Malignant Hyperthermia Syndrome is a dangerous reaction of the body’s skeletal muscles to some anesthesia medicines. In people who carry certain inherited changes (variants) in muscle-calcium control genes, a trigger drug can suddenly cause the muscle cells to open their calcium “floodgates.” The muscles then contract hard, burn a lot of energy, make a lot of heat and acid, and break down. This causes very fast breathing, rising end-tidal CO₂ (ETCO₂), fast heart rate, muscle rigidity, dark urine from myoglobin, high potassium, and a rapid rise in body temperature. Without quick treatment with the antidote dantrolene and supportive care, MH can cause heart rhythm problems, kidney failure, clotting problems, and death. MH is not an allergy; it is a genetic disorder of muscle calcium regulation. NCBI+2AANA+2
Malignant hyperthermia syndrome is a rare, inherited problem in skeletal muscle where certain anesthesia medicines (especially inhaled volatile anesthetics and the muscle relaxant succinylcholine) flip a “calcium switch” in muscle cells to the fully-on position. Calcium floods out of the sarcoplasmic reticulum through an over-reactive ryanodine receptor (RyR1), causing runaway muscle contraction and heat production. That hyper-metabolism drives a fast rise in carbon-dioxide, acidosis, dangerously high potassium, muscle breakdown (rhabdomyolysis), very high temperature (often late), arrhythmias, and can be fatal without rapid treatment. Most known genetic risks involve RYR1; a minority involve CACNA1S and STAC3. Outside the operating room, extreme heat or intense exertion may very rarely unmask susceptibility. NCBI+2NCBI+2
The main triggers are volatile anesthetic gases and succinylcholine; non-depolarizing relaxants and local anesthetics are considered safe. Typical early clues under anesthesia are an unexplained, rapid rise in end-tidal CO₂, tachycardia, muscle/jaw rigidity (after succinylcholine), and metabolic or respiratory acidosis. Fever is often late. Immediate action matters more than waiting for confirmatory testing. NCBI+2orphananesthesia.eu+2
Most MH crises start during anesthesia or soon after surgery when patients receive a volatile inhaled anesthetic (such as sevoflurane, desflurane, isoflurane) and/or the muscle relaxant succinylcholine. The earliest reliable sign during anesthesia is an unexplained rise in ETCO₂ despite adequate ventilation. Prompt recognition and treatment save lives. Medscape+2NCBI+2
Genetically, MH happens most often in people with pathogenic variants in the RYR1 gene (which encodes the skeletal-muscle ryanodine receptor calcium channel). Less commonly, variants in CACNA1S (a calcium channel subunit) or STAC3 are involved. Some people with these gene changes also have mild underlying myopathy or heat/exertion problems even without anesthesia. PMC+2PubMed+2
Other names
These terms all refer to the same clinical problem or its closely related states:
Malignant hyperthermia (MH)
Malignant hyperthermia crisis
Malignant hyperthermia susceptibility (MHS) — the genetic risk state without a crisis
Anesthesia-induced hypermetabolic crisis
Halothane–succinylcholine crisis (historic name)
RYR1-related crisis (genetic descriptor)
Pharmacogenetic hyperthermia of anesthesia
These names appear across anesthesia and genetics references describing the same syndrome and its susceptibility state. NCBI+1
Types
You may see MH described in a few practical “types,” which help clinicians think about when and how it presents:
Classic anesthetic-triggered MH — happens during or right after anesthesia with a volatile agent and/or succinylcholine. This is the most common pattern. Medscape
Abortive or evolving MH — early signs appear (rising ETCO₂, tachycardia, masseter spasm, mild rigidity) without full hyperthermia yet. Rapid treatment can stop progression. NCBI
Post-operative MH — begins in the recovery room or several hours after surgery when triggers were used. Same treatment is needed. Medscape
MH susceptibility (MHS) — the person carries a causative variant or has a positive muscle contracture test but has never had a crisis. Trigger avoidance and family counseling are key. NCBI
Exertional/heat-related crises in RYR1 disorders — some people with RYR1 variants get rhabdomyolysis or heat illness with intense exercise or high environmental heat. This overlaps biologically with MH but is not the same trigger mechanism. NCBI
Causes
Think of “causes” in two buckets: genetic susceptibility (the root cause) and triggers (what starts the crisis). Each item below is explained in one or two simple sentences.
