Annals of African Medicine
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Year : 2023  |  Volume : 22  |  Issue : 3  |  Page : 392-394  

Psychosis following caffeine consumption in a young adolescent: Review of case and literature

1 Department of Paediatrics, Alliance Hospital, Abuja; Faculty of Paediatrics, National Postgraduate Medical College of Nigeria, Lagos, Nigeria; Department of Maternal and Child Health, School of Public Health, James Lind Institute, Geneva, Switzerland
2 Department of Psychiatry, Federal Medical Centre, Keffi, Nasarawa State, Nigeria
3 Department of Ophthalmology, Alliance Hospital, Abuja, Nigeria
4 Department of Paediatrics, Alliance Hospital, Abuja, Nigeria

Date of Submission30-Jan-2022
Date of Decision18-May-2022
Date of Acceptance17-Jun-2022
Date of Web Publication4-Jul-2023

Correspondence Address:
Qadri Adebayo Adeleye
Department of Paediatrics, Alliance Hospital, Abuja

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aam.aam_28_22

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Caffeine, a popular over-the-counter methylxanthine, is widely consumed for its potent psychoactive properties. Toxicity generally occurs with intentional overdose and is often multisystemic and life-threatening. Consumption by children is rarely planned, and safe doses are potentially toxic in them. A 12-year-old boy whose parents had denied him coffee on several occasions eventually had access to it. The caffeine dose ingested was sub-toxic although he developed severe and life-threatening multisystemic caffeinism. Following ingestion, he became aggressive and was talking irrationally, with visual and auditory hallucinations. In addition, he had severe abdominal pain, multiple vomiting episodes, circulatory collapse, hypertension, angioedema, dysfunctional tear syndrome, hyperglycemia, ketonuria, hypokalemia, and metabolic acidosis. The clinical presentation, laboratory findings, and interventions are reviewed and discussed. Besides routine immunization, routine anticipatory guidance should be at the center of preventive pediatrics. Packaging of caffeinated beverages should also target the prevention of caffeine toxicity in children.
La caféine, une méthylxanthine en vente libre populaire, est largement consommée pour ses puissantes propriétés psychoactives. La toxicité se produit généralement avec surdosage intentionnel et est souvent multisystémique et potentiellement mortelle. La consommation par les enfants est rarement planifiée et les doses sûres sont potentiellement toxique chez eux. Un garçon de 12 ans dont les parents lui avaient refusé du café à plusieurs reprises a fini par y avoir accès. La caféine la dose ingérée était sub toxique bien qu'il ait développé un caféinisme multisystémique grave et menaçant le pronostic vital. Suite à l'ingestion, il est devenu agressif et parlait de manière irrationnelle, avec des hallucinations visuelles et auditives. De plus, il avait de fortes douleurs abdominales, des vomissements multiples épisodiques, collapsus circulatoire, hypertension, œdème de Quincke, syndrome lacrymal dysfonctionnel, hyperglycémie, cétonurie, hypokaliémie et troubles métaboliques acidose. La présentation clinique, les résultats de laboratoire et les interventions sont passés en revue et discutés. Outre la vaccination de routine, la routine le guidage préventif doit être au centre de la pédiatrie préventive. L'emballage des boissons contenant de la caféine devrait également cibler la prévention de la toxicité de la caféine chez les enfants.
Mots-clés: Conseils anticipatifs, caféine, toxicité potentiellement mortelle, toxicité paradoxale, organisme de réglementation, jeune ado

Keywords: Anticipatory guidance, caffeine, life-threatening toxicity, paradoxical toxicity, regulatory agency, young adolescent

How to cite this article:
Adeleye QA, Attama CM, Egbeobauwaye O, Angela O. Psychosis following caffeine consumption in a young adolescent: Review of case and literature. Ann Afr Med 2023;22:392-4

How to cite this URL:
Adeleye QA, Attama CM, Egbeobauwaye O, Angela O. Psychosis following caffeine consumption in a young adolescent: Review of case and literature. Ann Afr Med [serial online] 2023 [cited 2023 Sep 26];22:392-4. Available from:

   Introduction Top

Caffeine (1, 3, 7-trimethylxanthine) is commonly consumed by adults for its psychoactive properties.[1] It is a nonselective adenosine antagonist, a phosphodiesterase inhibitor, and a sympathomimetic agent. Typical over-the-counter (OTC) formulations include coffee, tea, chocolate, cola, cocoa, energy drinks, some OTC medicines, and appetite suppressants.[1] While intentional overdose is the most common cause of caffeinism in adults, inadvertent overdose is the most common cause in children. Safe caffeine doses have also been shown to be potentially toxic, especially in children.[2],[3]

To the best of our knowledge, there is no reported case of childhood caffeine toxicity in Africa.

