Bühler, Annette

von Braun, Amrei

Yuen, Bernd

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CE - LETTER TO THE EDITORSevere thyrotoxicosis: a rare cause of acute deliriumAmrei von Braun • Annette Bu¨hler •Bernd YuenReceived: 22 November 2010 / Accepted: 16 March 2011 / Published online: 31 March 2011 SIMI 2011Dear Sirs,A 56-year old woman presented to the emergency depart-ment (ED) with acute delirium ongoing since the previousday. Her family had initially contacted the general practi-tioner on call the night before. He found her agitated,confused and delirious. Being unfamiliar with her medicalhistory, he diagnosed an acute psychosis, and admitted herto the nearby psychiatric clinic for further treatment. Dueto the patients considerable aggression, it was impossible toimplement any kind of diagnostic procedures there, whichled to the referral to our clinic. On examination in the ED,the patient showed severe hyperactive delirium, exoph-thalmus, wasting (BMI 17 kg/m2), and a diffuse goitre. Thevital signs included: a body temperature 38.2C, bloodpressure 120/70 mmHg, heart rate 124 beats/min. As herfamily doctor later reported, she was diagnosed withGraves’ disease 30 years prior, and a subtotal thyroidec-tomy had been performed. Even after extensive search, nomedical report could be found on the exact type of surgicaltreatment. Shortly after surgical treatment, thyreostatictherapy for recurrence of the hyperthyroidism had to bere-implemented. Due to ‘‘intolerance of the medication,’’our patient subsequently stopped thyreostatic treatment,and refused any therapy, except homeopathic tablets tocontrol thyroid function. The laboratory tests on admissionshowed a severe hyperthyroidism (TSH \0.05 mlU/l, freeT4 60 pmol/l) and a mild leucocytosis of 12,200/ul, whilethe C-reactive protein was not elevated. With the diagnosisof acute delirium associated with thyrotoxicosis, the patientwas admitted to the ICU. In order to start thyreostatictherapy, high dose parenteral sedation for the first 24 h wasnecessary. Her therapy then consisted of 45 mg thiamazolper day, 20 mg propranolol administered every 8 h and200 mg hydrocortison per day. Four days after admission,she was transferred to the medical ward, her thyroidfunction had improved considerably with a free T4 of18.4 pmol/l. She was less confused, able to followinstructions and participate in conversations. The furtherclinical course was favourable with an uncomplicated totalthyroidectomy performed after 3 months of medicallywell-controlled thyroid function. Radioiodine as a treat-ment option was considered, but, because of the endocrineorbitopathy, although inactive, and the patient preference,was abandoned in the end.Our patient fulfilled the criteria for the diagnosis of a‘‘thyroid storm’’ introduced by Burch and Wartofsky [1].The most common underlying cause of this rare conditionis, as in our case, Graves’ disease, and mortality rates rangefrom 20 to 30% [2]. A challenge lies in early diagnosis andappropriate treatment of this medical emergency in order toprevent catastrophic outcomes up to multiple-organ failure.Most cases of thyroid storm occur following a precipitatingevent or intercurrent illness such as thyroid or non-thyroidalsurgery, trauma, infection, or an acute iodine load [3].Patients suffering from severe thyrotoxicosis frequentlypresent with psychiatric symptoms ranging from depressionto acute psychosis [4]. In contrast to the broad range ofliterature on psychosis in association with hypothyroidism,A. von BraunClinic for Internal Medicine, Buelach Hospital,8180 Buelach, SwitzerlandA. Bu¨hlerDivision of Endocrinology, Buelach Hospital,8180 Buelach, SwitzerlandB. Yuen (&)Interdisciplinary Intensive Care Unit, Buelach Hospital,8180 Buelach, Switzerlande-mail: bernd.yuen@spitalbuelach.ch123Intern Emerg Med (2012) 7 (Suppl 1):S27–S28DOI 10.1007/s11739-011-0572-0such as the well-known ‘‘myxoedema madness’’, little canbe found on delirium associated with hyperthyroidism.Psychological symptoms presented by patients with thyro-toxic crisis include depressive, manic, paranoid and schi-zoid features. In an emergency medicine setting