Pathogenic RYR1 variant — most common cause of MH susceptibility; the channel leaks or over-releases calcium during triggers. PMC
Pathogenic CACNA1S variant — rarer; alters the voltage sensor that talks to RYR1 and can permit runaway calcium release. PubMed
Pathogenic STAC3 variant — rare but established; disrupts excitation–contraction coupling and can cause MH. NCBI+1
Volatile inhalational anesthetics (e.g., sevoflurane, desflurane, isoflurane, halothane) — main pharmacologic triggers. Medscape
Succinylcholine — depolarizing neuromuscular blocker that can trigger or amplify MH, especially with volatile agents. Medscape
Combination of volatile anesthetic + succinylcholine — higher risk than either alone in susceptible patients. Medscape
Previous personal MH event — indicates susceptibility, so future exposure to triggers can cause recurrence. NCBI
First-degree family history of MH — because inheritance is often autosomal dominant, relatives are at risk. NCBI
Underlying RYR1-related myopathy — central core disease or other RYR1 myopathies can co-exist with MHS. NCBI
High-dose, rapid anesthesia trigger exposure — more intense exposure can push a marginal case into crisis. Medscape
Unrecognized masseter muscle rigidity after succinylcholine — an early “red flag” suggesting susceptibility. NCBI
Hypercarbia not explained by ventilation — rising ETCO₂ can be the earliest physiologic trigger clue. PMC
Metabolic stress from surgery — adds to the burden once a trigger starts calcium release. NCBI
Delayed recognition of early signs — allows the cascade to escalate; not a genetic cause but a practical precipitant. mhaus.org
Inadequate dantrolene availability — lack or delay of antidote lets crisis progress. mhaus.org
Exertional/heat stress in RYR1-positive individuals — can trigger rhabdomyolysis episodes outside anesthesia; highlights the shared pathway. NCBI
Unknown non-RYR1/CACNA1S/STAC3 factors — a minority of MH families test negative in known genes, showing genetic heterogeneity. ScienceDirect
Young age with heavy muscle mass — more muscle can mean bigger calcium release and heat production when triggered. NCBI
Concurrent illness or dehydration — may worsen acidosis and kidney risk once MH begins. NCBI
Use of triggering agents in out-of-OR settings without full monitoring — increases risk of late detection. mhaus.org
Symptoms and signs
Rapid rise in end-tidal CO₂ (ETCO₂) — most sensitive early sign during anesthesia; CO₂ climbs despite ventilation. PMC
Tachycardia — heart rate increases as the body enters a hypermetabolic state. NCBI
Generalized or jaw (masseter) muscle rigidity — muscles become very stiff; jaw may be hard to open after succinylcholine. NCBI
Rapidly rising body temperature — fever may rise late but can climb quickly once established. NCBI
Tachypnea (if breathing spontaneously) — fast breathing to blow off CO₂. NCBI
Acidosis (metabolic and/or respiratory) — lactate builds up; CO₂ retention adds respiratory acidosis. NCBI
Dark or cola-colored urine — myoglobin from muscle breakdown appears in urine. NCBI
Hyperkalemia — potassium leaks from damaged muscle; this can cause dangerous arrhythmias. NCBI
Rhabdomyolysis — muscle breakdown shown by high CK, myoglobin, and pain when awake. NCBI
Arrhythmias (PVCs, VT, VF) — due to acidosis, high potassium, and heat. NCBI
Warm, flushed skin and profuse sweating — from high metabolism and heat production. NCBI
Low oxygen saturation or rising oxygen needs — oxygen consumption increases; saturation may drop if unmet. NCBI
Elevated blood pressure early, then hypotension — sympathetic surge may be followed by cardiovascular collapse. NCBI
Coagulopathy or DIC in severe cases — widespread clotting activation can occur late. NCBI
Kidney injury — from myoglobin and shock if treatment is delayed. NCBI
Diagnostic tests
A) Physical exam and bedside monitoring
Continuous capnography (ETCO₂ trend) — the best early bedside indicator during anesthesia; a rising ETCO₂ that does not respond to ventilation is a red flag. PMC
Core temperature monitoring — rectal, esophageal, or bladder probes detect a rapid temperature climb; absence of early fever does not exclude MH. NCBI
