Anesthesia Emergencies: Malignant Hyperthermia and Bronchospasm

Intraoperative emergencies are among the most critical situations you can face as an anesthesiologist, OR nurse, or emergency physician. Malignant hyperthermia (MH) and severe bronchospasm are two entities that can rapidly become fatal without immediate, algorithmic action. Both emergencies share the fact that early signs are often subtle, the differential diagnoses are broad, and therapy is time-critical. This article provides you with a structured overview of pathophysiology, early signs, concrete treatment algorithms, and the necessary team management – so you don't lose any time in an emergency.

Malignant Hyperthermia

Pathophysiology Overview

Malignant hyperthermia is a pharmacogenetic disorder of skeletal muscle. In genetically predisposed individuals – usually carrying a mutation in the ryanodine receptor (RYR1) or, less commonly, in the DHPR calcium channel (CACNA1S) – volatile inhalational anesthetics (sevoflurane, desflurane, isoflurane) and/or depolarizing neuromuscular blocking agents (succinylcholine) trigger uncontrolled calcium release from the sarcoplasmic reticulum.

The result is a massive, self-sustaining muscle contraction with:

• Excessive O₂ consumption and CO₂ production
• Hypermetabolism with heat generation
• Rhabdomyolysis with hyperkalemia
• Lactic acidosis and mixed acidosis
• Potentially fatal circulatory collapse and multi-organ failure

The incidence is estimated at approximately 1:5,000 to 1:100,000 anesthetics, though the actual number is likely higher due to abortive episodes. Mortality was historically over 70% but has dropped to below 5% with consistent dantrolene therapy.

Recognizing Early Signs

The classic temperature rise is a late sign. If you wait for hyperthermia, you've lost valuable minutes. The actual early signs are:

• Unexplained rise in end-tidal CO₂ (etCO₂): Often the very first sign. A steadily rising etCO₂ despite adequate ventilation should alarm you.
• Tachycardia: Sinus tachycardia that does not respond to usual interventions.
• Masseter spasm (trismus): Particularly after succinylcholine administration. A rigid masseter is not a "normal" succinylcholine effect and must be regarded as an MH warning sign.
• Generalized muscle rigidity: Despite adequate neuromuscular blockade.
• Tachypnea: In spontaneously breathing patients.
• Mixed acidosis: Rapidly identifiable on blood gas analysis (metabolic + respiratory).
• Dark blood in the surgical field: A sign of massive O₂ extraction.

Only in the further course do the following develop:

• Temperature rise: Often >1 °C every 5 minutes, can exceed 43 °C.
• Hyperkalemia: Due to rhabdomyolysis, with risk of malignant arrhythmias.
• Myoglobinuria: Cola-colored urine.
• Disseminated intravascular coagulation (DIC).

Treatment Algorithm: Malignant Hyperthermia

Once MH is suspected: Start treatment immediately – do not wait for confirmation. The algorithm follows the principle "Stop the trigger – Give dantrolene – Provide supportive care":

1. Stop trigger substances immediately:

• Discontinue volatile anesthetics
• Remove the vaporizer from the anesthesia machine
• Set fresh gas flow to maximum (≥10 L/min with 100% O₂)
• Ideally switch to a trigger-free anesthesia machine or, if unavailable, continue ventilating with high fresh gas flow
• Continue anesthesia with trigger-free agents: propofol, opioids, non-depolarizing neuromuscular blocking agents, benzodiazepines

2. Call for help:

• Announce "MH emergency" – all available hands are needed
• Locate and retrieve the MH emergency cart/dantrolene supply
• Assign one person exclusively to dantrolene preparation

3. Dantrolene – the only specific antidote:

• Initial dose: 2.5 mg/kg IV bolus, as quickly as possible
• Repeat doses: 2.5 mg/kg every 5–10 minutes until symptoms resolve (etCO₂ decrease, heart rate normalization, resolution of rigidity)
• Maximum dose: 10 mg/kg, may be exceeded in severe cases
• Caution: Dantrolene preparation is time-consuming! Classic dantrolene (e.g., Dantrolene IV 20 mg per vial) must be dissolved in 60 mL of sterile water for injection – for an 80 kg patient, you initially need 10 vials. Newer formulations (e.g., Ryanodex®, 250 mg per vial) dissolve significantly faster and in a smaller volume.
• A dedicated person must mix dantrolene – this is essential for time management

