GC006 The Patient Is Very Ill After The Operation - Post-operative Management
Post-operative management of critically ill surgical patients involves systematic monitoring and treatment of complications such as hemorrhage, infection, respiratory failure, and organ dysfunction to ensure recovery and prevent deterioration.
The Patient is Very Ill After the Operation – Post-operative Management
This lecture (GC 006) by Dr Stanley Sau Ching Wong is an anaesthesia-focused lecture that addresses the early post-operative period — specifically what happens from the moment a patient arrives in the Post-Anaesthesia Care Unit (PACU) until they are stabilised. The lecture is structured around the ABC approach (Airway, Breathing, Circulation) and then systematically covers neurological, temperature-related, pain, and nausea/vomiting complications.
Why this matters clinically: The immediate post-operative period is one of the most dangerous windows for a surgical patient. Anaesthetic drugs are wearing off, the metabolic stress response to surgery is kicking in, and the patient is transitioning from a highly monitored operating theatre to a less-monitored environment. Any complication missed here can rapidly become fatal.
Why this matters for exams: This topic is a perennial favourite in both MCQ and SAQ/minicase formats. Examiners love to present a clinical scenario of a deteriorating post-op patient and expect you to systematically work through ABC, identify the cause, and manage appropriately. The 2023 minicase (Case 3, Section 4) directly tested airway manoeuvres, septic shock recognition, and acute management in a deteriorating post-op patient [1].
Learning Objectives (from the lecture) [2]
"Know the approach to patients arriving to PACU" "Recognize complications that could occur in PACU"
"Ensure patient safety. Prioritize → airway, breathing, circulation. Treat other common problems to enhance patient comfort." [2]
Complications post-anaesthesia at a glance [2]:
- A — Airway problems
- B — Hypoventilation, Hypoxaemia
- C — Hypotension, Hypertension, Arrhythmias
- Neurological — Confusion, Over-sedation, Stroke
- Others — Pain, Nausea and vomiting
The perioperative period is divided into: Preop → Intraop → Early post-op → Late post-op [3]
| Phase | Timeframe | Key Concerns |
|---|---|---|
| Pre-op | Before surgery | Fitness assessment, risk stratification, optimisation |
| Intra-op | During surgery | Anaesthetic management, surgical technique, monitoring |
| Early post-op | PACU → first 24–48 hours | This lecture's focus: ABC problems, pain, PONV, delirium, hypothermia |
| Late post-op | Day 2 onwards | Surgical site infection, DVT/PE, anastomotic leak, ileus, respiratory complications |
This lecture focuses on the early post-operative period, predominantly in the PACU setting.
On arrival need to check: (1) airway patency, (2) breathing + oxygenation, (3) vital signs: BP, pulse rate, temperature [4]
Give around 30–40% oxygen for GA patients [4]
The fixed 30–40% oxygen statement is the lecture's practical starting point, not a universal prescription. In current practice, give supplemental oxygen when needed and titrate it to a documented target saturation: usually 94–98%, or 88–92% for patients at risk of hypercapnic respiratory failure pending blood-gas results [56]. Do not withhold oxygen from a critically hypoxaemic patient while waiting for an ABG.
After general anaesthesia, multiple factors can reduce oxygenation:
- Residual anaesthetic agents depress ventilatory drive
- Atelectasis from intra-operative positioning and muscle relaxation
- V/Q mismatch from the supine position and abdominal distension
- Shivering increases oxygen consumption by 200-400%
Oxygen is a drug
Avoid the outdated explanation that oxygen is restricted in COPD because it "suppresses hypoxic drive." The clinically important problem is oxygen-induced hypercapnia in susceptible patients, mediated mainly by worsening V/Q mismatch and the Haldane effect. Prescribe a target range, monitor the response, and obtain a blood gas when hypercapnic respiratory failure is possible [56].
PACU Monitoring Checklist
Monitor: Pulse oximeter, non-invasive blood pressure, respiratory rate [5] Check fluid input and output (urine, drains) [5] Manage other problems: i.e. pain [5]
| Parameter | Why It Matters |
|---|---|
| SpO₂ | Earliest non-invasive indicator of hypoxaemia |
| NIBP | Detects hypo/hypertension — both dangerous post-op |
| Respiratory rate | Often the first vital sign to change in deterioration; detects hypoventilation before SpO₂ drops |
| Urine output | Useful perfusion/renal trend; oliguria is non-specific and must be interpreted with haemodynamics, fluid balance, renal function and catheter patency |
| Drain output | Detects surgical bleeding, bile leak, etc. |
| Temperature | Hypothermia is common and has significant consequences |
History: Story from patient (c/o or HPI), Pre-operative assessment, Anaesthetic record, Surgical record [6] Physical examination [6] Investigations: Blood tests, Imaging, Other monitoring devices [6]
Why is the anaesthetic record so important? It tells you:
- What drugs were given (and therefore what residual effects to expect)
- Intra-operative fluid balance (blood loss, fluids given)
- Any intra-operative events (hypotension, arrhythmias, difficult airway)
- Duration of anaesthesia (longer = more residual drug effect)
Why is the surgical record important? It tells you:
- What was done (risk of specific complications)
- Intra-operative blood loss
- Drain placement
- Any surgical concerns communicated to anaesthesia
General Approach
Simultaneous assessment & supportive treatment [7] Airway, Breathing, Circulation [7] Treat the patient, not the monitors [7]
Treat the Patient, Not the Monitors
This is a critical clinical principle. A monitor showing SpO₂ of 92% in a patient who is pink, talking, and comfortable may reflect a probe issue. Conversely, a patient who looks grey and distressed with "normal" numbers on the screen may be in serious trouble. Always correlate clinical findings with monitoring data.
