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Anesthesia Essentials & Complications

Name: Anesthesia Essentials & Complications
Creator: Veli Bakalov, MD

Catch the rising CO2, the potassium surge, and the numb lips before they turn lethal

Surgery·Perioperative Care·6 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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ASA I (healthy) to VI (brain-dead donor), with E for emergency; fasting is 2 h for clear liquids, 4 h breast milk, 6 h formula or light meal, 8 h fatty meal.
Malignant hyperthermia is an autosomal dominant RYR1 defect triggered by volatile anesthetics or succinylcholine; the earliest sign is rising end-tidal CO2, and fever is late.
Treat MH by stopping triggers, giving dantrolene 2.5 mg/kg IV repeatedly, cooling, and correcting hyperkalemia; avoid calcium channel blockers and test first-degree relatives.
Succinylcholine causes lethal hyperkalemia in burns or crush injury after 24–48 h, denervation, prolonged immobilization, and myopathies; use rocuronium instead.
Pseudocholinesterase deficiency causes hours of apnea after succinylcholine: keep ventilating until recovery; a low dibucaine number confirms the atypical enzyme.
Sugammadex encapsulates rocuronium or vecuronium and reverses deep block; neostigmine must be paired with glycopyrrolate; extubate at a train-of-four ratio ≥0.9.
LAST progresses from perioral numbness and tinnitus to seizures and arrhythmias (bupivacaine worst): give 20% lipid emulsion 1.5 mL/kg; lidocaine max is 4.5 mg/kg plain, 7 mg/kg with epinephrine.
Positional headache after dural puncture: fluids, caffeine, and analgesics, then an epidural blood patch.
Back pain and leg weakness after a neuraxial block in an anticoagulated patient: emergent MRI and decompression within about 8 h.

Preoperative assessment: ASA class and fasting

ASA physical status. The ASA classification grades how sick the patient is, independent of the operation. It tracks loosely with perioperative mortality but is not a cardiac risk tool; combine it with the procedure's own risk and the Revised Cardiac Risk Index.

ASA physical status classification

Class	Definition	Typical examples
ASA I	Normal healthy patient	Fit nonsmoker
ASA II	Mild systemic disease	Controlled hypertension or diabetes, smoker, pregnancy, BMI 30–40
ASA III	Severe systemic disease	Poorly controlled diabetes, COPD, BMI ≥40, ESRD on dialysis
ASA IV	Severe disease that is a constant threat to life	MI or stroke within 3 months, ongoing ischemia, sepsis
ASA V	Moribund; will not survive without the operation	Ruptured aortic aneurysm, massive trauma
ASA VI	Brain-dead organ donor	Organ procurement

The suffix E (for example, ASA IIIE) marks an emergency case.

Fasting: the 2-4-6-8 rule. Before elective anesthesia, clear liquids are allowed until 2 hours (water, pulp-free juice, carbohydrate drinks, clear tea, black coffee without milk), breast milk until 4 hours, infant formula, nonhuman milk, or a light meal until 6 hours, and fried or fatty food or meat until 8 hours. The aim is a small, less acidic gastric volume and less aspiration pneumonitis at induction. Emergencies cannot wait: assume a full stomach and use rapid-sequence induction, as also for bowel obstruction, gastroparesis, and late pregnancy.

Malignant hyperthermia

Mechanism. An autosomal dominant mutation in RYR1, the sarcoplasmic reticulum calcium-release channel (less often CACNA1S), floods the sarcoplasm with calcium after a trigger: any volatile anesthetic (sevoflurane, desflurane, isoflurane) or succinylcholine. Sustained contraction drives a hypermetabolic surge in CO₂ production and O₂ use, ATP depletion, and rhabdomyolysis. Propofol, nitrous oxide, opioids, ketamine, benzodiazepines, nondepolarizing blockers, and local anesthetics are safe. Central core disease carries the same susceptibility.

Recognition. The earliest sign is an unexplained rise in end-tidal CO₂ despite increased ventilation, with tachycardia; masseter spasm after succinylcholine may be the first warning. Generalized rigidity, mixed respiratory and metabolic acidosis, hyperkalemia with arrhythmias, and rhabdomyolysis (very high CK, myoglobinuria, AKI) follow. Fever is late.

Stop triggers, call for helpDiscontinue the volatile agent and succinylcholine; switch to IV anesthesia.
Hyperventilate100% O₂ at high flow to wash out CO₂.
Dantrolene2.5 mg/kg IV, repeated until signs resolve; it blocks RYR1 calcium release.
Cool and correctCold saline and ice packs; treat hyperkalemia (calcium, insulin with glucose), acidosis, and arrhythmias.
Protect the kidneys, monitorFluids against myoglobinuria; ICU for at least 24 h because MH can recur.

Do not give verapamil or diltiazem with dantrolene: the combination can cause hyperkalemia and cardiovascular collapse.

Afterward. Penetrance is variable, so an uneventful prior anesthetic does not exclude susceptibility. Refer first-degree relatives for RYR1 genetic testing or the caffeine-halothane contracture test on muscle biopsy (reference standard), and make every future anesthetic trigger-free: propofol-based total IV anesthesia, nondepolarizing blockers, a flushed machine. Look-alikes are neuroleptic malignant syndrome (days after a dopamine antagonist; bromocriptine) and serotonin syndrome (clonus, hyperreflexia; cyproheptadine).