4. Supportive measures:

• Active cooling: Cold infusions (4 °C normal saline), ice packs to axillae/groin, gastric lavage with cold water, possibly bladder irrigation. Target temperature: 38.5 °C (do not cool below this due to the risk of coagulopathy)
• Acidosis correction: Sodium bicarbonate 1–2 mEq/kg for pH <7.2
• Treat hyperkalemia: Calcium gluconate 10% (30 mL IV), glucose-insulin (10 IU regular insulin + 50 mL glucose 40%), salbutamol nebulization if needed
• Arrhythmias: Amiodarone for ventricular arrhythmias. Calcium channel blockers (verapamil, diltiazem) are contraindicated – in combination with dantrolene, refractory circulatory collapse may occur
• Force diuresis: Target urine output >2 mL/kg/h to prevent myoglobin-induced renal failure (mannitol is already contained in classic dantrolene preparations; additionally consider furosemide)
• Expand monitoring: Arterial line, central venous catheter, urinary catheter, frequent blood gas analysis (every 10–15 minutes), coagulation status

5. Post-event care:

• Intensive care unit admission for at least 24–48 hours
• Continue dantrolene: 1 mg/kg every 4–6 hours for 24–48 hours (recurrence risk up to 25%)
• Genetic counseling and in vitro contracture test (IVCT) for the patient and relatives
• Issue an MH identification card and document in the discharge summary

Differential Diagnoses of MH

Not every intraoperative tachycardia with CO₂ rise is MH. Important differential diagnoses include:

• Inadequate depth of anesthesia (most common cause of tachycardia and CO₂ rise)
• Thyrotoxic crisis
• Pheochromocytoma crisis
• Sepsis / Anaphylaxis
• Serotonin syndrome (particularly with SSRI use and perioperative opioid administration)
• Neuroleptic malignant syndrome (typically occurs more in the postoperative period)
• CO₂ insufflation during laparoscopic procedures (etCO₂ rise without other MH signs)
• Equipment malfunction (e.g., exhausted CO₂ absorber, rebreathing)

Severe Bronchospasm

Pathophysiology and Triggers

Intraoperative bronchospasm occurs through reflex-mediated or immunologically mediated contraction of bronchial smooth muscle with consequent mucosal edema and mucus secretion. The airways can narrow to the point of complete obstruction.

Common triggers in the OR setting:

• Mechanical stimulation: Intubation, suctioning, surgical stimulation under light anesthesia
• Anaphylaxis: Neuromuscular blocking agents (most common trigger!), antibiotics, latex, colloids
• Pre-existing airway disease: Bronchial asthma, COPD
• Aspiration: Gastric contents, blood
• Medications: Beta-blockers, NSAIDs (in aspirin-exacerbated respiratory disease), histamine-releasing agents (atracurium, morphine)
• Cold/dry airway gases

Early Signs and Diagnosis

The clinical presentation varies depending on severity:

• Auscultation: Expiratory wheezing and rhonchi; in the most severe spasm, a "silent chest" (no breath sounds despite ventilation attempts)
• Ventilation pressures: Peak inspiratory pressure rises dramatically, plateau pressure also rises (distinction from a pure tube problem: with tube obstruction, only peak pressure rises)
• etCO₂: Typical "shark fin" capnography (prolonged, upsloping expiratory plateau); subsequently etCO₂ rises due to hypoventilation
• Tidal volume: Decreases, with a high degree of air trapping (auto-PEEP)
• SpO₂ drop: Often a late sign, as FiO₂ is usually high intraoperatively

Treatment Algorithm: Severe Bronchospasm

1. Immediate measures:

• Increase FiO₂ to 100%
• Deepen anesthesia (propofol bolus 0.5–1 mg/kg or increase sevoflurane – volatile anesthetics are potent bronchodilators!)
• Ventilate manually to assess the degree of obstruction
• Interrupt surgical stimulation (if possible)

2. Rule out mechanical causes (DOPES):

• Displacement: Tube malposition? Endobronchial intubation?
• Obstruction: Secretions, blood, tube kinking?
• Pneumothorax: Unilateral breath sounds without a tube problem?
• Equipment: Ventilator functioning? Circuit intact?
• Stomach: Aspiration?