   Case Report Top

A 12-year-old boy, who developed incoherent speech, aggressive behavior, and visual and auditory hallucinations, admitted to surreptitiously consuming his father's coffee [Figure 1] shortly before the onset of symptoms. Associated complaints include severe periumbilical abdominal pain, several vomiting episodes, chest pain, eye itching and pain, and lip swelling. The vomitus and stool had black tinges on the 1st day; the stool consistency was however normal. He was referred to our facility on the 3rd day of illness, even though vomiting had stopped a day earlier. There was no fever, headache, jaundice, bleeding diathesis, or convulsion. He had no complaints before ingesting the coffee. He was reported to have been diagnosed of peptic ulcer about 3 years previously. He is the first of three children. He concluded his primary education a month before, and his academic performance was above average. There was no record of abnormal behavior, suicidal attempts, or drug reactions. He was not on any routine medications.
Figure 1: Sample of coffee sachet ingested by the boy

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On arrival, his Glasgow Coma Score was 12. He was listless, restless, and pale. The capillary refill time was 3 s, oxygen saturation was 99% in room air, and the axillary temperature was 35.3°C. The pulse was 140 bpm, regular and small in volume, and the blood pressure was 130/80 mmHg (Stage I systolic hypertension). His abdomen was exquisitely tender, especially at the epigastrium and right hypochondrium. His body weight, after fluid resuscitation, was 34 kg. The following day, he became aggressive and incoherent in speech again, with visual and auditory hallucinations. The blood pressure at the time was 150/90 mmHg (Stage II systolic hypertension); it normalized without antihypertensives.

Significant laboratory findings include random blood glucose of 7.9 mmol/L, marginally reduced plasma bicarbonate (21 mmol/L), ketonuria, and hypersthenuria (1.030). Serum potassium, which was normal at presentation (4.0 mmol/L), became low on the 4th day (2.7 mmol/L). Other findings (full blood count, plasma sodium, plasma urea, plasma creatinine, clotting profile, hemoglobin phenotype, liver enzymes, serology for Helicobacter pylori and human immunodeficiency, hepatitis B and hepatitis C viruses, and abdominal ultrasonography) were not remarkable. The facility for serum and urine caffeine levels was not available to us.

A diagnosis of severe caffeine toxicity was made; the features were psychosis, abdominal pain, emesis, lethargy, hypertension, circulatory collapse, angioedema, dysfunctional tear syndrome (DTS), hyperglycemia, ketonuria, hypokalemia, and metabolic acidosis.

He responded well to fluid resuscitation, diazepam, acetaminophen, oral potassium chloride, promethazine, omeprazole, amoxicillin-clavulanate, metronidazole, and topical hydroxypropyl methylcellulose (artificial tears).

He understood the implication of what he did and promised not to repeat similar actions in the future. His parents were also counseled on critical preventive strategies. He was discharged on the 8th day of hospitalization and scheduled for upper gastrointestinal endoscopy; he however did not turn up.

   Discussion Top

Although data on safe caffeine doses in children are scant, a systematic review shows that 2.5 mg/kg body weight per day is generally tolerable in them.[4] While a serum caffeine concentration of 15 mg/L is toxic, a level of 80–100 mg/L is generally considered lethal.[5] The brand of coffee ingested by our patient contains 34 mg of caffeine/g.[6] Thus, he consumed 51 mg of caffeine, equivalent to 1.5 mg/kg body weight. His young age and caffeine-naivety could explain the adverse effect of such a subtoxic dose.[7] Paradoxical caffeinism in children has also been attributed to genetic factors, pharmacologic intolerance, and incomplete brain development.[7],[8]

Neurotoxicity is a cardinal component of caffeine toxidrome;[9] it results from interference with adenosine-mediated dopamine-dependent neurotransmission.[10] The half-life is up to 24 h;[11] yet our patient's neurotoxicity persisted until the 4th day. In a similar report by Omi,[12] the psychiatric symptoms of a 19-year-old adolescent female persisted until the 3rd day. Caffeine metabolites are believed to be responsible for such “hangover” effect.[12] This aligns with the notion that the intensity of caffeine-induced neurostimulatory effect does not correlate well with serum caffeine level.[13]

Other presenting features in our patient (abdominal pain, emesis, lethargy, circulatory collapse, tachycardia, hypertension, angioedema, DTS, hyperglycemia, ketonuria, hypokalemia, and metabolic acidosis) are well-documented in the literature as independent features of caffeinism.[14],[15],[16]

Currently, no specific antidote exists for caffeine poisoning;[17] the management is mainly supportive.[5] Activated charcoal binds avidly to methylxanthines, hence, a useful gastric decontaminant in the setting of caffeine toxicity.[5] We did not consider activated charcoal in our patient due to the lost window period.

Benzodiazepines are the first-line treatment options in caffeine neurotoxicity.[11] High doses are recommended due to caffeine's blockade of benzodiazepine receptors.[9] A 34-month-old Caucasian girl, who ingested 14.4 mg/kg of caffeine, suffered intractable seizures despite repeated doses of 2.2 mg/kg diazepam; pentobarbital was the last resort.[14] On the other hand, our patient responded to only two doses of low-dose diazepam (0.15 mg/kg). The difference may be related to age, race, and caffeine dose ingested. It may also suggest that benzodiazepines are only helpful in nonconvulsive caffeine-induced neurotoxicity.

