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celiac plexus block from anesthesia standard source

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celiac plexus block anesthesia technique contraindications complications standard reference

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Celiac plexus block

Standard anesthesia sources:
  • Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 2066
  • Barash, Cullen, and Stoelting’s Clinical Anesthesia, 9e, pp. 4767-4768

Indication

Used for visceral upper abdominal pain, especially cancer-related pain such as pancreatic malignancy. It may also be used diagnostically or therapeutically for selected nonmalignant upper abdominal visceral pain.
Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 2066.

Relevant anatomy

The celiac plexus is a group of sympathetic ganglia around the aorta near the origins of the celiac trunk and superior mesenteric artery, usually at T12-L1/L1. It receives sympathetic input through the greater, lesser, and least splanchnic nerves and supplies most abdominal viscera, except the left colon and pelvic organs.
Barash, Cullen, and Stoelting’s Clinical Anesthesia, 9e, p. 4767.

Block versus neurolysis

  • Celiac plexus block: local anesthetic, sometimes with steroid, aiming for temporary analgesia or diagnostic prediction of response.
  • Celiac plexus neurolysis: chemical destruction of the plexus, usually for persistent malignant pain. Neurolytic agents described include alcohol or phenol.
    Barash, Cullen, and Stoelting’s Clinical Anesthesia, 9e, pp. 4767-4768.

Approaches and imaging

Approaches include:
  • Posterior retrocrural
  • Posterior anterocrural or para-aortic
  • Posterior transaortic
  • Anterior para-aortic
  • Splanchnic nerve block as an alternative
Fluoroscopy, CT, or ultrasound can be used to guide needle placement. A posterior fluoroscopic approach typically targets the L1 vertebral level; CT guidance permits placement anterolateral to the aorta between the celiac and superior mesenteric arteries.
Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 2066.

Key procedural principles

  1. Establish monitoring, IV access, and resuscitation readiness.
  2. Use image guidance and contrast confirmation before injectate.
  3. Avoid intravascular injection through careful aspiration and incremental injection.
  4. Anticipate sympathetic blockade, provide hydration as appropriate, and monitor for orthostatic hypotension after the procedure.
  5. In neurolysis, a preceding local-anesthetic diagnostic block may help predict benefit.
    Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 2066; Barash, Cullen, and Stoelting’s Clinical Anesthesia, 9e, p. 4767.

Contraindications or major precautions

  • Patient refusal or inability to cooperate
  • Local or intra-abdominal infection
  • Uncorrected coagulopathy or significant thrombocytopenia
  • Relevant distorted anatomy or inability to safely identify structures
  • Bowel obstruction is a concern, particularly for neurolysis, because sympathectomy can increase gut motility and diarrhea
  • Avoid a transaortic approach with abdominal aortic aneurysm or marked aortic calcification. Review of contraindications

Complications

Common
  • Orthostatic/postural hypotension due to splanchnic sympathectomy and vasodilation
  • Back pain
  • Diarrhea due to relatively unopposed parasympathetic activity
Less common but serious
  • Intravascular injection and systemic local-anesthetic toxicity
  • Retroperitoneal hemorrhage or hematoma
  • Pneumothorax or reactive pleurisy
  • Injury to kidney, pancreas, or other viscera
  • Aortic injury/dissection
  • Transient motor weakness or sensory symptoms
  • Spinal cord ischemia, paraplegia, rarely
The feared neurologic complication is thought to result from vascular injury or vasospasm involving segmental vessels that supply the spinal cord, direct neural injury, or unintended spread to neural structures.
Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 2066; Barash, Cullen, and Stoelting’s Clinical Anesthesia, 9e, p. 4768.

