Adrenergic storm
Other namesSympathomimetic toxicity
Sympathomimetic toxidrome
ComplicationsTachycardia, hypertension
CausesCocaine, stimulant abuse, subarachnoid hemorrhage, methamphetamine, foods high in tyramine, rabies
Treatmentdiazepam, benzodiazepines, beta blockers, anti-hypertensives

An adrenergic storm is a sudden and dramatic increase in serum levels of the catecholamines adrenaline and noradrenaline (also known as epinephrine and norepinephrine respectively), with a less significant increase in dopamine transmission. It is a life-threatening condition because of extreme tachycardia and hypertension, and is especially dire for those with prior heart problems. If treatment is prompt, prognosis is good; typically large amounts of diazepam or other benzodiazepines are administered alongside beta blockers. Beta blockers are contraindicated in some patients, so other anti-hypertensive medication such as clonidine may be used.[1] Antipsychotics are also used to treat the most severe psychiatric reactions such as psychosis, paranoia or terror, after their use was formerly discouraged because of their potential to prolong the QT interval; however, more recent research performed since 2019 has revealed that this and other severe side effects are rare and their occurrence does not warrant banning antipsychotics from the treatment of adrenergic crises for which they can be extremely useful.[2][3][4][5][6][7][8]

Adreneric storms are usually caused by overdoses of stimulants, especially cocaine or methamphetamine, or eating foods high in tyramine while taking monoamine oxidase inhibitors.[9] A subarachnoid hemorrhage can also cause an adrenergic storm.[9] A catecholamine storm is part of the normal course of rabies infection, and is responsible for the severe feelings of agitation, terror, and dysautonomia present in the pre-coma stage of the disease.[10]

Signs and symptoms

The behavioral symptoms are similar to those of an amphetamine, cocaine or caffeine overdose. Overstimulation of the central nervous system results in a state of hyperkinetic movement and unpredictable mental status including mania, rage and suicidal behavior; hyperthermia is also prominently present.[11] Delirium can also be present but rarely.[12]

Physical symptoms are more serious and include heart arrhythmias as well as outright heart attack or stroke in people who are at risk of coronary disease. Breathing is rapid and shallow while both pulse and blood pressure are dangerously elevated.[13]

Other complications would include rhabdomyolysis, a breakdown of the voluntary muscles because of the excessive physical movement, causing the components of the muscle, most notably myoglobin, to be released into the bloodstream and then clog the kidneys, causing renal failure.[14] In all, rhabdomyolysis is especially common in adrenergic storms caused by the use of stimulant drugs, most notably those of the phenethylamines such as cathinones or amphetamines.[15]

Causes

There are several known causes of adrenergic storms; in the United States, cocaine overdose is the leading cause.[16] Any stimulant drug has the capacity to cause this syndrome if taken in sufficient doses, but even non-psychotropic drugs can very rarely provoke a reaction.[17]

Monoamine oxidase inhibitors (MAOIs) are a class of drugs that inhibit the enzyme monoamine oxidase. This enzyme is responsible for breaking down many compounds; basically, anything with a primary amine moiety is likely to be oxidized by monoamine oxidase. An important substrate of the enzyme MAO is tyramine. MAOIs inhibit the enzyme either reversibly, in which MAO is inhibited only until the drug is cleared from the system, or irreversibly, in which the substrate binds permanently to the enzyme, rendering it inactive and effectively destroying it. Irreversible MAOIs are potentially more dangerous, because the body takes about two weeks to regenerate MAO enzymes to functional levels.[18] Two subtypes of MAO exist: MAO-A and MAO-B; this is relevant to adrenergic storms, as there are significant differences between the two types, such as their differential expression throughout the body, and range of substrates. While both MAO-A and MAO-B metabolize tyramine, only MAO-A is present in the gastrointestinal tract and singularly metabolizes the majority of consumed tyramine.[9] (The small portion normally passing into circulation is mostly degraded in the liver where both MAO types act.[9]) Consequently, MAOIs that irreversibly inhibit MAO-A will permit high levels of circulating tyramine able to cause tyramine-induced hypertensive crisis. Aged cheese, beer, red wine, some mushrooms, and fermented products such as pickles are foods containing high levels of tyramine that passed into circulation can cause such a hypertensive crisis.

Adrenergic storms are not provoked often from MAOI-tyramine interactions; hypertensive crisis alone does not diagnose adrenergic storm, although there will always be hypertension in an adrenergic storm, along with tachycardia and rapid, shallow breathing. However, if a patient on MAOIs uses recreational quantities of any drug with stimulant effects on the CNS, it can provoke an adrenergic crisis (along with the inevitable hypertensive crisis). Deaths have occurred from individuals attempting to combine MAOIs with various entheogens to attain a stronger psychedelic experience, both from adrenergic storms and serotonin syndrome. Combining drugs like MDMA, 2C-B, mescaline, 2C-T-7, etc. with even small quantities of MAOIs - small quantities of both drugs - is still extremely risky. Nevertheless, some users claim to use certain combinations successfully.