A — Airway Problems
Tongue falling back, Laryngospasm, Secretions, Vomitus, Blood, External pressure on trachea, Foreign body (e.g. gauze packing) [8]
Let's understand each:
| Cause | Mechanism | Why It Happens Post-Op |
|---|---|---|
| Tongue falling back | Loss of pharyngeal muscle tone → tongue falls posteriorly against posterior pharyngeal wall | Most common cause; residual anaesthetic/sedative/opioid effects reduce genioglossus tone |
| Laryngospasm | Protective reflex closure of vocal cords; glottis snaps shut | Triggered by blood, secretions, or airway manipulation during emergence from anaesthesia |
| Secretions | Mucus pools in hypopharynx | Reduced swallowing reflex during emergence; some drugs (e.g. ketamine) increase secretions |
| Vomitus | Gastric contents in the airway | Risk increased with emergency surgery, obesity, full stomach, opioids |
| Blood | From surgical site (especially ENT, oral, thyroid surgery) | Accumulates in airway if patient is semi-conscious |
| External pressure on trachea | Haematoma compressing trachea externally | Post-thyroidectomy or neck surgery haematoma is a surgical emergency |
| Foreign body | Gauze, dental prostheses, throat packs left in situ | Human error; should be checked at end of surgery |
Partial obstruction: noisy respiration [9] Total obstruction: cessation of airflow at mouth, no breath sounds, no chest expansion [9] Do not wait till oxygen desaturation [9]
High Yield Exam Point
"Do not wait till oxygen desaturation" — This is a critical teaching point. SpO₂ is a LAGGING indicator. By the time SpO₂ drops, the patient has already been hypoxaemic for seconds to minutes due to the oxygen reservoir in the lungs (functional residual capacity). Recognise airway obstruction by CLINICAL SIGNS (noisy breathing, paradoxical chest movements, accessory muscle use, tracheal tug) BEFORE the numbers change.
Clinical pearl: The character of noisy breathing tells you the level of obstruction:
- Snoring → tongue/soft palate (most common in PACU)
- Stridor (inspiratory) → supraglottic/glottic level (laryngospasm)
- Gurgling → liquid in airway (secretions, blood, vomitus)
- Wheeze (expiratory) → lower airway (bronchospasm)
- Silence with respiratory effort → total obstruction (emergency!)
Triple airway manoeuvre: head tilt, chin lift, jaw thrust [10] Give oxygen [10] Airway adjuncts: nasopharyngeal airway [10] Suction blood, vomitus, remove FB [10] Endotracheal intubation [10]
Stepwise escalation:
- Triple airway manoeuvre — This physically lifts the tongue off the posterior pharyngeal wall and opens the airway. Head tilt + chin lift is the simplest; jaw thrust is used if cervical spine injury is suspected.
- High-flow oxygen — Buy time while you fix the obstruction.
- Airway adjuncts — Nasopharyngeal airway (NPA) is preferred in semi-conscious patients as it is better tolerated than an oropharyngeal airway (OPA), which can trigger gagging/vomiting/laryngospasm in patients with intact reflexes.
- Suction — Under direct vision for vomitus/blood; blind deep suction can worsen laryngospasm.
- Endotracheal intubation — Definitive airway if above measures fail.
Visual concept — Relief of airway obstruction [2]: A sagittal diagram contrasts a blocked airway (tongue displaced posteriorly, obstructing the pharynx) with an open airway (hand performing head-tilt/jaw manoeuvre, tongue lifted away from the posterior wall, airway passage patent). This illustrates why the triple airway manoeuvre works — it mechanically displaces the tongue anteriorly.
For laryngospasm specifically:
- Call for anaesthetic help, remove the provoking stimulus, apply a firm jaw thrust and 100% O₂ with continuous positive airway pressure through a tight mask seal.
- If it persists, the anaesthetist may deepen anaesthesia and give a rapid-onset neuromuscular blocker according to the local emergency protocol.
- Persistent obstruction, hypoxaemia or inability to ventilate may require tracheal intubation. Continue oxygenation/ventilation support throughout.
The 2023 minicase (Q11-12) asked directly for "three simple airway manoeuvres" and "the most appropriate simple airway adjunct" — the answers are head tilt, chin lift, jaw thrust (3 marks each), and nasopharyngeal airway [1].
B — Breathing Problems
Hypoventilation
Causes of hypoventilation: [11] Poor respiratory drive: Residual anaesthetic effect, opioid, CNS problem Poor respiratory muscle function: Residual muscle relaxant, diaphragmatic splinting Pulmonary diseases: Pneumothorax, severe COPD, asthma
| Agent | Mechanism | Clinical Clue |
|---|---|---|
| Residual volatile anaesthetic | Depresses medullary respiratory centre | Drowsy patient, slow RR, shallow breathing |
| Opioids | μ-receptor activation in brainstem respiratory centres → ↓ respiratory rate and tidal volume | RR < 8/min, small pupils, responds to naloxone |
| Benzodiazepines | GABA-A potentiation → CNS depression | Drowsy but usually less respiratory depression than opioids alone |
| CNS problem | Stroke, raised ICP | Focal neurological signs, asymmetric pupils |
Residual muscle paralysis, Pain — 60% reduction in vital capacity after upper abdominal operations, External compression: Obesity, Gastric distention, Tight dressings [12]
High Yield Fact
"Pain causes 60% reduction in vital capacity after upper abdominal operations" — This is a commonly cited statistic. Upper abdominal and thoracic incisions cause the most respiratory impairment because they inhibit diaphragmatic and intercostal muscle contraction through reflex splinting and pain. This is WHY good post-operative analgesia is not just about comfort — it prevents respiratory complications like atelectasis and pneumonia.
Residual neuromuscular blockade: Even after reversal, incomplete recovery can cause upper-airway obstruction, weak cough and hypoventilation. Weak grip, inability to sustain head lift and paradoxical breathing are warning signs, but clinical tests alone cannot exclude residual blockade. Current guidance recommends quantitative monitoring at the adductor pollicis and confirmation of a train-of-four ratio ≥0.9 before extubation [57].
ABC, Oxygenation and ventilation, May need endotracheal intubation [13] Find and treat underlying cause Consider antidote if opioid or BDZ overdose (naloxone, flumazenil) Reverse any residual muscle relaxant effect
| Drug problem | Immediate principle | Definitive step |
|---|---|---|
| Opioid-induced ventilatory depression | Open the airway and support ventilation; do not wait for naloxone to work | Titrate naloxone to restore adequate ventilation while avoiding abrupt complete analgesia reversal; observe for recurrent depression because naloxone may wear off first |
| Benzodiazepine effect | Support airway and ventilation first | Flumazenil is for selected, known iatrogenic benzodiazepine sedation; avoid routine use when dependence, seizure risk or mixed/pro-convulsant overdose is possible |
| Residual neuromuscular blockade | Escalate to the anaesthetist and support ventilation | Use quantitative train-of-four monitoring; choose reversal according to the blocker and depth of block, then confirm TOF ratio ≥0.9 [57] |
Common Exam Trap
Naloxone has a shorter half-life (~30 min) than most opioids (morphine ~3-4 hrs). A patient may initially improve with naloxone then re-sedate as the naloxone wears off. Always monitor these patients closely and consider a naloxone infusion if repeated doses are needed.