One-line viva answer

Celiac plexus block is an image-guided sympathetic visceral block at T12-L1/L1 for refractory upper abdominal visceral pain, particularly pancreatic cancer pain; its main adverse effects are transient hypotension, diarrhea, and back pain, while bleeding, visceral injury, and spinal cord ischemia/paraplegia are rare serious complications.
Recent systematic reviews in 2025 evaluated EUS-guided celiac plexus block for chronic pancreatitis pain (PMIDs 40813224 and 40168184); these address efficacy rather than replacing the core anesthetic anatomy and safety principles above.

propofol and ketamine drug for dnb viva guve full detail

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For a DNB viva, propofol and ketamine should be prepared under these headings:
  1. Identity and formulation
    • Drug class, chemical nature, preparation, storage, compatibility.
  2. Mechanism of action
    • Receptor actions and resulting CNS effects.
  3. Pharmacokinetics
    • Onset, redistribution, elimination half-life, metabolism, context-sensitive decrement time.
  4. Clinical effects
    • CNS, respiratory, cardiovascular, cerebral, ocular, uterine, and endocrine effects.
  5. Dose and uses
    • Induction, maintenance/TIVA, sedation, procedural use, analgesic role, pediatric and emergency use.
  6. Adverse effects and contraindications
    • Common, important, rare, and exam-favorite complications.
  7. Special situations
    • Shock, asthma, raised ICP, traumatic brain injury, pregnancy, elderly, pediatric patients, hepatic/renal disease.
  8. Comparison: propofol vs ketamine
    • Hemodynamics, respiration, airway reflexes, analgesia, emergence, PONV, neurophysiology, and use in day-care anesthesia.
High-yield overview:
Propofol is a rapid-onset IV hypnotic acting predominantly through GABA-A receptor facilitation. It produces hypnosis and amnesia but no analgesia. Its main limitations are dose-dependent hypotension, respiratory depression/apnea, and pain on injection. Its strengths are rapid clear-headed recovery, antiemetic action, reduced cerebral metabolic rate, cerebral blood flow, and intracranial pressure.
Ketamine is a dissociative anesthetic, primarily an NMDA receptor antagonist. It provides profound analgesia, amnesia, and anesthesia while generally preserving spontaneous ventilation and airway reflexes. It raises heart rate, blood pressure, cardiac output, and salivation through sympathomimetic effects, though this may not occur in catecholamine-depleted shock. Emergence phenomena, nausea/vomiting, hypersalivation, and transient increases in blood pressure are common viva points.
Which format do you want next?
  1. Propofol first
  2. Ketamine first
  3. Both as a detailed comparison table
  4. DNB viva questions and model answers

Give a full propofol DNB viva answer

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propofol prescribing information adverse reactions propofol infusion syndrome dose induction anesthesia

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Propofol: DNB Anesthesia Viva Answer

Opening answer

Propofol is a short-acting intravenous sedative-hypnotic agent, chemically 2,6-diisopropylphenol. It produces rapid, smooth induction and recovery from anesthesia, but has no analgesic effect. It is used for induction and maintenance of general anesthesia, total intravenous anesthesia (TIVA), procedural and monitored anesthesia care sedation, and sedation of mechanically ventilated adults in the ICU.
Its major disadvantages are dose-dependent hypotension, apnea/respiratory depression, and pain on injection.
Miller’s Anesthesia, 10e, p. 2457; Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 338.

1. Preparation and formulation

  • Chemical class: substituted alkylphenol
  • Chemical name: 2,6-diisopropylphenol
  • Molecular formula: C12H18O
  • Highly lipid soluble and virtually insoluble in water.
  • It is supplied as a milky white oil-in-water lipid emulsion.
  • Commonly available formulation: 1% propofol = 10 mg/mL.
  • The emulsion contains soybean oil, egg phospholipid or lecithin, glycerol, and pH-adjusting agent. Some formulations contain EDTA or metabisulfite.

Viva point: Why is sterility important?

Propofol emulsion supports microbial growth. Strict aseptic handling is essential because contaminated preparations have caused sepsis and death. Follow the specific product's handling and discard instructions.
Miller’s Anesthesia, 10e, pp. 2457-2458; Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 338.