Neuromuscular and jaw tone check — note masseter spasm or generalized rigidity; alerts clinicians to possible MH. NCBI
Urine inspection — dark urine suggests myoglobinuria; prompt fluids and alkalinization help protect kidneys. NCBI
Clinical Grading Scale (Larach score) — uses observed signs (e.g., ETCO₂, rigidity, CK) to estimate the likelihood that an event is MH; supports urgent treatment decisions. PubMed+1
B) Manual and specialized functional tests
Caffeine–halothane contracture test (CHCT/IVCT) — the gold-standard diagnostic test on a fresh muscle biopsy; MH-susceptible muscle contracts more to caffeine/halothane. PMC+2Medscape+2
Family cascade testing pathway — using CHCT or genetics in relatives after an index case to identify who must avoid triggers. NCBI
Dantrolene therapeutic test (clinical response) — in a suspected crisis, improvement in ETCO₂, rigidity, and vitals after dantrolene supports the diagnosis (therapy should not be delayed for a test). mhaus.org
Anesthesia machine trigger elimination checklist — immediate stopping of volatile agents, 100% oxygen, high fresh-gas flows, and circuit change; clinical improvement after these steps supports MH over other causes. mhaus.org
C) Laboratory and pathological tests
Arterial blood gas (ABG) with lactate — shows mixed metabolic and respiratory acidosis; lactate is often high. NCBI
Serum creatine kinase (CK) — rises as muscle breaks down; very high levels support MH or rhabdomyolysis. NCBI
Serum potassium — detects hyperkalemia that can trigger arrhythmias; guide urgent treatment. NCBI
Serum/urine myoglobin — confirms rhabdomyolysis risk to kidneys; aligns with cola-colored urine. NCBI
Coagulation panel (PT/INR, aPTT, fibrinogen, D-dimer) — looks for DIC in severe crises. NCBI
Comprehensive metabolic panel (creatinine, AST/ALT, bicarbonate) — assesses kidney/liver stress and acidosis. NCBI
Genetic testing for RYR1, CACNA1S, STAC3 — confirms susceptibility in many families and guides relatives; a negative test does not fully exclude MH. NCBI+1
Muscle biopsy pathology (if obtained for CHCT) — processed strips are used for the contracture test; histology may show core-type changes in some RYR1 disorders. PMC
D) Electrodiagnostic and physiologic monitoring
Electrocardiogram (ECG/telemetry) — detects tachyarrhythmias or conduction changes from hyperkalemia and acidosis; helps guide calcium and antiarrhythmic therapy. NCBI
Train-of-four or neuromuscular monitoring — persistent rigidity despite neuromuscular blocker raises concern for MH rather than light anesthesia alone. NCBI
Pulse oximetry and noninvasive blood pressure — show rising oxygen needs and hemodynamic instability; trend data support the global hypermetabolic picture. NCBI
Non-pharmacological management
These are the evidence-based non-drug steps used to treat an acute crisis and to prevent one in susceptible people. They complement (not replace) dantrolene.
Stop all triggers immediately. Turn off volatile anesthetics, discontinue succinylcholine, and switch to total intravenous anesthesia if surgery must continue. This is the single most important first step. mhaus.org
Maximize oxygen and hyperventilate. Deliver 100% oxygen at high flow and hyperventilate to wash out CO₂ and correct acidosis while other steps are mobilized. mhaus.org
Flush/prepare the anesthesia machine or use a trigger-free system. Remove/disable vaporizers; use fresh circuits and high fresh-gas flows per MHAUS guidance to minimize residual volatile anesthetics. mhaus.org
Active cooling (external). Use ice packs to axillae/groin/neck, cooling blankets, and cold air; stop when core temp approaches 38–38.5 °C to avoid overshoot. mhaus.org
Active cooling (internal). Consider cold IV saline, cold gastric/rectal/bladder lavage when available and appropriate, especially in severe hyperthermia. mhaus.org
Continuous capnography and core temperature monitoring. Rising ETCO₂ and core temperature trends are critical for early recognition and to track response. mhaus.org
Frequent arterial blood gases and electrolytes. Track pH, PCO₂, potassium, calcium, CK, and lactate to steer therapy and detect complications (e.g., hyperkalemia). Medscape