Hypoxaemia
SpO₂ < 90% or PaO₂ < 8 kPa [14]
This is the lecture threshold for significant hypoxaemia, not a complete clinical definition. SpO₂ of about 90% corresponds to PaO₂ of roughly 8 kPa (60 mmHg) on the oxygen-haemoglobin dissociation curve — near the "steep part," where small further drops in PaO₂ cause larger drops in saturation. Treat the patient and trajectory rather than waiting for this threshold.
Poor perfusion, Hypotension, Hypothermia, Motion, Inaccurate at low SpO₂ levels [14]
Why these limitations exist: Pulse oximetry works by detecting the pulsatile component of arterial blood flow and measuring the ratio of absorption of red (660 nm) and infrared (940 nm) light. When there is poor pulsatile flow (hypotension, hypothermia, vasoconstriction), the device cannot distinguish arterial from venous blood. Motion creates artefactual pulsations. At very low SpO₂ levels, the calibration algorithms become unreliable because they were derived from volunteer studies where desaturation below ~75% was ethically impossible.
Other limitations not on slides but worth knowing:
- Carbon monoxide poisoning → falsely high SpO₂ (carboxyhaemoglobin absorbs at same wavelength as oxyhaemoglobin)
- Methaemoglobinaemia → SpO₂ trends toward 85% regardless of true saturation
- Nail polish (dark colours) → may interfere
- Anaemia → SpO₂ may be normal despite inadequate O₂ delivery
Hypoventilation, Atelectasis, Lobar/Segmental Collapse, Aspiration, Pulmonary Oedema, Pneumothorax, Bronchospasm [15]
| Cause | Mechanism | Clinical Clue |
|---|---|---|
| Atelectasis | Small airway closure → microatelectasis → V/Q mismatch → shunt | Most common cause of post-op hypoxaemia; worse in obese, upper abdominal surgery, prolonged surgery |
| Lobar/Segmental Collapse | Mucus plugging or endobronchial intubation → complete collapse | Sudden desaturation, reduced breath sounds, tracheal deviation toward collapsed side |
| Aspiration | Gastric contents in airways → chemical pneumonitis ± bacterial pneumonia | History of vomiting on emergence, bilateral crackles, rapid deterioration |
| Pulmonary oedema | Fluid overload, cardiogenic (MI, HF), negative-pressure (post-laryngospasm) | Pink frothy sputum, bilateral crackles, raised JVP, CXR: bat-wing opacities |
| Pneumothorax | Air in pleural space → lung collapse | Unilateral reduced breath sounds, hyperesonant percussion, subcutaneous emphysema; after central line insertion or thoracic/upper abdominal surgery |
| Bronchospasm | Airway smooth muscle constriction | Wheeze, prolonged expiration; triggered by cold air, ET tube irritation, drugs, aspiration, asthma/COPD |
Hypotension, Reduced cardiac output [16] Fever, Shivering [16]
Why does low cardiac output cause hypoxaemia? When cardiac output drops, blood spends more time in pulmonary capillaries (longer transit time should actually help), BUT more importantly, mixed venous oxygen tension drops (tissues extract more O₂), and when this desaturated blood passes through lung regions with V/Q mismatch, the resulting arterial hypoxaemia is worse.
Why does shivering/fever cause hypoxaemia? Both increase metabolic rate → increased O₂ consumption → if the cardiorespiratory system cannot increase O₂ delivery proportionally, hypoxaemia results. Shivering can increase O₂ consumption by 200-400%.
History & physical examination, Pulse oximetry, Arterial blood gas measurement, CXR, Bronchoscopy [17]
ABG is the gold standard for assessing oxygenation. It gives you:
- PaO₂ (true arterial oxygen tension)
- PaCO₂ (tells you if hypoventilation is contributing)
- pH and base excess (metabolic status)
- P/F ratio (PaO₂/FiO₂ — assesses severity of gas exchange impairment)
CXR — first-line imaging; can diagnose pneumothorax, pulmonary oedema, collapse, pleural effusion, aspiration.
Bronchoscopy — indicated if mucus plugging causing lobar collapse, suspected foreign body, massive haemoptysis.
ABC, Give oxygen, Find and treat underlying cause [18]
The lecture includes a slide on this [19] — this is a clinical scenario emphasising that aspiration is a real risk during the vulnerable period of emergence from anaesthesia, when protective laryngeal reflexes are partially restored but not fully intact. Management: lateral/recovery position, suction, high-flow O₂, be prepared for reintubation if aspiration occurs.
CXR finding in aspiration [2]: The lecture slide shows a frontal chest radiograph with patchy right lower-zone air-space opacity after vomiting during extubation. This is compatible with dependent aspiration injury, but it is not diagnostic by itself; the distribution depends on patient position, and early aspiration pneumonitis can have a normal radiograph. Interpret the image with the witnessed event, oxygenation and clinical trajectory.
