBP and sepsis worsen vasodilation and renal failure, with albumin improving outcomes.

Renal dysfunction is functional, not structural. Albumin plus vasoconstrictors can restore perfusion. Nutrition is critical: early enteral feeding with adequate protein supports recovery and ammonia clearance.

Bottom line: cirrhosis care works when physiology drives every decision.

In this episode, I walk through the real-world critical care management of acute decompensated alcohol-related liver disease, using a high-risk ICU case to anchor the discussion. The focus is on understanding the underlying physiology—portal hypertension, rebalanced haemostasis, hepatic encephalopathy, infection, and hepatorenal syndrome—and translating that physiology into clear first-hour priorities at the bedside.

Listeners are guided through airway and circulatory decision-making, rational use of albumin, vasopressors, antibiotics, lactulose and rifaximin, and careful blood product transfusion, while avoiding common pitfalls such as reflexive FFP or over-resuscitation.

The episode emphasises early recognition of red flags, the central role of infection as a precipitant, and the interconnected nature of multi-organ failure in acute-on-chronic liver disease, all framed within pragmatic UK ICU practice.

This episode offers a structured, bedside-focused exploration of Non-Invasive Ventilation (NIV) for acute hypercapnic respiratory failure in COPD, aligned with NICE NG115 and BTS/ICS 2016 guidance. Aimed at early-career critical care nurses, it breaks the topic down into physiology, practical setup, monitoring, and escalation.

Key Topics Covered

• Mechanisms behind acute-on-chronic hypercapnic respiratory failure in COPD.

• How NIV improves ventilation, reduces CO₂, and decreases work of breathing.

• Evidence-based indications for NIV initiation.

• Practical bedside steps for the first hour of therapy.

• How to titrate settings, troubleshoot problems, and recognise failure.

• Common complications and when to escalate to invasive ventilation.

Case-Based Learning The episode follows Mr. Harris, a 68-year-old man with severe COPD presenting with type 2 respiratory failure. His clinical deterioration, ABG results (pH 7.25, pCO₂ 9.8 kPa), and work of breathing set the scene for understanding when and why NIV is beneficial.

Physiology Essentials Listeners are guided through the impact of airway obstruction, air trapping, hyperinflation, respiratory muscle fatigue, and CO₂ narcosis. NIV's core actions—improving tidal volume with IPAP and splinting airways with EPAP—are linked directly to these mechanisms.

Practical Bedside Framework

• Start with IPAP 12 cmH₂O / EPAP 4 cmH₂O and FiO₂ around 28%, aiming for SpO₂ 88–92%.

• Reassure the patient, optimise positioning, secure a comfortable mask seal, and monitor synchrony.

• Repeat ABG at 1 hour; look for rising pH and falling CO₂.

• Adjust pressures in small increments if needed while monitoring for leaks, agitation, hypotension, or gastric distension.

Monitoring and Escalation Success indicators include reduced respiratory rate, improved alertness, and trending normalisation of pH. Red flags include worsening acidosis, declining consciousness, mask intolerance, or inability to maintain the airway—prompting urgent senior review.

Common Complications Facial pressure sores, gastric distension, aspiration risk, anxiety, and haemodynamic compromise are highlighted with practical prevention strategies.

Five Golden Rules

1. Recognise early and initiate NIV promptly.

2. Start simple with standard pressures and controlled oxygen.

3. Reassess rapidly with a 1-hour ABG.

4. Escalate quickly if failure criteria develop.

5. Protect the patient with meticulous care and communication.

Outcome After an hour of NIV, Mr. Harris' pH rises to 7.32 and pCO₂ falls to 8.2 kPa, with clear clinical improvement—illustrating the value of timely, well-managed NIV in COPD.

Closing The episode reinforces the importance of physiological understanding in delivering confident, effective NIV care at the bedside.