High-volume IV fluids. Aggressive crystalloid resuscitation helps maintain perfusion, supports cooling, and protects kidneys from myoglobin. Medscape
Urine output targeting and alkalinization strategy. Aim ≥2 mL/kg/h with fluids ± (drug diuretics if needed—see drug section) and consider urine alkalinization for myoglobinuria risk. Medscape
Avoid calcium channel blockers with dantrolene. This non-drug rule prevents fatal hyperkalemia/rhabdomyolysis from drug interactions; communicate it to the whole team. pie.med.utoronto.ca
Dedicated MH cart and posted crisis checklist. Institutions should stock dantrolene and supplies, and post a step-by-step algorithm where it’s instantly visible. Anesthesia Patient Safety Foundation
Team drills and rapid role assignment. Regular simulation shortens time-to-dantrolene and improves outcomes. Assign roles (airway, drugs, cooling, labs, documentation). Anesthesia Patient Safety Foundation
ICU observation after stabilization (≥24 hours). Recrudescence can occur; ongoing monitoring of CK, potassium, temperature, and renal function is standard. Medscape
Trigger-free anesthesia plans for known/suspected MHS. Use regional/neuraxial techniques or total intravenous anesthesia; have a contingency for airway emergencies without volatile agents. PMC
Machine preparation before known MHS cases. Follow MHAUS flush times or use activated charcoal filters when available to rapidly reduce volatile levels. mhaus.org
Medical alert identification and family notification. Patients should carry MHS identification and inform relatives because risk is inherited. NCBI
Genetic counseling and test referral. Post-event, refer to centers that offer contracture testing and gene panels to guide family risk and future anesthetics. NCBI
Perioperative warming used judiciously. Avoid unnecessary heat burden during suspected events; resume normothermia strategies once stable. orphananesthesia.eu
Rapid recognition of “late fever.” Teach teams that temperature may spike late; do not wait for high fever to start treatment. NCBI
Use of crisis hotlines and expert support. The MHAUS emergency hotline can support frontline teams during events. AANA
Drug treatments
Only dantrolene treats the root mechanism. The rest are supportive drugs for complications (acidosis, hyperkalemia, arrhythmias, renal protection, hypotension). Where possible, I cite FDA labels and MH guidance. Always avoid calcium channel blockers with dantrolene.
Dantrolene (Ryanodex® or Dantrium® IV) — Skeletal muscle relaxant; the only specific antidote.
Class/Purpose: Direct RyR1 calcium release inhibitor; stops the hypermetabolic cascade. Dose: Initial 2.5 mg/kg IV; repeat until control (commonly up to 10 mg/kg); then maintenance per protocol. Timing: Give immediately once MH is suspected—do not wait for labs. Mechanism: Lowers calcium release from SR in skeletal muscle, reversing rigidity and heat generation. Key adverse effects: Muscle weakness, phlebitis; do not co-administer calcium channel blockers. Evidence/Labels: FDA Ryanodex dossier/label; clinical guidance. pie.med.utoronto.ca+4FDA Access Data+4FDA Access Data+4Sodium bicarbonate (IV) — For severe metabolic acidosis/hyperkalemia.
Class/Purpose: Systemic alkalinizer. Dose: Titrate to ABGs; common boluses 1–2 mEq/kg in severe acidosis per clinician judgment. Mechanism: Buffers H⁺, shifts K⁺ intracellularly, mitigates arrhythmia risk. Not MH-specific but used in crises. Label evidence: FDA sodium bicarbonate labeling. U.S. Food and Drug Administration+1Regular insulin (IV) + Dextrose (IV) — Treats life-threatening hyperkalemia.
Class/Purpose: Temporizing shift of K⁺ into cells. Dose: Typical 10 units regular insulin IV with 25 g dextrose; adjust per glucose/chemistry. Mechanism: Insulin drives K⁺ intracellularly; dextrose prevents hypoglycemia. Labels: Humulin R; Dextrose Injection. FDA Access Data+2FDA Access Data+2Nebulized albuterol — Adjunct for hyperkalemia.
Class/Purpose: β₂-agonist bronchodilator that also shifts K⁺ intracellularly. Dose: Typical 10–20 mg continuous nebulization as an adjunct. Mechanism: β₂ stimulation activates Na⁺/K⁺-ATPase. Label: Albuterol solution/HFA. FDA Access Data+1Furosemide (IV) — Supports high urine output to protect kidneys from myoglobin.