C — Cardiovascular Problems
Hypotension, Hypertension, Arrhythmias [20]
Hypotension
Hypovolaemic, Cardiogenic, Distributive (Low systemic vascular resistance), Obstructive [21]
This is the classic four-category shock classification. Understanding it is essential because management differs fundamentally between types:
| Type | Mechanism | Heart Rate | JVP/CVP | Cardiac Output | SVR | Key Post-Op Causes |
|---|---|---|---|---|---|---|
| Hypovolaemic | Insufficient circulating volume | ↑ | ↓ | ↓ | ↑ | Dehydration: long fasting, fluid shift, fever, vomiting, diarrhoea; Blood loss [22] |
| Cardiogenic | Pump failure | ↑ | ↑ | ↓ | ↑ | Myocardial ischaemia/infarction, Arrhythmia, Ventricular dysfunction, Valvular pathology [23] |
| Distributive | Pathological vasodilation | ↑ | ↓/N | ↑ (initially) | ↓ | Drugs (anaesthetic, anti-hypertensive), Regional anaesthesia (EA, high spinal), Sepsis, Anaphylaxis [24] |
| Obstructive | Mechanical obstruction to cardiac filling/output | ↑ | ↑ | ↓ | ↑ | Pneumothorax, Cardiac tamponade, Pulmonary embolism, Fat/air/amniotic fluid embolism [25] |
High Yield: Hypovolaemia Signs
The slide lists tachycardia, reduced urine output and CVP assessment as clues to hypovolaemia [22]. These findings are non-specific, and a single static CVP value does not establish volume depletion or predict fluid responsiveness. Look for bleeding, capillary refill and peripheral temperature; review fluid balance and lactate; and use response to passive leg raise, a carefully monitored bolus, or bedside echocardiography when appropriate [58].
Common Exam Trap: Regional Anaesthesia Causing Hypotension
Epidural anaesthesia (EA) and high spinal cause distributive shock via sympathetic blockade → vasodilation + venodilation → reduced preload and SVR. This is NOT hypovolaemia even though the patient looks "underfilled." Treatment: fluid loading + vasopressors (phenylephrine/ephedrine). A high spinal can also block cardiac sympathetic fibres (T1-T4) causing bradycardia — treat with atropine.
Reliable BP monitor [26] Organ perfusion: Brain — consciousness; Kidney — urine output; Heart — ischaemia [26] Central venous pressure (CVP), A-line, echocardiogram [26]
Why focus on organ perfusion rather than just a number? Blood pressure is just a surrogate for tissue perfusion. A patient with chronic hypertension may have inadequate organ perfusion at a BP that would be "normal" for someone else. Conversely, a fit young patient may tolerate a MAP of 55 without organ damage.
Monitoring nuance: CVP can be useful for trends and for recognising some obstructive/right-heart patterns, but it should not be used alone as a measure of circulating volume. Confirm a surprising non-invasive BP with cuff size/position and repeat measurement; use an arterial line when continuous beat-to-beat data will change management.
Arterial line (A-line): Provides continuous, beat-to-beat BP monitoring and allows repeated arterial blood sampling. Indications: haemodynamic instability, need for frequent ABGs, intra-operative major surgery [27].
Example arterial line monitor display [2]: A bedside monitor showing ECG (HR 155 bpm), plethysmography (SpO₂ 96%), and arterial blood pressure waveform (ABP 82/40 mmHg) — illustrating a tachycardic, hypotensive patient requiring urgent assessment and intervention despite an apparently adequate SpO₂.
ABC, ECG and tight BP monitoring, Fluid resuscitation, Vasopressors/inotropes, Find and treat underlying cause [28]
Fluid resuscitation is indicated only when hypovolaemia or fluid responsiveness is plausible. For an adult who needs crystalloid resuscitation, NICE advises a 500 mL bolus over less than 15 minutes, followed by immediate reassessment of ABCDE, perfusion and the risk of overload [58]. A smaller aliquot may be appropriate in frailty, cardiac/renal impairment or when diagnostic uncertainty is high. In haemorrhage, activate local major-haemorrhage/source-control pathways and use blood components rather than repeatedly substituting crystalloid [29].
Vasopressors/inotropes — chosen by shock type:
- Hypovolaemic: control the loss and replace volume; vasopressors may be a bridge, not a substitute for haemostasis
- Cardiogenic: inotropes (dobutamine) if adequate filling; vasopressors if severely hypotensive [30]
- Distributive (septic): give crystalloid with frequent reassessment and start noradrenaline when hypotension persists or fluids are unlikely to help [31]
- Obstructive: treat the obstruction (needle decompression for tension pneumothorax, pericardiocentesis for tamponade, thrombolysis/embolectomy for massive PE)
Hypertension
Systolic > 180 mmHg, diastolic > 100 mmHg [32] 20% more than baseline [32] Why is treatment required? [32]
These are lecture thresholds for concern, not an instruction to lower every postoperative reading immediately. Repeat the measurement, compare with baseline and determine whether there is acute target-organ injury. The presence of encephalopathy, myocardial ischaemia, pulmonary oedema, aortic syndrome or acute kidney injury makes this a hypertensive emergency requiring monitored, diagnosis-specific treatment; otherwise correct triggers such as pain, agitation, urinary retention, hypoxaemia or hypercapnia first.
Why treat post-operative hypertension?
- Risk of surgical site bleeding (suture line disruption)
- Risk of myocardial ischaemia/infarction (increased afterload → increased myocardial O₂ demand)
- Risk of stroke (especially in patients with cerebrovascular disease)
- Risk of end-organ damage (hypertensive encephalopathy, acute kidney injury)
Pain, Discomfort (e.g. Foley, full bladder, confusion), Hypoxia/hypercapnia [33] Iatrogenic, Metabolic: thyroid storm, malignant hyperthermia [33] Raised intracranial pressure, Pre-existing hypertension [33]
Clinical Pearl
Pain is the most common cause of post-operative hypertension. Before reaching for anti-hypertensives, always ask: Is the patient in pain? Do they have a full bladder? Are they hypoxic? Treating the underlying cause often resolves the hypertension without additional drugs.
Malignant hyperthermia is a rare but life-threatening complication triggered by volatile anaesthetics (sevoflurane, desflurane, isoflurane) and suxamethonium in genetically susceptible individuals (RYR1 mutation). Features: rapidly rising temperature, rigidity, tachycardia, hypertension, metabolic acidosis, rhabdomyolysis. Treatment: dantrolene (the specific antidote), stop triggering agent, active cooling.
Cushing reflex (raised ICP): hypertension + bradycardia + irregular respirations — consider post-neurosurgery or head injury patients.