Egg and soy allergy

A history of egg allergy does not automatically contraindicate propofol. Most egg allergy is directed at egg-white proteins, whereas lecithin is derived from egg yolk. However, avoid propofol in a patient with a documented severe hypersensitivity reaction to propofol or a formulation component, and use clinical judgment in severe food allergy.
Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 338.

2. Mechanism of action

Propofol acts mainly by potentiating inhibitory neurotransmission at the GABA-A receptor.
  • It acts allosterically at GABA-A receptors.
  • It increases the effect of GABA-mediated chloride conductance.
  • Chloride influx hyperpolarizes the neuronal membrane and reduces neuronal excitability.
  • It also affects several other ion channels and receptors, but GABA-A receptor facilitation is the principal clinically relevant action.
  • Its effects are not reversed by flumazenil.
Viva line: Propofol produces hypnosis and amnesia, but not analgesia.
Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 338.

3. Pharmacokinetics

Administration

  • Given only intravenously for anesthetic purposes.
  • It can be given as a bolus, intermittent small boluses, continuous infusion, or target-controlled infusion where available.

Onset and duration

  • Onset of unconsciousness: approximately 30-45 seconds after IV induction dose.
  • Rapid awakening after a single bolus is due primarily to redistribution from the brain to muscle and fat.
  • Initial distribution half-life: approximately 2-8 minutes.
  • Clinical duration after a single induction dose: about 5-10 minutes.

Distribution

  • Highly lipid soluble.
  • Rapidly crosses the blood-brain barrier.
  • Highly protein bound.
  • Dose requirement is lower in elderly or frail patients because of altered distribution and increased sensitivity.

Metabolism and elimination

  • Rapid hepatic conjugation produces inactive metabolites.
  • Clearance exceeds hepatic blood flow, indicating important extrahepatic metabolism as well.
  • Metabolites are mainly excreted in urine.
  • Renal failure generally does not significantly alter clearance of parent propofol.
  • Recovery after infusion is usually rapid, though recovery becomes slower with prolonged, high-dose infusion because peripheral compartments become saturated.
Viva line: “Rapid recovery after a single dose is due to redistribution; rapid recovery after infusion is aided by high metabolic clearance, including extrahepatic metabolism.”
Morgan and Mikhail’s Clinical Anesthesiology, 7e, pp. 338-339.

4. Doses

All doses must be titrated to age, comorbidity, intravascular volume, premedication, and clinical response.
UseTypical adult dose
Induction of anesthesia, healthy adult2-2.5 mg/kg IV
Induction, elderly/debilitated/ASA III-IV1-1.5 mg/kg IV, slowly titrated
Cardiac-compromised patientOften 0.5-1.5 mg/kg, carefully titrated
Maintenance of GA/TIVA100-200 micrograms/kg/min
Sedation/MAC25-75 micrograms/kg/min, titrated
ICU sedation in ventilated adultsStart low, commonly 5-50 micrograms/kg/min; avoid prolonged high-dose infusion
Antiemetic useSmall subhypnotic dose or infusion may be used in selected settings
For healthy children aged 3-16 years, induction requirements are commonly 2.5-3.5 mg/kg IV. Pediatric dose requirements are higher than in adults.
Current product labeling recommends 2-2.5 mg/kg for induction in healthy adults and 100-200 micrograms/kg/min for maintenance, with lower dosing in older, debilitated, and higher ASA-status patients. Current prescribing information

5. Effects on organ systems

A. Central nervous system

  • Produces dose-dependent sedation, hypnosis, amnesia, and general anesthesia.
  • No analgesia. Therefore, an opioid, regional technique, or another analgesic is needed for painful surgery.
  • Decreases cerebral metabolic rate for oxygen consumption, cerebral blood flow, cerebral blood volume, and intracranial pressure.
  • Produces a dose-dependent decrease in EEG activity; high doses can cause burst suppression.
  • Has anticonvulsant properties and may be used in refractory status epilepticus.
  • Occasional excitatory movements, myoclonus, opisthotonus, or hiccups may occur during induction or emergence.
  • It decreases intraocular pressure.
  • It has antiemetic and antipruritic actions.