Subarachnoid hemorrhage is an extremely serious condition in which a neural membrane is breached and the brain itself is compromised. The onset is sudden, described as "the worst headache of one's life," and many grave symptoms follow. Adrenergic storm is often present among these symptoms, and is responsible for some of the dangers, both long-term and short, of subarachnoid hemorrhage adrenergic storm, through a complex cascade of processes starting with the movement of subarachnoid blood into the brain. Apparently, as the intracranial pressure increases, the brain is squeezed and catecholamines are forced out of their vesicles into the synapses and extracellular space.[19]

Rare causes

Rarely, a pheochromocytoma (tumor of the medullar tissue of the adrenal glands, which are located anterior to the kidney), may result in an adrenergic storm.[20] This type of tumor is not common to begin with, and furthermore, the subtype that can cause massive adrenaline release is rarer still. Patients with pheochromocytoma can unexpectedly fly into a rage or sink into trembling fear, possibly dangerous to themselves and others as their judgment is impaired, their senses and pain threshold are heightened, and the level of the adrenaline in their bloodstream is more than most people ever experience; pheochromocytoma can, very rarely, kill by internal adrenaline overdose.[21] But overall, adrenergic storm is an uncommon but certainly not rare phenomenon associated with the also uncommon condition of pheochromocytoma.[22]

Diagnosis

Differential diagnosis

Because the adrenergic storm overlaps with so many other similar conditions, such as hypertensive crises, stimulant intoxication or overdose, or even panic attack, and because the treatments for these overlapping conditions are largely alike, it is not necessary to obtain a differential and definitive diagnosis before initiating treatment. However, analysis of the patient's medical history, checked against the possible causes of the adrenergic storm such as those above, should be done, because some adrenergic storms can be caused by serious underlying conditions.[10] If a patient has an adrenergic storm and all or most of the other factors are ruled out, the adrenergic storm could lead to the discovery of a pheochromocytoma, which can become malignant. However, not all cases of adrenergic storm have an identifiable cause. Like a seizure, sometimes a patient has a single one, or perhaps a few, and then does not for the rest of their life.[23] The mechanisms of idiopathic adrenergic storm are very poorly understood.

Serotonin syndrome, in which an excess of serotonin in the synapses causes a similar crisis of hypertension and mental confusion, could be confused with an adrenergic storm. Serotonin, being a tryptamine (non-catecholamine) involved in higher brain functions, can cause dangerous hypertension and tachycardia from its effects on the sympathetic nervous system.[23] Symptoms caused by excessive adrenergic signalling can occur alongside those of serotonergic signalling. One example would be: overdose of drug(s) influencing multiple targets including serotonin, and adrenergic systems, with concurrent MAOI use). Abnormal echocardiograms, or chest pain are indicative of adrenergic crisis.[23] On the other hand, uncontrollable slow, rhythmic, and/or jerky movements, contractions and tension-often in every part of the body, dangerously high fever, eye rolling, and bruxism are more indicative of serotonin syndrome.[10][24]

Treatment

If there is evidence of overdose or it is suspected, the patient should be given gastric lavage, activated charcoal, or both; this could make the difference between life and death in a close situation.[25] It can however aggravate the patient which should be taken into account.[10]

The first line treatments are diazepam and a non-selective beta blocker; other antihypertensive drugs may also be used. It is important to note that not all benzodiazepines and beta blockers are safe to use in an adrenergic storm; for instance, alprazolam and propranolol;[10] alprazolam weakly agonizes dopamine receptors and causes catecholamine release while propranolol mildly promotes some catecholamine release - each worsening the condition.[23]

Antipsychotics are also used to treat the psychiatric symptoms such as aggression, agitation, psychosis, paranoia or anxiety. Originally, the use of antipsychotics was discouraged because of their potential to prolong the QT interval;[3] however, newer research has revealed that their careful use does not carry the potential for any significant side effects and today their judicious use is encouraged.[3][2][4][26]

Adrenergic storms are often idiopathic in nature; however if there is an underlying condition, then that must be addressed after bringing the heart rate and blood pressure down.[1]