Class/Purpose: Loop diuretic. Dose: Tailored to urine output and hemodynamics. Mechanism: Increases diuresis to flush myoglobin once volume replete. Label: Furosemide Injection. FDA Access Data+1Mannitol (IV) — Osmotic diuretic for renal protection if volume status allows.
Class/Purpose: Promote osmotic diuresis. Mechanism: Opposes tubular pigment cast formation. Label: Osmitrol/Mannitol Injection. FDA Access Data+1Amiodarone (IV) — For ventricular arrhythmias caused by hyperkalemia/acidosis when needed.
Class: Class III antiarrhythmic. Mechanism/Purpose: Stabilizes myocardium without calcium-channel blockade. Caution: Continuous monitoring; correct underlying K⁺/acidosis. Label: Nexterone. FDA Access DataProcainamide (IV) — Alternative antiarrhythmic for wide-complex tachycardia if selected by the treating team.
Class: Class Ia antiarrhythmic. Note: Titrate with close QRS/pressure monitoring. Label/data: SPL dosing information. FDA Access DataLidocaine (IV) — Antiarrhythmic option for ventricular ectopy.
Class: Class Ib antiarrhythmic. Label: Lidocaine injection. FDA Access DataCalcium chloride (IV) — For life-threatening hyperkalemic arrhythmia when indicated.
Important: This is not a calcium channel blocker; however, do not give calcium channel blockers with dantrolene. Use calcium chloride only for classic hyperkalemia indications per ACLS with careful risk–benefit judgment. Label: Calcium chloride injection. mhaus.org+1Norepinephrine (IV infusion) — For refractory hypotension after adequate volume.
Class: Vasopressor (α-predominant). Label: Norepinephrine injection. FDA Access DataPhenylephrine (IV) — Bolus/infusion for anesthesia-related vasodilatory hypotension.
Class: α-agonist vasoconstrictor. Label: Phenylephrine injection. FDA Access DataMagnesium sulfate (IV) — For torsades de pointes if QT instability occurs.
Class: Antiarrhythmic/electrolyte. Label: Magnesium sulfate injection. FDA Access DataRocuronium (IV) — Safe non-depolarizing neuromuscular blocker if paralysis is needed after stopping succinylcholine.
Class: NDMB; does not trigger MH. Label: Rocuronium (Zemuron). FDA Access DataOpioid analgesics (e.g., fentanyl) — For analgesia without triggering MH (use per standard care).
Note: Not MH-specific; avoids added sympathetic surge. Label: (General class labels; use institution formulary.) Not cited as a key source to avoid over-quoting labels unrelated to MH.Vasopressin (IV) — Second-line vasopressor if needed for refractory vasoplegia.
Label: (FDA vasopressin injection labeling exists; use per shock guidelines.) Not a primary MH source; kept brief to prioritize core evidence.Crystalloid solutions (cold when cooling) — To support perfusion and aid cooling.
Note: Product labels vary; clinical guidance prioritizes volume resuscitation. MedscapeActivated charcoal filters for machines — Device adjunct to reduce volatile levels quickly (non-drug supply used alongside other steps). mhaus.org
Antiemetics/acid suppression (supportive) — Standard perioperative care, not MH-specific; used as clinically indicated. Kept generic; not central to MH control.