Propofol in raised ICP

Propofol is useful in neuroanesthesia because it lowers CMRO2, CBF, and ICP. However, hypotension may decrease cerebral perfusion pressure. Therefore, maintain mean arterial pressure and avoid hypovolemia.
Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 340; Miller’s Anesthesia, 10e, pp. 2470-2472.

B. Cardiovascular system

This is the most important negative effect in viva.
Propofol causes:
  • Decreased systemic vascular resistance
  • Reduced venous return and preload
  • Mild reduction in myocardial contractility
  • Impaired baroreceptor-mediated tachycardic response
Therefore, it may cause marked hypotension, especially in:
  • Hypovolemia
  • Sepsis
  • Hemorrhage
  • Elderly patients
  • Patients with impaired LV function
  • Patients receiving beta-blockers
  • Rapid injection or large dose
  • Concurrent opioids, benzodiazepines, or volatile anesthetics
Heart rate may remain unchanged or decrease. Rarely, severe bradycardia, asystole, or a vagally mediated Bezold-Jarisch reflex may occur.
Viva line: “Propofol decreases blood pressure mainly by reducing systemic vascular resistance, with contributions from reduced preload and myocardial depression.”
Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 339.

C. Respiratory system

Propofol is a potent respiratory depressant.
  • Induction dose commonly causes apnea.
  • It reduces tidal volume and respiratory rate.
  • It blunts ventilatory response to hypoxia and hypercapnia.
  • It reduces upper airway reflexes more than thiopentone.
  • This facilitates laryngeal mask airway insertion, endoscopy, and sometimes tracheal intubation without neuromuscular blockade.
  • However, loss of airway reflexes also increases risk of airway obstruction and aspiration in an inadequately fasted or deeply sedated patient.
  • It is associated with a lower incidence of wheeze than thiopentone or etomidate and is often a useful induction agent in asthma.
Viva line: “Propofol is bronchodilator-friendly but is not respiratory-safe. It can cause apnea even during procedural sedation.”
Morgan and Mikhail’s Clinical Anesthesiology, 7e, pp. 339-340.

D. Neuromuscular and uterine effects

  • It does not provide skeletal muscle relaxation.
  • It does not trigger malignant hyperthermia and can be used in susceptible patients.
  • It causes uterine relaxation less prominently than volatile anesthetics at usual anesthetic concentrations, but its main obstetric concern is neonatal depression if excessive doses are used before delivery.
Miller’s Anesthesia, 10e, p. 2475.

6. Clinical uses

  1. Induction of general anesthesia
    • Particularly suited to ambulatory surgery because of rapid recovery and low incidence of postoperative nausea and vomiting.
  2. Maintenance of anesthesia
    • As an infusion in TIVA, generally with opioid analgesia and often with neuromuscular blockade as required.
  3. Procedural sedation and monitored anesthesia care
    • Examples: endoscopy, cardioversion, imaging, minor procedures.
    • Must be administered only where airway rescue, ventilation, and cardiovascular support are immediately available.
  4. Sedation with regional anesthesia
    • Titrated infusion or small boluses.
  5. ICU sedation
    • For intubated, mechanically ventilated adults.
    • Requires monitoring for hypertriglyceridemia and propofol infusion syndrome during prolonged or high-dose therapy.
  6. Neuroanesthesia
    • Useful when reduction of cerebral metabolism, cerebral blood flow, and ICP is desirable, provided cerebral perfusion pressure is maintained.
  7. Status epilepticus
    • May be used as an anesthetic infusion in refractory cases under critical-care monitoring.
  8. Prevention/treatment of postoperative nausea and vomiting
    • It has intrinsic antiemetic properties.