patientsadmitted to the hospital with acute delirium are common[5]. When handling such a case it is essential to rule outunderlying somatic causes before assuming an intrinsicpsychiatric disorder (Table 1). Besides a profound generaland neurological examination, effective diagnostic mea-sures include laboratory testing to screen for fluid orelectrolyte disturbances, infections or sepsis, the with-drawal from alcohol or drugs, and the search for metabolicdisorders such as hypoglycemia, hypercalcemia, uremia,liver failure and, last but not least, thyrotoxicosis. Furtherdiagnostic procedures such as lumbar puncture, EEG andneuroimaging may be necessary if no cause is apparent, or ifthe delirium does not improve despite seemingly appro-priate treatment.Our patient was sent to a psychiatric clinic beforeunderlying somatic conditions were ruled out because thephysician involved was unfamiliar with the clinical pictureof ‘‘thyroid storm’’ and routine laboratory tests did notinclude thyroid function. Concerning the clinical picture,we consider the clinical criteria offered by Burch andWartofsky to be helpful for emergency physicians. Yet,with regard to the realities of working in an ED setting, wefirst and foremost propose to routinely check thyroidfunction in patients with acute delirium in order to preventmissing this potentially fatal but treatable condition. Afterestablishing the diagnosis of severe thyrotoxicosis, thepatient should undergo immediate emergency therapy withvigourous intravenous fluid replacement, and treatment ofhyperthermia as well as all supportive measures. Addi-tionally, a multidrug approach with several targets is vitallyimportant; thyreostatic therapy to stop the synthesis of newhormone within the thyroid gland, corticosteroids for pre-venting conversion of T4–T3 and Beta-adrenergic blockadefor controlling adrenergic symptoms [3]. Thus, early rec-ognition and prompt implementation of all the treatmentmodalities is essential for successful management of life-threatening thyrotoxicosis.Conflict of interest None.References1. Burch HB, Wartofsky L (1993) Life-threatening thyrotoxicosis.Thyroid storm. Endocrinol Metab Clin North Am 22:263–2772. Sarlis NJ, Gourgiotis L (2003) Thyroid emergencies. Rev EndocrMetab Disord 4:129–1363. Nayak B, Burman K (2006) Thyrotoxicosis and thyroid storm.Endocrinol Metab Clin North Am 35:663–6864. Brownlie BEW, Rae AM, Walshe JWB, Wells JE (2000)Psychoses associated with thyrotoxicosis—‘thyrotoxic psychosis’.A report of 18 cases, with statistical analysis of incidence. Eur JEndocrinol 142:438–4445. Han JH, Shintani A, Eden S et al (2010) Delirium in theEmergency Department: an independent predictor of death within6 months. Ann Emerg Med 56:244–252Table 1 Common causes of delirium and confusional states Adoptedby 2010 uptodate, online version 18.1Drugs and toxinsPrescription drugs: i.e. Opioids, sedatives–hypnotics,antipsychotics etc.Drugs of abuse: i.e. ethanol, heroin, hallucinogensWithdrawal states: i.e. ethanol, benzodiazepinesMedication side effects: i.e. hyperammonemia from valproic acid,serotonin syndromeInfectionsSepsisSystemic infections; fever related deliriumMetabolic derangementsElectrolyte disturbance: elevated or decreased (sodium, calcium,magnesium)Endocrine disturbance: depressed or increased (thyroid,parathyroid, adrenal, pituitary)Hyperglycemia and hypoglycemiaHyperosmolar and hypoosmolar statesHypoxemia and hypercarbiaInborn errors of metabolism: i.e. Wilson’s disease etc.Nutritional: i.e. Wernicke’s encephalopathy, vitamin B12deficiencyBrain disordersCNS infections: encephalitis, meningitis, brain or epiduralabscessEpileptic seizures, non-convulsive status epilepticusHead injuryHypertensive encephalopathyPsychiatric disordersSystemic organ failureCardiac, renal or liver failure; acute or chronicHematologic disordersPhysical disordersHypo-, HyperthermiaBurns, Trauma with SIRSS28 Intern Emerg Med (2012) 7 (Suppl 1):S27–S28123

Severe thyrotoxicosis: a rare cause of acute delirium

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Severe thyrotoxicosis: a rare cause of acute delirium

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