ABC, Exclude and treat pain, Exclude other discomfort (e.g. Foley, bowel distention), Rule out sinister causes, Drug therapy: e.g. beta blockers, GTN [34]
| Drug | Mechanism | When to Use |
|---|---|---|
| Labetalol | Combined α + β blocker | Most post-op hypertension; good first-line |
| GTN (nitroglycerin) | Venodilator > arteriolar dilator | When myocardial ischaemia suspected |
| Hydralazine | Direct arteriolar vasodilator | Safe in pregnancy; used in some centres |
| Esmolol | Ultra-short acting β₁ blocker | Precise control needed; wears off in minutes |
| Nicardipine | Calcium channel blocker | Alternative to labetalol |
Causes: Hypoxia/hypercapnia, Electrolyte/acid-base disturbances, Myocardial ischaemia, Fever/hypothermia, Pre-existing heart disease, Pain & anxiety, Endocrine disorders [35]
The key teaching point here is that post-operative arrhythmias are usually secondary to a reversible cause. The approach is to find and fix that cause, not just treat the rhythm.
The "H's and T's" mnemonic for reversible causes overlaps heavily with this list:
- Hypoxia, Hypovolaemia, Hypo/hyperkalaemia, Hypothermia, Hydrogen ion (acidosis)
- Tension pneumothorax, Tamponade, Toxins, Thrombosis (coronary/pulmonary)
Electrolyte disturbances are particularly important post-operatively:
- Hypokalaemia (from fluid shifts, diuretics, metabolic alkalosis) → U waves, ST depression, risk of VT/VF
- Hyperkalaemia (from tissue damage, renal dysfunction, transfusion) → peaked T waves, wide QRS, risk of VF/asystole
- Hypomagnesaemia (often accompanies hypokalaemia) → prolongs QT, risk of torsades de pointes
Post-Operative Delirium
Acutely altered and fluctuating mental status with inattention and an altered level of consciousness [36] Increased risk of poor outcome [36] Elderly, cognitive impairment, vascular surgery, hip fracture surgery [36]
Why is post-operative delirium important?
- Associated with increased mortality, prolonged hospital stay, and long-term cognitive decline
- Up to 50% of elderly surgical patients develop delirium
- It is often missed, especially the hypoactive subtype (quiet, withdrawn, mistaken for depression or "just tired")
Causes of Post-Operative Delirium
Pain or other discomfort, Hypoxia, Hypotension, Cerebral hypoxia, Cerebral injury, Electrolyte or endocrine imbalances, Drugs: ketamine, drug withdrawal, anticholinergic [37]
| Category | Specific Causes |
|---|---|
| Metabolic | Hypoxia, hypercarbia, hypo/hyperglycaemia, hyponatraemia, uraemia, hepatic encephalopathy |
| Drugs | Opioids, benzodiazepines, ketamine, anticholinergics, drug withdrawal (alcohol, benzodiazepines) |
| Infectious | Urinary tract infection, pneumonia, wound infection, sepsis |
| Neurological | Stroke, post-ictal state, raised ICP |
| Other | Pain, urinary retention, constipation, sleep deprivation |
Evaluation and Management
ABC, history, Neurological exam: Focal signs, GCS [38] Electrolytes, sugar, temperature [38] CT brain [38] Consider sedation if treatable cause excluded; anti-psychotics [38] — historical slide wording; see the current-practice note below.
Management algorithm:
- ABC — always first
- Exclude and treat reversible causes — this is the PRIORITY
- Check glucose, electrolytes, calcium, renal function, LFTs
- Check urine output (retention?), temperature (infection?)
- Pulse oximetry (hypoxia?)
- Review drug chart (new drugs? withdrawal?)
- CT brain — if focal neurological signs, new headache, history of falls/head trauma, or anticoagulated patient
- Non-pharmacological management — reorientation, familiar faces, night-day cycle, glasses/hearing aids, avoid restraints
- Medication is not routine delirium treatment. If the patient is distressed or poses a risk to self/others, use verbal and non-verbal de-escalation first. Only if this is ineffective or inappropriate should short-term haloperidol be considered at the lowest appropriate dose, with particular caution about cardiac/neurological adverse effects and avoidance in Parkinson disease or dementia with Lewy bodies [59]. Benzodiazepines are generally avoided except for a specific indication such as alcohol/benzodiazepine withdrawal.
Hypothermia
Core temperature < 35°C [39] — the lecture's older threshold. Increased heat loss & reduced heat generation during general anaesthesia [39] Risk factors: Paediatric & elderly patients, Exposure, Administration of cold fluids e.g. Blood products [39]
For adult perioperative care, current NICE guidance defines inadvertent hypothermia as core temperature < 36.0°C, not < 35°C [60]. In recovery, measure temperature on arrival and every 15 minutes; if it is below 36°C, use active forced-air warming and do not arrange ward transfer until it is at least 36°C [60].
Why does GA cause hypothermia?
- Redistribution (most important in first hour): Anaesthetic-induced vasodilation redistributes warm core blood to cooler periphery → rapid core temperature drop of ~1.5°C
- Reduced metabolic heat production: Anaesthesia reduces basal metabolic rate by ~20%; muscle relaxants abolish shivering
- Increased heat loss: Operating room is cold (~18–21°C); surgical exposure of body cavities; cold irrigation fluids
- Impaired thermoregulation: GA raises the threshold for vasoconstriction and shivering by 2–4°C
Consequences of Hypothermia
CVS: myocardial ischaemia, arrhythmias [40] Coagulopathy [40] Left shift O₂-Hb dissociation curve [40] Shivering → increased oxygen consumption [40] Decreased drug metabolism → prolonged drug effect [40] ↑ wound infection [40]
| Consequence | Mechanism | Clinical Impact |
|---|---|---|
| Myocardial ischaemia | Shivering → ↑ O₂ demand + ↑ catecholamines → coronary vasoconstriction | Post-op MI, especially in patients with IHD |
| Arrhythmias | Direct effect on cardiac conduction system | AF, VF (severe hypothermia < 30°C) |
| Coagulopathy | Impaired platelet function + impaired coagulation enzyme activity | ↑ Bleeding, ↑ need for transfusion |
| Left-shifted O₂-Hb curve | Haemoglobin holds onto O₂ more tightly → less O₂ delivered to tissues | Tissue hypoxia despite "normal" SpO₂ |
| ↑ O₂ consumption (shivering) | Skeletal muscle contraction generates heat but consumes 200–400% more O₂ | Can precipitate myocardial ischaemia and respiratory failure |
| Prolonged drug effect | Hepatic enzyme activity is temperature-dependent | Delayed emergence, prolonged muscle relaxation |
| ↑ Wound infection | Vasoconstriction → reduced wound perfusion → reduced delivery of O₂ and immune cells | 3× increased risk of surgical site infection per 1.9°C drop |
High Yield: Hypothermia and Wound Infection
Even mild hypothermia (1–2°C below normal) significantly increases surgical site infection rates. This is why perioperative warming (forced-air warming blankets, warmed IV fluids) is standard of care and a quality metric in many hospitals.