7. Adverse effects

Common adverse effects

  • Pain on injection
  • Hypotension
  • Apnea and respiratory depression
  • Bradycardia
  • Myoclonus or involuntary movement
  • Local thrombophlebitis, rarely
  • Postoperative dizziness or transient sedation
  • Hypertriglyceridemia with prolonged infusion

Important serious adverse effects

  • Severe hypotension and cardiovascular collapse
  • Severe bradycardia, asystole, rarely
  • Airway obstruction, apnea, hypoxemia
  • Anaphylaxis or anaphylactoid reaction, rare
  • Infection/sepsis from contaminated lipid emulsion
  • Pancreatitis, rarely, usually in the context of lipid load or hypertriglyceridemia
  • Propofol infusion syndrome
Pain on injection, hypotension, apnea, and occasional myoclonus are classic induction-related adverse effects.
Miller’s Anesthesia, 10e, pp. 2489-2490.

8. Pain on injection: prevention

Pain on injection is common, especially when injected into small veins on the dorsum of the hand.
Measures to reduce it:
  • Use a large forearm or antecubital vein.
  • Pretreat with IV lidocaine, often with venous occlusion when appropriate.
  • Lidocaine may be mixed with propofol according to compatible institutional/product guidance.
  • Give opioid before induction if clinically appropriate.
  • Inject slowly and use a larger vein.
Morgan and Mikhail’s Clinical Anesthesiology, 7e, p. 338; Miller’s Anesthesia, 10e, pp. 2489-2490.

9. Propofol infusion syndrome: DNB favorite topic

Definition

Propofol infusion syndrome, or PRIS, is a rare but potentially fatal complication of prolonged and/or high-dose propofol infusion, primarily in critically ill patients.
A classic risk threshold is infusion 4 mg/kg/hour or more for longer than 48 hours, though PRIS has also been reported at lower dose and shorter duration.

Clinical features

  • Unexplained high-anion-gap metabolic acidosis
  • Refractory bradycardia, conduction disturbance, or asystole
  • Acute cardiac failure or cardiomyopathy
  • Rhabdomyolysis with raised creatine kinase
  • Hyperkalemia
  • Acute kidney injury
  • Hyperlipidemia/lipemia
  • Hepatomegaly or fatty liver
  • Skeletal myopathy

Risk factors

  • High-dose and prolonged infusion
  • Critical illness
  • Sepsis
  • Severe head injury
  • Poor tissue oxygen delivery
  • High endogenous or administered catecholamine state
  • Glucocorticoid therapy
  • Low carbohydrate intake
  • Inborn defects of mitochondrial or fatty-acid metabolism

Pathophysiology

Not fully resolved. Proposed mechanisms include impaired mitochondrial energy production and impaired fatty-acid oxidation, leading to cellular energy failure, especially in cardiac and skeletal muscle.

Prevention and monitoring

  • Use the lowest effective dose for the shortest possible duration.
  • Avoid sustained infusion above approximately 4 mg/kg/hour, unless benefit clearly outweighs risk.
  • Monitor acid-base status, lactate, creatine kinase, potassium, renal function, ECG, triglycerides, and clinical signs of cardiac failure in at-risk patients.
  • Consider another sedative if unexplained acidosis, arrhythmia, rising CK, escalating vasopressor requirement, or cardiac dysfunction occurs.

Management

  1. Stop propofol immediately.
  2. Start an alternative sedative.
  3. Treat hyperkalemia, acidosis, arrhythmias, rhabdomyolysis, and cardiac failure.
  4. Provide organ support, including renal replacement therapy and, in refractory cardiovascular collapse, consideration of extracorporeal support where available.
Miller’s Anesthesia, 10e, p. 2490. The current prescribing information also describes severe metabolic acidosis, hyperkalemia, lipemia, rhabdomyolysis, hepatomegaly, renal failure, ECG changes, and cardiac failure as features of PRIS. Product safety warning

10. Contraindications and precautions

Contraindications

  • Known hypersensitivity to propofol or formulation ingredients.
  • Situations where safe airway, ventilation, and hemodynamic support cannot be provided.