HHS (Hyperosmolar Hyperglycaemic State) is the quiet counterpart to DKA. It develops slowly in older type 2 diabetics with residual insulin, leading to extreme hyperglycaemia and dehydration without ketosis. In this 2-hour deep dive, Jonathan explains why HHS kills through water loss and hyperviscosity rather than acid, and how to manage it safely.

Key Learning Points:

· Pathophysiology: Relative insulin deficiency → no ketones, but relentless osmotic diuresis → hyperosmolarity > 320 mOsm/kg.

· Recognition: Elderly, confused, profoundly dehydrated, glucose often > 30 mmol/L, Na⁺ high, pH > 7.3.

· Fluids first: Replace ~½ deficit in 12 h with 0.9 % saline; adjust for heart/kidney function.

· Insulin later: 0.05 u/kg/hr once osmolality is falling; aim glucose fall 3–6 mmol/L/hr.

· Add dextrose when glucose ≈ 14 mmol/L to avoid cerebral oedema.

· Potassium vigilance: Replace according to level; withhold insulin if

· Thromboprophylaxis essential.

· Monitoring: Hourly glucose & neuro obs, 2–4-hourly U&Es/osmolality, strict fluid balance.

· Complications: Cerebral oedema, VTE, renal injury, electrolyte shifts, rhabdomyolysis.

· Take-home: In HHS, correct the water slowly, the sugar gently, and never forget the brain.

Diabetic ketoacidosis (DKA) is not just "high blood sugar" — it's a hormonal storm caused by absolute insulin deficiency and a surge of counter-regulatory hormones. The result is a triad of hyperglycaemia, dehydration, and metabolic acidosis.

We follow Sophie, a 23-year-old with type 1 diabetes who arrives with vomiting, Kussmaul breathing, glucose 28 mmol/L, ketones 5.6 mmol/L, and pH 7.08.

• No insulin → cells can't use glucose → liver produces more.

• Glucose spills into urine → osmotic diuresis → 6–8L fluid + electrolyte loss.

• Fat breakdown produces ketones → metabolic acidosis.

• Potassium appears normal or high, but total body stores are low.

1. Fluids first – 1L 0.9% NaCl over 30 mins (slower if frail/cardiac issues). Restores perfusion, lowers stress hormones.

2. Potassium next – replace before insulin if K⁺ <3.5 mmol/L; add to fluids if 3.5–5.5.

3. Insulin third – fixed-rate 0.1 units/kg/h to stop ketone production, not to chase glucose.

4. Add 10% dextrose when glucose falls to ~14 mmol/L to safely continue insulin.

5. Treat the trigger – infection, missed insulin, MI, etc.

DKA isn't chaotic when understood physiologically. Fluids, potassium, insulin — in that order. You're not treating the number; you're fixing the metabolic storm.

Summary: In this episode, we spotlight a stealthy ICU disruptor — hypophosphataemia. Based on a 2024 narrative review in the Journal of Clinical Medicine, we explore why phosphate matters, how it goes missing in critically ill patients, and why you should care even when it's just "a little low."

What's Covered:

• The vital role of phosphate in energy, oxygen delivery, and muscle function

• Why hypophosphataemia affects 20–80% of ICU patients

• Clinical consequences, from muscle weakness to respiratory failure, arrhythmias, and delirium

• Common causes: refeeding, DKA, diuretics, malnutrition, and sepsis

• Replacement options — and why there's no universal guideline

• When to go IV, when oral might suffice, and what risks to watch for

Key Takeaways:

• Don't overlook mild phosphate drops — they're not always benign

• Severe hypophosphataemia (

• Consider protocols for screening and replacement in high-risk ICU patients

• More research is needed, but clinical awareness matters now

Final Thought: Phosphate might be the quiet ninja of the ICU — when it vanishes, chaos isn't far behind. Check your labs, trust your gut, and give phosphate the respect it deserves.

• What is DKA? – The triad of hyperglycaemia, ketonaemia, and metabolic acidosis (JBDS 2023 definitions).

• Pathophysiology explained – Insulin deficiency, ketone production, and why potassium is so tricky.