Acetaminophen, which antagonizes caffeine at the site of action, has also been shown to be helpful in management.[18] Its use in our patients may have contributed to the favorable outcome.

In extreme situations, hemodialysis and peritoneal dialysis are employed as management modalities;[5],[14] we did not consider any of them necessary for our patient.

Regulatory agencies have a big role to play in preventing childhood caffeine toxicity. Beyond ensuring the amount of caffeine in a caffeinated beverage is written, authorities should also mandate manufacturers to clearly state the potential adverse effects of caffeine and warn against childhood access. Child-proof and child-resistant packaging should also be considered for caffeinated beverages.

   Conclusion Top

Similar to overdose, safe caffeine doses are potentially toxic in children. Our patient's ingestion of coffee stemmed from adolescent exploratory tendency. Hence, routine anticipatory guidance should be central to preventive pediatrics. Warning labels on caffeinated beverages should also caution against consumption by children.

Informed consent

The parent gave consent to publish the case, and the patient assented.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given their consent for images and other clinical information to be reported in the journal. The guardian understands that name and initials of the patient will not be published and due efforts will be made to conceal the patient's identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

   References Top

Quadra GR, Paranaíba JR, Vilas-Boas J, Roland F, Amado AM, Barros N, et al. A global trend of caffeine consumption over time and related-environmental impacts. Environ Pollut 2020;256:113343.  Back to cited text no. 1
Rivenes SM, Bakerman PR, Miller MB. Intentional caffeine poisoning in an infant. Pediatrics 1997;99:736-8.  Back to cited text no. 2
Beauchamp GA, Johnson AR, Crouch BI, Valento M, Horowitz BZ, Hendrickson RG. A retrospective study of clinical effects of powdered caffeine exposures reported to three US poison control centers. J Med Toxicol 2016;12:295-300.  Back to cited text no. 3
Wikoff D, Welsh BT, Henderson R, Brorby GP, Britt J, Myers E, et al. Systematic review of the potential adverse effects of caffeine consumption in healthy adults, pregnant women, adolescents, and children. Food Chem Toxicol 2017;109:585-648.  Back to cited text no. 4
Murray A, Traylor J. Caffeine toxicity. StatPearls Publishing. 2021. Available from: [Last accessed on 2022 Jul 3].  Back to cited text no. 5
Jeukendrup A. How much Caffeine is in Coffee?. Mysportscience; 2021. Available from: [Last accessed on 2021 Nov 12].  Back to cited text no. 6
Beauchamp G, Amaducci A, Cook M. Caffeine toxicity: A brief review and update. Clin Pediatr Emerg Med 2017;18:197-202.  Back to cited text no. 7
Reissig CJ, Strain EC, Griffiths RR. Caffeinated energy drinks – A growing problem. Drug Alcohol Depend 2009;99:1-10.  Back to cited text no. 8
Winston AP, Hardwick E, Jaberi N. Neuropsychiatric effects of caffeine. Adv Psychiatr Treat 2005;11:432-9.  Back to cited text no. 9
Cauli O, Morelli M. Caffeine and the dopaminergic system. Behav Pharmacol 2005;16:63-77.  Back to cited text no. 10
FitzSimmons CR, Kidner N. Caffeine toxicity in a bodybuilder. J Accid Emerg Med 1998;15:196-7.  Back to cited text no. 11
Omi T. Protracted effects of caffeine after hemodialysis for severe caffeine intoxication. Toxicol Commun 2021;5:73-5.  Back to cited text no. 12
Kitamura J, Miyabe H, Uenishi N, Kano H, Hirakawa A, Hara K, et al. Two cases of fatal caffeine poisoning. J Jpn Soc Emerg Med 2014;17:711-5.  Back to cited text no. 13
Walsh I, Wasserman GS, Mestad P, Lanman RC. Near-fatal caffeine intoxication treated with peritoneal dialysis. Pediatr Emerg Care 1987;3:244-9.  Back to cited text no. 14
Tognetti L, Murdaca F, Fimiani M. Caffeine as a cause of urticaria-angioedema. Indian Dermatol Online J 2014;5:S113-5.  Back to cited text no. 15
Amaechi OU, Savia J. The effect of caffeine on tear formation. J Niger Optom Assoc 2005;12:14-6.  Back to cited text no. 16
Carreon CC, Parsh B. How to recognize caffeine overdose. Nursing 2019;49:52-5.  Back to cited text no. 17
Deng JF, Spyker DA, Rall TW, Steward O. Reduction in caffeine toxicity by acetaminophen. J Toxicol Clin Toxicol 1982;19:1031-43.  Back to cited text no. 18


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