Prevention of hypothermia:
- Forced air warming blankets (most effective)
- Warm IV fluids and blood products
- Increase operating room temperature
- Minimize exposure
- Humidified warm inspired gases
Post-Operative Pain
Unpleasant, poor patient satisfaction [41] Prolonged recovery and hospital stay [41] Chronic post-surgical pain [41] Morbidity: Respiratory: pneumonia, atelectasis; CVS: myocardial, cerebral ischaemia [41]
Pain assessment visual [2]: The slide combines a 0–10 numeric scale with progressively distressed faces: 0 at a smiling face, 4 near the neutral midpoint and 10 at a crying face. Treat these as communication aids rather than objective measurements. Use the same validated tool serially, ask about pain at rest and on movement/coughing, and reassess function and adverse effects after treatment.
Why is treating post-operative pain so important beyond comfort?
Uncontrolled pain triggers a stress response: catecholamine release → tachycardia, hypertension, ↑ myocardial O₂ demand → risk of MI. It also causes splinting → reduced deep breathing and coughing → atelectasis → pneumonia. Additionally, immobility from pain → DVT/PE risk. Chronic pain can develop through central sensitisation if acute pain is poorly managed ("wind-up" phenomenon).
Multimodal approach [42] Systemic drugs: Opioids (PCA, IV bolus), Non-opioids: paracetamol, NSAID, ketamine [42] Regional anaesthesia/analgesia: Epidural, Peripheral nerve blocks/catheters [42] Procedure-specific analgesia [42]
Key Concept: Multimodal Analgesia
Multimodal analgesia means combining drugs and techniques with different mechanisms of action to provide superior pain relief with fewer side effects of any single agent. For example: paracetamol (central COX inhibition) + NSAID (peripheral COX inhibition) + opioid (μ-receptor activation) + regional block (nerve conduction blockade) = better pain control with lower opioid requirement.
| Modality | Agent/Technique | Mechanism | Notes |
|---|---|---|---|
| Opioid - PCA | Morphine, fentanyl | μ-receptor agonist → ↓ pain transmission | Patient self-administers small boluses; a lockout reduces but does not eliminate respiratory-depression risk, so monitoring remains essential |
| Opioid - IV bolus | Morphine 1-2 mg titrated | Same | Nurse-administered; risk of oversedation if not monitored |
| Paracetamol | IV/PO | Central analgesic mechanisms | Check all combination products and use the local weight-, frailty- and liver-risk-adjusted maximum; overdose can cause severe hepatotoxicity |
| NSAIDs | Ketorolac, diclofenac | COX-1/2 inhibition → ↓ prostaglandins | Anti-inflammatory + analgesic; beware: renal impairment, GI bleeding, impaired platelet function, asthma exacerbation |
| Ketamine | Low-dose IV infusion | NMDA receptor antagonist | Prevents central sensitisation; opioid-sparing; useful in opioid-tolerant patients |
| Epidural | Local anaesthetic ± opioid | Blocks nerve roots in epidural space | Excellent for thoracic/abdominal surgery; requires monitoring for complications |
| Peripheral nerve block | Local anaesthetic via catheter | Blocks specific peripheral nerves | Procedure-specific; e.g., femoral nerve block for knee surgery, TAP block for abdominal surgery |
General — allergy [43] Opioids: respiratory depression, sedation, dizziness, GI: N+V, constipation [43] Epidural: hypotension, respiratory depression, infection, neurological impairment [43]
Epidural complications in detail:
- Hypotension: Sympathetic blockade → vasodilation → ↓ preload and SVR. More pronounced if block extends above T4 (cardiac sympathetic fibres). Rx: fluid bolus, vasopressors (ephedrine/phenylephrine).
- Respiratory depression: If epidural opioid migrates cephalad. Delayed onset (6-12 hours with hydrophilic opioids like morphine). Rx: naloxone, may need intubation.
- Infection: Epidural abscess — rare but devastating. Signs: back pain, fever, progressive neurological deficit. Emergency MRI → surgical decompression.
- Neurological impairment: Epidural haematoma (risk increased with anticoagulation) → new/progressive weakness, numbness, severe back pain or sphincter dysfunction. Stop the infusion, escalate urgently for MRI and specialist decompression; delay risks permanent deficit.
Post-Operative Nausea and Vomiting (PONV)
Common [44] Patient risk factors: Female, history of PONV/motion sickness, non-smoker, post-op use of opioids [44] Anaesthetic risk factors: duration, N₂O, etomidate [44] Surgical risk factors: middle ear surgery, laparoscopic [44]
The Apfel Score is a validated risk scoring system for PONV [45]:
| Risk Factor | Points |
|---|---|
| Female sex | 1 |
| Non-smoker | 1 |
| History of PONV or motion sickness | 1 |
| Post-operative opioid use | 1 |
| Score | Risk of PONV |
|---|---|
| 0 | ~10% |
| 1 | ~20% |
| 2 | ~40% |
| 3 | ~60% |
| 4 | ~80% |
Apfel score — historical slide table [2]:
| Risk Factors | PONV Incidence | Prophylaxis Strategy |
|---|---|---|
| 0 | ~10% | None |
| 1 | ~20% | 4 mg dexamethasone ± 2nd anti-emetic |
| 2 | ~40% | Avoid inhalation agents if possible + 4 mg dexamethasone ± 2nd anti-emetic |
| 3 | ~60% | Avoid inhalation agents if possible + 4 mg dexamethasone + another prophylactic anti-emetic (e.g. scopolamine patch) |
| 4 | ~80% | Avoid inhalation agents if possible + 4 mg dexamethasone + NK-1 receptor antagonist ± another prophylactic anti-emetic (e.g. scopolamine patch) |
The risk percentages and four predictors remain useful, but the drug-by-score table is an older protocol, not a universal contemporary prescription. The 2025 Fifth Consensus Guideline retains general multimodal prevention: use baseline-risk reduction (such as opioid-sparing analgesia and propofol-based TIVA where appropriate) and combination prophylaxis with different mechanisms; patients with 3 or more risk factors should receive at least two prophylactic agents [61]. Follow the local anaesthetic protocol for drug choice, timing, contraindications and dosing.