Neuromuscular blockers: succinylcholine and reversal

Succinylcholine. A depolarizing nicotinic agonist with the fastest onset and a 5–10-minute duration, used for rapid-sequence intubation. It causes fasciculations, myalgias, bradycardia (especially in children), raised intraocular and intracranial pressure, and a normal potassium rise of about 0.5 mEq/L.

Hyperkalemic arrest. Denervation and injury spread extrajunctional acetylcholine receptors across the muscle membrane, so succinylcholine releases a massive potassium load. At risk: burns and crush injury after about 24–48 hours, spinal cord injury, stroke, Guillain-Barré syndrome, prolonged immobilization, and muscular dystrophy. Use rocuronium instead; if arrest occurs, give IV calcium first, then insulin with glucose.

Pseudocholinesterase deficiency. Plasma cholinesterase normally ends succinylcholine's effect within minutes. An inherited atypical enzyme (autosomal recessive) or acquired deficiency (liver disease, pregnancy, malnutrition, organophosphates) prolongs paralysis for hours. Keep the patient sedated and ventilated until strength returns; neostigmine would worsen the block because it also inhibits plasma cholinesterase, and sugammadex does not bind succinylcholine. A low dibucaine number (about 20 vs 80 normally) confirms the variant, and relatives should be tested.

Reversing neuromuscular blockade

Feature	Sugammadex	Neostigmine + glycopyrrolate
Mechanism	Modified γ-cyclodextrin that encapsulates the blocker	Acetylcholinesterase inhibitor; extra ACh outcompetes the blocker
Works on	Rocuronium, vecuronium	All nondepolarizing blockers
Depth of block	Reverses even deep block within minutes	Only after partial recovery (ceiling effect)
Companion drug	None	Glycopyrrolate blocks muscarinic bradycardia, bronchospasm, secretions
Cautions	Rare anaphylaxis, bradycardia; hormonal contraception needs a backup method for 7 days	Bradycardia if the antimuscarinic is omitted

Confirm a train-of-four ratio ≥0.9 before extubation. Neither drug reverses succinylcholine.

Local anesthetic systemic toxicity

Cause and signs. LAST follows intravascular injection or overdose; systemic absorption is highest after intercostal blocks and lowest after subcutaneous infiltration. CNS signs usually lead: circumoral numbness, metallic taste, tinnitus, and agitation, then seizures, coma, and apnea. Cardiotoxicity brings bradycardia, a widened QRS, ventricular arrhythmias, and collapse. Bupivacaine is the most cardiotoxic agent and can cause collapse with little CNS warning.

4.5 mg/kgmaximum lidocaine without epinephrine (≤300 mg)

7 mg/kgmaximum lidocaine with epinephrine (≤500 mg)

2.5 mg/kgapproximate maximum bupivacaine

Dose arithmetic. A 1% solution holds 10 mg/mL, so a 70-kg adult may receive at most 300 mg (30 mL of 1%) plain lidocaine — 4.5 mg/kg would be 315 mg, but the 300-mg ceiling applies. Epinephrine vasoconstricts, slows absorption, and prolongs the block, which permits the higher dose.

Management. Stop injecting, give 100% O₂, and secure the airway, since hypoxia and acidosis worsen toxicity. Treat seizures with a benzodiazepine. At the first sign of serious toxicity, give 20% lipid emulsion: a 1.5 mL/kg bolus (100 mL if over 70 kg), then an infusion. Modify ACLS by keeping epinephrine ≤1 μg/kg and avoiding vasopressin, calcium channel blockers, β-blockers, and more local anesthetic; resuscitation may need to be prolonged.

Lipid emulsion acts as a lipid sink that draws lipophilic anesthetic out of the myocardium. Give it early, not as a last resort.

Neuraxial anesthesia complications

Post-dural puncture headache. CSF leaking through the dural hole lowers intracranial pressure. The frontal-occipital headache begins within about 1–3 days, worsens sitting or standing, and eases lying flat, sometimes with neck stiffness, tinnitus, or diplopia from sixth nerve traction. Risk is highest in young women, obstetric patients, and after large-bore or cutting needles; pencil-point needles lower it. Start with fluids, caffeine, and analgesics; an epidural blood patch is definitive for severe or persistent headache. A nonpositional headache, fever, or focal deficit needs imaging instead.

Spinal epidural hematoma. Bleeding after needle or catheter placement or removal is linked to anticoagulants, antiplatelet drugs, coagulopathy, and thrombocytopenia. New back pain, progressive bilateral leg weakness or numbness, and bowel or bladder dysfunction call for emergent MRI and surgical decompression; recovery is best within about 8 hours. Prevention depends on timing:

Prophylactic-dose LMWH: puncture or catheter removal at least 12 h after the last dose.
Therapeutic-dose LMWH: at least 24 h.
Clopidogrel 5–7 days; DOACs usually about 72 h, longer for dabigatran with renal impairment.
Aspirin or NSAIDs alone need no interruption.

New back pain or leg weakness after a neuraxial block is an epidural hematoma until MRI proves otherwise; never blame it on residual block.