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Case report

Thyrotoxicosis-Induced Cardiogenic Shock with Encephalopathy and Acute Respiratory Distress: A Case Report and Literature Review


Thyrotoxicosis-induced cardiomyopathy and cardiogenic shock (CS) can lead to sudden mortality in adults. Hemodynamic instability and collapse occur due to functional alterations in both peripheral circulation and myocardium. Thyroid storm (TS) increases preload and decreases afterload along with an increase in cardiac contractility and heart rate leading to high output acute failure. We present a case of a 30-year-old female who presented with a complaint of watery diarrhea and dehydration for almost a week. At her visit to the emergency room, she was unresponsive with hemodynamic collapse leading to altered mental status and tachycardia. The computed tomography (CT) scan of head was non-contributory. The condition worsened with respiratory distress, and eventually, mechanical ventilation with intubation was completed. Further, laboratory workup showed acute thyrotoxicosis. The severe cardiomyopathy on echocardiography with compromised left ventricle function and diffuse pulmonary congestion led to acute respiratory distress syndrome (ARDS). The multi-organ failure, impending ARDS and CS with encephalopathy led to the sudden death of a patient within 24 hours of intensive care unit (ICU) stay before even extracorporeal membrane oxygenation (ECMO) could be started.


Thyrotoxic cardiomyopathy (TCM) is an uncommon presentation in hyperthyroid patients. TCM has been reported in 6% of hyperthyroidism cases, with less than 1% developing dilated cardiomyopathy (DCM) and severe left ventricular dysfunction [1]. The effects of thyroid hormone at the cellular level may cause alterations of peripheral circulation by interacting with the sympathetic nervous system [2].

Case Presentation

We present a case of a 30-year-old female who presented with a complaint of watery diarrhea for almost one week. She went to a primary care physician with a complaint of watery stools, wherein she presented with an elevated heart rate of >200 beats per minute. The patient was transferred to an emergency room with an altered mental status, unresponsiveness, and hemodynamic instability. We initiated fluid resuscitation and gave her procainamide for arrhythmia or tachycardia with heart rate >200 per minute. Afterward, her heart rate decreased to around 170 beats per minute. However, she was subsequently on continuous positive airway pressure (CPAP) in the setting of acute respiratory distress. Considering the worsening of respiratory distress despite being on CPAP, the patient was intubated. She also required vasopressor support, including dobutamine, norepinephrine, and vasopressin. The neurological assessment revealed diffuse hyperreflexia. The computed tomography (CT) scan was non-contributory. Chest X-ray showed pulmonary vascular congestion with right pleural effusion and cardiomegaly (Figure 1).

Electrocardiogram on admission showed atrial flutter with right axis deviation, incomplete right bundle branch block, and ST elevation indicative of septal ischemia (Figure 2). 

The elevated troponins with delta trend pushed further diagnostic workup. Echocardiography (ECHO) showed an ejection fraction of 10% to 15%, global hypokinesis, and dilated left ventricle with small pericardial effusion (Figure 3).

The patient was brought to the cardiac catheterization lab emergently for mechanical circulatory support. Due to the elevated lactic acid levels and mixed acidosis on arterial blood gas (ABG), we started her on broad-spectrum empiric antibiotics. The serum ammonia and procalcitonin levels were within normal limits. Continuous renal replacement therapy (CRRT) initiated due to worsening acute kidney injury and hyperkalemia secondary to thyrotoxicosis induced rhabdomyolysis. The laboratory investigations are shown in Table 1.