Rescue treatment: Review what prophylaxis was already given and use a different agent and/or pharmacological class. Routine redosing of the same class after failed prophylaxis offers no benefit; if more than 6 hours have elapsed and no alternative is available, repeat short-acting 5-HT₃ antagonist/butyrophenone dosing may be considered [61]. The slide's ondansetron 1 mg IV example should therefore not be memorised as a universal rescue dose.
How to interpret the predictors: Female sex, non-smoking status and a history of PONV/motion sickness are reproducible epidemiological predictors; they should not be reduced to unproven single-receptor explanations. Postoperative opioids are both a predictor and a modifiable driver through central emetic pathways and delayed gastric emptying.
Anaesthetic factors:
- N₂O (nitrous oxide): Increases middle ear pressure → vestibular stimulation; also may diffuse into bowel causing distension
- Etomidate: Strong emetogenic induction agent
- Duration of surgery: More anaesthetic exposure → more risk
Surgical factors:
- Middle ear surgery: Direct vestibular stimulation
- Laparoscopic surgery: Peritoneal CO₂ insufflation → diaphragmatic irritation; also CO₂ absorption → mild hypercarbia
ABC, Check BP, heart rate, Rule out surgical/neurological problems [46] Ensure adequate hydration, correct electrolyte abnormality [46] Treat pain and anxiety [46] Drug therapy [46]
Important Clinical Point
Before just giving anti-emetics, always rule out sinister causes of post-operative vomiting: raised intracranial pressure (Cushing reflex), intestinal obstruction (distended abdomen, absent bowel sounds), bleeding causing hypotension and vagal stimulation, hypoglycaemia.
Serotonin antagonists: ondansetron, tropisetron [47] Steroid: Dexamethasone [47] Dopamine antagonists: droperidol, metoclopramide [47] Antihistamine: Cyclizine [47] Anticholinergic: scopolamine, hyoscine hydrobromide [47] Others: propofol, benzodiazepine, clonidine [47]
The final "others" line reflects the lecture list, not equal first-line status. The 2025 consensus specifically advises against using benzodiazepines solely for PONV prophylaxis because of sedation risk [61].
| Class | Drug | Receptor | Site of Action | Notes |
|---|---|---|---|---|
| 5-HT₃ antagonist | Ondansetron 4 mg IV | 5-HT₃ | CTZ + vagal afferents | First-line; well-tolerated; may cause headache, QT prolongation |
| Steroid | Dexamethasone 4-8 mg IV | Unknown (anti-inflammatory?) | Central? | Given at induction for prophylaxis; onset delayed ~2 hrs; perineal pruritus with rapid IV injection |
| Dopamine antagonist | Metoclopramide 10 mg IV | D₂ | CTZ + prokinetic (GI) | Also promotes gastric emptying; risk of dystonic reactions (especially in young women) |
| Dopamine antagonist | Droperidol 0.625-1.25 mg IV | D₂ | CTZ | Very effective; risk of sedation, QT prolongation |
| Antihistamine | Cyclizine 50 mg IV/IM | H₁ | Vomiting centre | Sedating; anticholinergic side effects |
| Anticholinergic | Hyoscine (scopolamine) | mACh | Vomiting centre + vestibular | Transdermal patch for prophylaxis; dry mouth, blurred vision, urinary retention |
| Other | Propofol | Multiple | Central | Sub-anaesthetic doses have anti-emetic effect; TIVA (total IV anaesthesia) has lower PONV than volatile anaesthesia |
Multimodal anti-emetic approach: For high-risk patients (Apfel ≥ 3), use at least two prophylactic interventions with different mechanisms, plus baseline-risk reduction; follow local guidance for the exact regimen [61].
From GC 001 [48]:
Disposition: Where do the patient go from here? Home, Ward, High Dependency Unit, Intensive Care Unit. If you are not sure, ask the anaesthesiologist.
| Disposition | Criteria |
|---|---|
| Home (day surgery) | Stable vitals, pain controlled, no PONV, can drink, responsible adult escort, lives close to hospital |
| Ward | Routine post-op; stable ABC; can monitor on ward |
| High Dependency Unit (HDU) | Needs closer monitoring than ward (e.g., epidural, PCA, single organ support) |
| Intensive Care Unit (ICU) | Multi-organ support, ventilatory support, complex surgery, significant comorbidities, intra-op complications |
Integration with Related Material
Good pre-operative assessment identifies risk factors (ASA grade, cardiac/respiratory disease, medications) that predict post-operative complications. A patient identified as high-risk pre-operatively (e.g., ASA III-IV) should have appropriate post-operative monitoring level (HDU/ICU) planned in advance.
Surgery triggers a catabolic stress response (↑ cortisol, catecholamines, GH, ADH → sodium/water retention, potassium loss, protein catabolism, hyperglycaemia). This explains why post-operative patients develop:
- Sodium/water retention and transient oliguria can occur, but do not label postoperative oliguria "normal" without assessment. Recheck perfusion, bleeding, obstruction/catheter patency, renal injury and fluid balance; avoid both reflex fluid loading and missed shock.
- Hyperglycaemia (even in non-diabetics)
- Increased O₂ consumption The 2024 MCQ Q21 tested understanding that post-operative weight loss is primarily due to "mobilisation of amino acid and fatty acid from muscle and fat" — the correct answer reflecting the catabolic stress response [50].
Hypothermia → ↑ wound infection risk. Also, prophylactic antibiotics should be given within 60 minutes before skin incision for clean-contaminated or prosthetic procedures — this is a pre-operative step but its impact is measured post-operatively.
Malnourished patients have impaired wound healing, immune function, and respiratory muscle strength. Perioperative nutritional support (oral → enteral → parenteral) reduces major complications by 21% [51].
Post-operative bleeding requiring transfusion must consider: hypothermia-induced coagulopathy, dilutional coagulopathy after massive fluid resuscitation, and transfusion reactions as additional post-op complications.