• Clinical features – Polyuria, dehydration, Kussmaul breathing, acetone breath, and red flags for deterioration.

• Investigations – Capillary ketones, blood gases, electrolytes, ECG, and screening for precipitants.

• Management (UK guidelines) – Fluids first, fixed-rate insulin infusion, careful potassium replacement, and always treat the trigger.

• Pitfalls – Starting insulin before fluids, forgetting potassium, dropping glucose too quickly, or missing the underlying cause.

• Case vignette – A young woman with type 1 diabetes presenting in DKA, walking through priorities and pitfalls in real time.

🔑 Key takeaways:

• DKA = fluids first, insulin second, potassium throughout.

• Monitor closely and stick to the JBDS 2023 UK protocol.

• Always identify and treat the precipitating cause.

Mobilisation in the ICU raises two big questions: is it safe, and will staff embrace it?

In this discussion, Jonathan explores both sides of the story:

• Safety first:

  • Large prevalence studies show mobilisation is happening, though often inconsistently.

  • A systematic review of 1,800+ sessions found serious adverse events in only 0.6% — most minor and short-lived.

  • Even patients on CRRT can safely mobilise with planning, adequate staff, and the right equipment.

  • Consensus guidelines outline clear safety screens, covering oxygen, ventilator settings, vasopressors, and line security.

• Culture and barriers:

  • Staff concerns include safety fears, deep sedation, lack of hands, limited kit, and "whose job is this anyway?"

  • Interviews reveal gaps in knowledge and confidence, differing beliefs about risks and benefits, and role confusion between professions.

  • Success breeds success: once teams see mobilisation working, attitudes shift.

  • Daily goals, interdisciplinary huddles, and local champions help make mobilisation the default, not the exception.

Takeaway: Mobilisation in ICU is both safe and achievable — but safety checks alone aren't enough. Embedding it into everyday culture is the real key to making it routine.

Summary For much of critical care history, immobility was the norm: patients were sedated, kept still, and "protected." But decades of research have revealed the hidden costs — profound muscle wasting, delirium, and long-term disability.

Jonathan explores how our understanding of mobilisation in ICU has evolved — from the recognition of harm caused by bedrest, to the first landmark studies proving that early movement is both feasible and beneficial.

• ICU-acquired weakness: Patients can lose 15–20% of muscle mass within the first week of critical illness.

• Long-term outcomes: ARDS survivors tracked for five years showed persistent disability and reduced independence.

• Sedation & delirium: Deep sedation increases delirium risk; mobilisation reduces both incidence and duration.

• Physiological rationale: Even minimal movement supports cardiovascular tone, respiratory function, circulation, and cognition.

• Core message: Bedrest is not neutral — it is actively harmful. Mobilisation offers protection for both brain and body.

• Feasibility (Morris et al., 2008): Protocol-led mobilisation cut time to first mobilisation (5 vs 11 days), with no increase in adverse events.

• Landmark RCT (Schweickert et al., 2009):

  • Early PT/OT + daily sedation interruption vs SAT alone.

  • 59% vs 35% regained independence at discharge.

  • Patients had less delirium and spent fewer days ventilated.

• Implementation (Needham et al.): Demonstrated how embedding mobilisation into daily ICU practice improves outcomes and serves as a model for quality improvement.

• Core message: Early mobilisation is not only possible — it improves patient-centred outcomes safely.

• Bedrest and heavy sedation accelerate weakness, delirium, and disability.

• Mobilisation is both biologically plausible and clinically effective.

• Early trials proved feasibility, safety, and functional benefits.

• Success requires:

  • Lighter sedation targets and daily SATs.

  • Interdisciplinary teamwork (nursing, PT/OT, medical).

  • Structured protocols and safety screens.

Overall message: Mobilisation should no longer be an afterthought in ICU. It is a therapeutic intervention — one that supports recovery, preserves dignity, and helps patients walk out of intensive care with more than just survival.