See also

References

  1. 1 2 King, Andrew; Dimovska, Mirjana; Bisoski, Luke (24 February 2018). Oparil, Suzanne (ed.). "Sympathomimetic toxidromes and other pharmacological causes of acute hypertension". Current Hypertension Reports. Basingstoke, United Kingdom: Springer Nature. 20 (1): 8. doi:10.1007/s11906-018-0807-9. ISSN 1522-6417. OCLC 46464855. PMID 29478133. S2CID 3530495.
  2. 1 2 Malashock, Hannah R.; Yeung, Claudia; Roberts, Alexa R.; Snow, Jerry W.; Gerkin, Richard D.; O'Connor, Ayrn D. (13 January 2021). Mycyk, Mark B.; Chai, Peter (eds.). "Pediatric Methamphetamine Toxicity: Clinical Manifestations and Therapeutic Use of Antipsychotics—One Institution's Experience". Journal of Medical Toxicity. Phoenix, Arizona, United States of America: American College of Medical Toxicology (ACMT)/Springer. 17 (2): 168–175. doi:10.1007/s13181-020-00821-4. ISSN 1556-9039. OCLC 163567183. PMC 8017059. PMID 33442836.
  3. 1 2 3 Connors, Nicholas J.; Alsakha, Ahmed; Larocque, Alexandre; Hoffman, Robert S.; Landry, Tara; Gosselin, Sophie (1 October 2019). White, J. Douglas; Brady, William J. (eds.). "Antipsychotics for the treatment of sympathomimetic toxicity: A systematic review". The American Journal of Emergency Medicine. Amsterdam, Netherlands: Elsevier. 37 (10): 1880–1890. doi:10.1016/j.ajem.2019.01.001. ISSN 0735-6757. OCLC 08996781. PMID 30639129. S2CID 58631990 – via ScienceDirect.
  4. 1 2 Richards, John R.; Derlet, Robert W. (10 December 2019). White, J. Douglas; Brady, William J. (eds.). "Another dogma dispelled? Antipsychotic treatment of sympathomimetic toxicity". The American Journal of Emergency Medicine. Amsterdam, Netherlands: Elsevier. 37 (12): 2256–2257. doi:10.1016/j.ajem.2019.05.013. ISSN 0735-6757. OCLC 08996781. PMID 31088749. S2CID 155090660. Retrieved 28 July 2021 – via ScienceDirect.
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  6. ↑ Connors, Nicholas J.; Alsakha, Ahmed; Larocque, Alexandre; Hoffman, Robert S.; Landry, Tara; Gosselin, Sophie (1 December 2019). White, J. Douglas; Brady, William J. (eds.). "Evidence over dogma and anecdotes". The American Journal of Emergency Medicine. Amsterdam, Netherlands: Elsevier. 37 (12): 2257. doi:10.1016/j.ajem.2019.05.014. ISSN 0735-6757. OCLC 08996781. PMID 31128936. S2CID 167206288. Retrieved 28 July 2021.
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  12. ↑ von Braun, Ammrei; Bühler, Annette; Yuen, Bernd (31 March 2011). Prisco, Domenico (ed.). "Severe thyrotoxicosis: a rare cause of acute delirium" (PDF). Internal and Emergency Medicine. Rome, Italy: Italian Society of Internal Medicine (Società Italiana di Medicina Interna)/Springer. 7 (Supplement 1): S27–S28. doi:10.1007/s11739-011-0572-0. ISSN 1828-0447. OCLC 889552819. PMID 21451989. S2CID 207310201.
  13. ↑ Mayersohn, Michael; Guentert, Theodor W. (1 November 1995). "Clinical pharmacokinetics of the monoamine oxidase-A inhibitor moclobemide". Clinical Pharmacokinetics. Amsterdam, Netherlands: Springer. 29 (5): 292–332. doi:10.2165/00003088-199529050-00002. ISSN 0312-5963. PMID 8582117. S2CID 25628650.
  14. ↑ Lombard, J.; Wong, B.; Young, J. H. (1 April 1988). Wilkes, Michael (ed.). "Acute renal failure due to rhabdomyolysis associated with cocaine toxicity". Western Journal of Medicine. London, United Kingdom: BMJ Group (British Medical Association. 148 (4): 466–468. ISSN 0093-0415. LCCN 75642547. OCLC 1799362. PMC 1026152. PMID 3388853.
  15. ↑ O'Connor, Ayrn D.; Padilla-Jones, Angie; Gerkin, Richard D.; Levine, Michael (1 June 2015). Mycyk, Mark B.; Greller, Howard (eds.). "Prevalence of Rhabdomyolysis in Sympathomimetic Toxicity: a Comparison of Stimulants". Journal of Medical Toxicity. Phoenix, Arizona, United States of America: American College of Medical Toxicology (ACMT)/Springer. 11 (2): 195–200. doi:10.1007/s13181-014-0451-y. ISSN 1556-9039. OCLC 163567183. PMC 4469713. PMID 25468315.