High Yield Summary
-
Post-operative management centres on a systematic ABC approach
-
A — Airway
- Most common obstruction = tongue fall-back. Manage with triple airway manoeuvre → O₂ → airway adjuncts → intubation. Do not wait for SpO₂ to drop.
-
B — Breathing
- Hypoventilation (residual drugs, pain, muscle relaxants) and hypoxaemia (atelectasis, aspiration, PE, pneumothorax).
- Give O₂, find cause, consider antidotes (naloxone, flumazenil), reverse relaxants.
- Pain causes 60% ↓ vital capacity after upper abdominal surgery.
-
C — Circulation
- Classify hypotension by shock type (hypovolaemic most common). Hypertension — exclude pain/discomfort first. Arrhythmias — usually secondary to reversible cause.
-
Neurological
- Delirium is common in older people; treat reversible causes and use reorientation/de-escalation first. Consider short-term haloperidol only for distress or risk when de-escalation fails, with contraindications and adverse effects checked.
-
Temperature
- Inadvertent perioperative hypothermia (core temperature < 36°C) → coagulopathy, arrhythmias, ↑ wound infection, ↑ O₂ consumption from shivering. Prevent and treat with active warming.
-
Pain
- Multimodal approach (opioids + non-opioids + regional). Untreated pain → respiratory complications, ischaemia, chronic pain.
-
PONV
- Use Apfel score. Multimodal anti-emetics. Always exclude sinister causes before treating.
-
Golden rule: Treat the patient, not the monitors. Start supportive treatment while working up the diagnosis.
Active Recall - Post-operative Management
[1] Past papers: 2023 Fourth Summative Minicase.pdf (Case 3, Section 4, Q11-14) [2] Lecture slides: GC 006 - The patient is very ill after the operation - Post-operative management.pdf (p2) [3] Lecture slides: GC 006 (p3) [4] Lecture slides: GC 006 (p7) [5] Lecture slides: GC 006 (p8) [6] Lecture slides: GC 006 (p9) [7] Lecture slides: GC 006 (p10) [8] Lecture slides: GC 006 (p11) [9] Lecture slides: GC 006 (p12) [10] Lecture slides: GC 006 (p13) [11] Lecture slides: GC 006 (p16) [12] Lecture slides: GC 006 (p17) [13] Lecture slides: GC 006 (p18) [14] Lecture slides: GC 006 (p19) [15] Lecture slides: GC 006 (p20) [16] Lecture slides: GC 006 (p21) [17] Lecture slides: GC 006 (p23) [18] Lecture slides: GC 006 (p22) [19] Lecture slides: GC 006 (p24) [20] Lecture slides: GC 006 (p25) [21] Lecture slides: GC 006 (p26) [22] Lecture slides: GC 006 (p27) [23] Lecture slides: GC 006 (p29) [24] Lecture slides: GC 006 (p28) [25] Lecture slides: GC 006 (p30) [26] Lecture slides: GC 006 (p31) [27] Lecture slides: GC 006 (p32) [28] Lecture slides: GC 006 (p33) [29] Senior notes: Ryan Ho Critical Care.pdf (p21) [30] Senior notes: Ryan Ho Critical Care.pdf (p22) [31] Senior notes: Ryan Ho Critical Care.pdf (p22) [32] Lecture slides: GC 006 (p34) [33] Lecture slides: GC 006 (p35) [34] Lecture slides: GC 006 (p36) [35] Lecture slides: GC 006 (p37) [36] Lecture slides: GC 006 (p38) [37] Lecture slides: GC 006 (p39) [38] Lecture slides: GC 006 (p40) [39] Lecture slides: GC 006 (p41) [40] Lecture slides: GC 006 (p42) [41] Lecture slides: GC 006 (p44) [42] Lecture slides: GC 006 (p45) [43] Lecture slides: GC 006 (p46) [44] Lecture slides: GC 006 (p47) [45] Lecture slides: GC 006 (p48) [46] Lecture slides: GC 006 (p49) [47] Lecture slides: GC 006 (p50) [48] Lecture slides: GC 001 - How would you anaesthetise me - Pharmacology of anaesthetic drugs.pdf (p49) [49] Lecture slides: GC 006 (p51) [50] Past papers: 2024 Fourth Summative MCQ.pdf (Q21) [51] Senior notes: Ryan Ho Fluids and Nutrition.pdf (p8) [56] British Thoracic Society. Guideline for oxygen use in adults in healthcare and emergency settings (2017): https://www.brit-thoracic.org.uk/document-library/guidelines/emergency-oxygen/bts-guideline-for-oxygen-use-in-adults-in-healthcare-and-emergency-settings/ [57] American Society of Anesthesiologists Task Force. 2023 Practice Guidelines for Monitoring and Antagonism of Neuromuscular Blockade: https://pubmed.ncbi.nlm.nih.gov/36520073/ [58] NICE CG174. Intravenous fluid therapy in adults in hospital — recommendations: https://www.nice.org.uk/guidance/cg174/chapter/recommendations [59] NICE CG103. Delirium: prevention, diagnosis and management — recommendations: https://www.nice.org.uk/guidance/cg103/chapter/Recommendations [60] NICE CG65. Hypothermia: prevention and management in adults having surgery: https://www.nice.org.uk/guidance/CG65 [61] Gan TJ, et al. Fifth Consensus Guidelines for the Management of Postoperative Nausea and Vomiting (2025): https://pubmed.ncbi.nlm.nih.gov/41237407/ [62] NICE NG158. Venous thromboembolic diseases: diagnosis, management and thrombophilia testing — recommendations: https://www.nice.org.uk/guidance/ng158/chapter/Recommendations
GC005 The Patient Is Critically Ill - Intensive Care Medicine; Unstable Vital Organ Function
Unstable vital organ function refers to the acute failure or impending failure of one or more vital organ systems—such as cardiovascular, respiratory, neurological, or renal—requiring immediate monitoring and intervention in an intensive care setting to prevent irreversible damage or death.
GC012 Abnormal Lung Shadow On Chest Radiograph CXR, CT
An incidental or symptomatic radiographic finding on chest X-ray or CT scan representing a localized or diffuse opacity that requires systematic evaluation to determine its etiology, which may include infection, malignancy, inflammation, or vascular abnormality.