Insulin infusion (after bolus phase) — For ongoing K⁺ management and glycemic control in ICU if needed. Labels: Regular insulin. FDA Access Data
Caution: Do not use calcium channel blockers with dantrolene (risk of hyperkalemia and cardiovascular collapse). pie.med.utoronto.ca
Dietary molecular supplements
There are no dietary supplements proven to prevent, treat, or shorten an MH crisis. The only disease-specific therapy is dantrolene plus the supportive measures above. Supplements should not be used in place of urgent care; they can delay life-saving treatment and some (e.g., high-dose potassium, stimulants) can worsen complications. Focus patient-facing content on avoidance of triggers, preparedness, and post-event follow-up, not supplements. mhaus.org+1
Immunity-booster, regenerative,” and “stem-cell” drugs
MHS is an acute pharmacogenetic reaction to anesthetic triggers, not an immune deficiency or a degenerative tissue disorder. There are no immune-boosting, regenerative, or stem-cell drugs indicated for MHS prevention or treatment; including them alongside MH content risks implying benefit where none exists. Keep your medication section centered on dantrolene and evidence-based supportive drugs only. NCBI
Surgeries
Surgery does not treat MH. In fact, MH usually occurs during surgery with triggering anesthetics. Management is medical and supportive. If surgery must continue once the crisis is controlled, it should proceed trigger-free with close ICU-level monitoring after. PMC
Practical preventions
Documented MH history and family screening before procedures. NCBI
Trigger-free anesthesia plans for known/suspected MHS (regional/TIVA). PMC
MH machine preparation (flush, remove vaporizers, consider charcoal filters). mhaus.org
Stock an MH cart with dantrolene and supplies; check expiry. Anesthesia Patient Safety Foundation
Post visible crisis checklists in ORs and PACUs. Anesthesia Patient Safety Foundation
Run team MH drills at regular intervals. Anesthesia Patient Safety Foundation
Continuous ETCO₂ and core temperature monitoring for GA >30 min. mhaus.org
Educate staff on early signs (rapid ETCO₂ rise, rigidity) and the rule to avoid CCBs with dantrolene. pie.med.utoronto.ca
Plan ICU handoff/observation for at least 24 hours after an event. Medscape
Patient carries medical alert info and informs relatives for possible testing. NCBI
When to seek urgent medical care / call for help
During anesthesia or recovery: any sudden, unexplained rise in ETCO₂; generalized or masseter rigidity; fast metabolic acidosis; dark cola-colored urine; rapid temperature climb; or unstable arrhythmia. Treat as MH until proven otherwise and give dantrolene. Medscape
After discharge: severe muscle pain, dark urine, fever, confusion, palpitations, or reduced urine output within 24–48 h after anesthesia—seek emergency care and tell clinicians “possible MH exposure.” NCBI
Family members of a known case: ask about referral for contracture testing/genetic counseling before any future anesthetic. NCBI
What to eat and what to avoid
Diet does not prevent or treat an MH episode. After recovery from rhabdomyolysis, clinicians often advise adequate hydration, balanced electrolytes, and avoiding excessive heat/exertion until labs normalize. Avoid “performance” supplements or stimulants that can raise temperature or heart rate during early recovery. This is general convalescent advice—not MH-specific therapy. Always follow the treating team’s instructions. NCBI
FAQs
1) What exactly causes MH?
An inherited change (usually in RYR1) makes the calcium channel in skeletal muscle over-react to certain anesthetics; calcium floods muscle cells, causing a dangerous metabolic storm. NCBI
2) Who is at risk?
Anyone with a personal or family history of MH, certain myopathies, or a positive contracture test. It’s usually inherited in an autosomal-dominant pattern. NCBI
3) What medicines trigger it?
Volatile anesthetic gases and succinylcholine are the classic triggers; most other anesthetic drugs are safe. NCBI
4) What are the earliest signs in the OR?
A rapid rise in end-tidal CO₂ and tachycardia; rigidity after succinylcholine is a red flag; fever is often late. Medscape
5) What’s the life-saving drug?
Dantrolene—give it immediately when MH is suspected; don’t wait for labs or fever. Medscape
6) Can calcium channel blockers be used?
No. Avoid calcium channel blockers with dantrolene—combination can be fatal. pie.med.utoronto.ca
7) Does acetaminophen help the fever?
Not meaningfully for MH; you must stop triggers, hyperventilate, cool actively, and give dantrolene. mhaus.org
8) Do vitamins or supplements prevent MH?
No. No supplement prevents or treats MH. Focus on anesthesia planning and preparedness. mhaus.org
9) Can MH happen outside anesthesia?
Rarely, extreme heat/exertion may unmask susceptibility, but the classic setting is triggered anesthesia. NCBI
10) Is testing available?
Yes—caffeine–halothane contracture testing and genetic testing at expert centers. NCBI
11) If I’m susceptible, can I still have surgery?
Yes—with a trigger-free plan (regional/TIVA) and an MH-ready team. PMC
12) How long must I be observed after an event?
Typically at least 24 hours in ICU because MH can recur after initial control. Medscape
13) What about children?
Incidence is higher in pediatrics; vigilance and preparation are the same or greater. MDPI
14) Where can clinicians get real-time help?
The MHAUS emergency hotline and online algorithms. AANA
15) Why does temperature sometimes rise late?
Because the metabolic storm starts with CO₂ and muscle rigidity; heat accumulation follows—so don’t wait for fever to treat. NCBI
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: October 16, 2025.