3. Pharmacological therapy – Stepwise approach:

Step 1 – Inhaled beta-2 agonists:

• Salbutamol 2–4 puffs via MDI adapter on the ventilator circuit, or
• Salbutamol nebulization 2.5–5 mg via the breathing circuit
• Repeat every 5–15 minutes based on response

Step 2 – Systemic therapy:

• Epinephrine IV: Start with 10–20 µg (= 0.1–0.2 mL of a 1:10,000 solution), titrated to effect. In severe spasm, escalate stepwise to 100–200 µg. In hemodynamic instability: epinephrine infusion (0.05–0.5 µg/kg/min)
• Alternatively, if hemodynamically stable: Reproterol 90 µg IV slowly (over 1–2 minutes), may repeat after 10 minutes
• Magnesium sulfate: 2 g IV over 20 minutes – bronchodilatory and well tolerated
• Corticosteroids: Methylprednisolone 1–2 mg/kg IV or hydrocortisone 200 mg IV. Onset of action not until 4–6 hours, so administer early – does not help acutely, but in the subsequent course

Step 3 – Refractory bronchospasm:

• Ketamine: 1–2 mg/kg IV bolus, then 0.5–1 mg/kg/h as continuous infusion. Ketamine is a potent bronchodilator through direct smooth muscle relaxation and sympathomimetic effects
• Deepen volatile anesthetics: Sevoflurane is best suited (strongest bronchodilatory potency among volatile agents)
• Ipratropium bromide: 0.5 mg nebulized – additive effect to beta-2 stimulation
• In extremis: Subcutaneous epinephrine (0.3–0.5 mg), theophylline IV (5 mg/kg loading dose over 20 minutes – caution: narrow therapeutic index)

4. Ventilation management in severe bronchospasm:

• Reduce respiratory rate (8–12/min)
• Prolong I:E ratio to 1:3 to 1:4 (long expiratory time!)
• Keep PEEP low (caution: auto-PEEP!)
• Moderate tidal volumes (6–8 mL/kg), accept permissive hypercapnia
• Target peak pressure <40 cmH₂O as a guide (barotrauma risk)

Differential Diagnosis: Bronchospasm vs. Anaphylaxis

An intraoperative bronchospasm may be the first or sole manifestation of anaphylaxis. The following accompanying signs suggest an anaphylactic etiology:

• Skin signs (urticaria, flushing, angioedema) – often hidden by surgical drapes intraoperatively!
• Cardiovascular collapse / hypotension
• Temporal association with drug administration (especially neuromuscular blocking agents, antibiotics)
• Elevated serum tryptase (draw 1–2 hours after the event)

If anaphylaxis is suspected: Epinephrine is the first-line therapy – not salbutamol alone. The epinephrine dose in anaphylactic shock is 0.5–1 mg IM or titrated IV.

Team Management and Communication in the OR

Both emergencies require a well-coordinated team. The following principles of Crisis Resource Management (CRM) are critical:

• Speak up early and clearly: "I am thinking about malignant hyperthermia" or "Severe bronchospasm – I need help." Verbally naming the problem activates the team.
• Clear role assignment: Who administers dantrolene? Who provides cooling? Who documents? Who calls the ICU?
• Closed-loop communication: Have orders confirmed. "Give 200 mg dantrolene IV" – "200 mg dantrolene IV has been given."
• Use cognitive aids: Emergency checklists for MH and bronchospasm should be available in every OR and familiar to the team. The MH hotline (available in Austria) can provide additional expert assistance.
• Maintain situational awareness: Regular team updates every 5 minutes: "We have given X mg of dantrolene so far, etCO₂ has dropped from Y to Z, the temperature is…"
• Debriefing: After every critical event, a structured debriefing should take place promptly – both for medical review and for the mental well-being of the team.

Prevention and Preparedness

The best therapy begins before the emergency:

• Screen for MH susceptibility preoperatively: Personal history (unexplained anesthetic incidents, muscle disorders) and family history. If suspected: plan a trigger-free anesthetic.
• Ensure dantrolene availability: A minimum of 36 vials of dantrolene (= sufficient for an initial dose of 10 mg/kg in a 70 kg patient) must be readily available at every anesthesia workstation. The location must be known to all team members.
• Evaluate bronchospasm risk: Identify patients with asthma and COPD. Optimize maintenance medications preoperatively. Prefer a supraglottic airway over intubation when surgically appropriate. Ensure deep anesthesia before airway instrumentation.
• Regular simulation training: Rare emergencies can only be managed reliably through repeated training in realistic scenarios. Studies consistently show that teams respond faster and with fewer errors to MH and other anesthesia emergencies after simulation training.

Practical Training

Intraoperative emergencies such as malignant hyperthermia or severe bronchospasm are rare enough that most anesthesia teams will experience them only a few times in their careers – but frequent enough that everyone must be prepared. Algorithmic action, safe pharmacotherapy, and structured team communication can be trained most effectively in realistic simulation scenarios. In the ACLS Refresher Course by Simulation Tirol, you deepen exactly these competencies: from recognizing critical situations to correct drug therapy to structured team management under time pressure. If you want to keep your skills up to date, you can find all information at simulation.tirol.