  16. ↑ Jones, Chris; Owens, Dave (1 June 1996). Dawson, Deborah; Bench, Suzanne (eds.). "The recreational drug user in the intensive care unit: A review". Intensive and Critical Care Nursing. London, United Kingdom: British Association of Critical Care Nurses/Elsevier. 12 (3): 126–130. doi:10.1016/S0964-3397(96)80418-6. ISSN 0964-3397. OCLC 173733887. PMID 8717812.
  17. ↑ Gupta, Anish; Omender, Singh; et al. (Foreword by Fahrad N. Kapadia) (31 May 2019). "Chapter 8: Sympathomimetic Drugs". In Singh, Omender; Juneja, Deven (eds.). Principles and Practice of Critical Care Toxicology. New Delhi, India: Jaypee Brothers Medical Publishers. p. 84. ISBN 9789352706747 – via Google Books.
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  19. ↑ Rodman, Karen A.; Awad, Issam A. (1993). "CHAPTER 2: Clinical Presentation". In Awad, Isam A.; Barrow, Daniel L.; Miller, Linda S. (eds.). Cuerrent Management of Cerebral Aneurysms. Neurosurgical Topics. Vol. 15. Rolling Meadows, Illinois, United States of America: AANS Publications Committee (American Association of Neurological Surgeons (AANS)). pp. 21–43. ISBN 9781879284425 – via Google Books.
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  21. ↑ Whalen, Raymond K.; Althausen, Alex F.; Daniels, Gilbert H. (1 January 1992). Smith Jr., Joseph A.; Chai, Toby C.; Kaufman, Melissa R.; Clark, Peter E.; Klotz, Laurence (eds.). "Extra-adrenal pheochromocytoma". The Journal of Urology. Linthicum, Maryland, United States of America: American Urological Association (American Urological Association Education and Research, Inc.). 147 (1): 1–10. doi:10.1016/s0022-5347(17)37119-7. ISSN 0022-5347. OCLC 01754854. PMID 1729490.
  22. ↑ Manger, William M. (7 September 2006). Braaten, Douglas; Lo, Patrick C.; Murphy, Anar; Bohall, Steven E. (eds.). "An overview of pheochromocytoma: History, current concepts, vagaries, and diagnostic challenges". Annals of the New York Academy of Sciences. New York City, New York, United States of America: The New York Academy of Sciences/John Wiley & Sons, Inc. 1073 (1): 1–20. Bibcode:2006NYASA1073....1M. doi:10.1196/annals.1353.001. ISSN 0077-8923. LCCN 12037287. OCLC 01306678. PMID 17102067. S2CID 21423113. Retrieved 28 July 2021 – via Wiley Online Library.
  23. 1 2 3 4 Williams, Robert H.; Erickson, Timothy; Broussard, Larry A. (1 September 2000). Bertholf, Roger L. (ed.). "Evaluating sympathomimetic intoxication in an emergency setting". Laboratory Medicine. Chicago, Illinois, United States of America: American Society for Clinical Pathology (ASCP)/Oxford University Press. 31 (9): 497–508. doi:10.1309/WVX1-6FPV-E2LC-B6YG. OCLC 423776763.
  24. ↑ Vizcaychipi, Marcela P. (8 December 2007). Hemmings, Hugh C. (ed.). "Serotonin Syndrome triggered by Tramadol". BJA: British Journal of Anaesthesia. Oxford, United Kingdom: Oxford University Press/The British Journal of Anaesthesia Ltd. 99 (Supplement 8): 919. doi:10.1093/bja/el_2126. ISSN 0007-0912. OCLC 01537271. PMID 18006535. Retrieved 28 July 2021.
  25. ↑ Hughes, Joshua D.; Rabinstein, Alejandro A. (1 June 2014). Diringer, Michael N.; Wijdicks, Eelco F. (eds.). "Early diagnosis of paroxysmal sympathetic hyperactivity in the ICU". Neurocritical Care. Chicago, Illinois, United States of America: Neurocritical Care Society/Springer. 20 (3): 454–459. doi:10.1007/s12028-013-9877-3. ISSN 1541-6933. OCLC 909921680. PMID 23884511. S2CID 6433256. Retrieved 28 July 2021.
  26. ↑ Jerry, Jason; Collins, Gregory; Streem, David (10 April 2012). Mandell, Brian F.; Batur, Pelin; Nielsen, Craig; Studer, Peter G.; Cusick, Mary T. (eds.). "The emerging 'incense' and 'bath salt' phenomenon" (PDF). Cleveland Clinic Journal of Medicine. Lyndhurst, Ohio, United States of America: The Cleveland Clinic Foundation. 79 (4): 258–264. doi:10.3949/ccjm.79a.11147. ISSN 0891-1150. LCCN 87640278. OCLC 14576751. PMID 22473725. S2CID 40623460. Archived from the original (PDF) on 21 April 2021.
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