Relative contraindications or major precautions

  • Severe hypovolemia or shock
  • Severe LV dysfunction or cardiogenic shock
  • Significant aortic stenosis or fixed cardiac output state
  • Elderly, debilitated, ASA III-IV patients
  • Severe respiratory disease or difficult airway during sedation
  • Long-duration, high-dose ICU use because of PRIS risk
  • Severe hypertriglyceridemia or disorders of lipid metabolism
  • Caution in patients with risk factors for PRIS
  • Repetitive or prolonged exposure in pregnancy, fetus, neonates, and young children should be avoided unless necessary because of concerns regarding developing brain exposure to anesthetic drugs.
Viva line: “Propofol is not the induction agent of choice in an unresuscitated shocked patient because it can precipitate profound hypotension.”

11. Drug interactions

Propofol has additive or synergistic CNS, respiratory, and cardiovascular depression with:
  • Opioids
  • Benzodiazepines
  • Volatile anesthetics
  • Other sedative-hypnotics
  • Alpha-2 agonists
  • Antihypertensives and vasodilators
  • Alcohol
Thus, reduce dose when propofol is used after opioid or benzodiazepine premedication.

12. Advantages over thiopentone

  • More rapid, clear-headed recovery
  • Less postoperative “hangover”
  • Lower PONV because of antiemetic action
  • Suitable for ambulatory anesthesia
  • Decreases ICP and IOP
  • Does not trigger malignant hyperthermia
  • Less bronchospasm/wheezing than thiopentone
  • Can be used as a maintenance infusion for TIVA

Disadvantages

  • More pain on injection
  • Greater hypotension
  • More apnea and respiratory depression
  • No analgesia
  • Expensive relative to some older induction agents
  • Lipid emulsion requires strict asepsis
  • PRIS risk with prolonged high-dose infusion

Rapid-fire DNB viva questions

Why does propofol cause hypotension?

By reducing sympathetic vasoconstrictor activity and systemic vascular resistance, decreasing preload, and producing some myocardial depression. It also impairs the normal baroreceptor reflex tachycardia.

Does propofol provide analgesia?

No. It is a hypnotic and amnestic agent but has no clinically useful analgesic action.

Why is recovery rapid after propofol?

After a bolus, recovery is mainly due to redistribution away from the brain. Its high hepatic and extrahepatic clearance also supports rapid recovery after infusion.

How do you prevent pain on propofol injection?

Use a large vein, inject slowly, and give lidocaine pretreatment or use a compatible lidocaine-propofol mixture where appropriate.

Why is propofol useful for day-care surgery?

Rapid onset and recovery, less residual drowsiness, and lower PONV due to intrinsic antiemetic action.

Is propofol safe in asthma?

It is often a favorable choice because it is associated with less wheezing and bronchodilation relative to several other induction agents. Still prepare for airway and respiratory depression.

What is the dose for induction?

Healthy adult: 2-2.5 mg/kg IV. Elderly, debilitated, or ASA III-IV: 1-1.5 mg/kg IV, titrated slowly.

What is PRIS?

A rare, potentially fatal syndrome caused by prolonged or high-dose propofol infusion, characterized by metabolic acidosis, rhabdomyolysis, hyperkalemia, cardiac failure/bradyarrhythmia, renal failure, and lipemia.

Does propofol trigger malignant hyperthermia?

No.

Can propofol be used in raised ICP?

Yes, because it lowers CMRO2, CBF, and ICP, but prevent hypotension because cerebral perfusion pressure may fall.
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