Laboratory Variables Findings Normal Values
Serum Sodium (Na)   132 mEq/L 135-145 mEq/L
Serum Potassium (K)   6.7 mEq/L 3.5-5.0 mEq/L
Serum Chloride   101 mEq/L 98-108 mEq/L
Serum Bicarbonate (HCO3) 13 mEq/L   21-32 mEq/L
Anion Gap   18 mEq/L 5-14 mEq/L
Serum Total Calcium (Ca) 7.2 mg/dl   8.5-10.1 mg/dl
Serum Magnesium (Mg)   2.3 mg/dl 1.8-2.4mg/dl
Blood Glucose   79 mg/dl 70-100 mg/dl
Serum Creatinine (Cr)   2.3 mg/dl 0.6-1.1 mg/dl
Glomerular Filtration Rate (GFR)   25 mL/min/1.73 m2 =/>60 mL/min/1.73 m2
Blood Urea Nitrogen (BUN) 53 mg/dl 7-18 mg/dl  
Total Creatinine Kinase (CK)   2141 U/L 26-192 U/L
Alanine Aminotransferase (ALT)   1944 U/L 12-78 U/L
Aspartate Aminotransferase (AST)   5336 U/L 15-37 U/L
Alkaline Phosphatase (ALP)   235 U/L 45-117 U/L
Total Bilirubin   4.3 mg/dl 0.2-1 mg/dl
Bilirubin Direct 3.3 mg/dl 0.0-0.2 mg/dl  
Albumin   2.7 g/dl 3.1-4.5 g/dl
Procalcitonin   0.06 nanogram/milliliter (ng/ml) 0.15 ng/mL or less
Thyroid Stimulating Hormone (TSH)    <0.005 milliunits per liter (mU/L) 0.358-3.740 (mU/L)
Free Triiodothyronine (fT3)   >30 ng/dl 2.18-3.98 ng/dl
Free Thyroxine (fT4) >8.00 ng/dl 0.76-1.46 ng/dl

She suffered from multi-organ failure and sepsis with elevated levels of liver function enzymes. Thionamides were discontinued after the development of acute transaminitis. She was treated with hydrocortisone 100 mg every intravenous (IV) eight hours, potassium iodide five drops every six hours, and cholestyramine IV 4 g every eight hours.

There were multifaceted management plans under consideration at that stage ranging from extracorporeal membrane oxygenation (ECMO), intra-aortic balloon pump (IABP), and left the ventricular assisted device (LVAD). Unfortunately, the patient coded blue and lost pulse during heart catheterization for IABP. Cardiopulmonary resuscitation (CPR) was done for 30 minutes without the return of spontaneous circulation (ROSC). The decision to stop CPR was made by her family, the primary service, and the consulting cardiology team.


Heart failure is an unusual presentation of hyperthyroidism and can only occur in 6% of cases. About 50% of such cases come under the sub-group of high output failure with preserved ventricular ejection fractions (>50%). TCM cases are also highly associated with coexisting atrial fibrillation [1]. Cardiogenic shock (CS) is a rare complication of thyroid storm (TS), and minimal data exists on its incidence and outcomes. Mohananey D et al. mentioned some of the preluding factors for thyrotoxicosis-induced CS. These include preexisting congestive heart failure, valvular disorders, atrial fibrillation, coagulopathy, alcohol or drug abuse, fluid and electrolyte disorders, liver, renal or pulmonary disorders, and weight loss as compared to those without CS [2]. The decreased contractile reserve with impaired left ventricular filling might contribute to CS with encephalopathy [3]. The pathophysiology of TCM is unclear and complicated in literature. It is multifactorial with both the toxicogenic effects of thyroid hormones and hyperdynamic cardiogenic stress [4]. However, antithyroid treatment has shown to reverse the cardiomyopathy effects of thyrotoxicosis [5-6].

In a recent study by Smith et al., the disappearance of cardiovascular outcomes with the achievement of euthyroid state after treatment was observed in patients with long-term subclinical hyperthyroidism [7]. We tried thionamides but discontinued later due to the development of acute transaminitis in the setting of sepsis. Kim S et al. reported the reversibility of TCM-associated reduced ejection fraction to almost normal after venous-arterial ECMO [8]. Unfortunately, in our case, the patient expired before getting ECMO from hemodynamic collapse. The management of hyperthyroidism associated with acute heart failure is complicated. It demands invasive monitoring with circulatory support. Some patients might lead to CS despite the reversible nature of TCM with aggressive treatment [8-9]. Therefore, early recognition and successful treatment of cardiac symptoms in patients with hyperthyroidism are essential.

The limitation in our case was time; the patient went to ARDS and cardiogenic shock with encephalopathy within 24 hours. The aggressive progression of TCM leaves us with a dilemma of realizing the gravity of the problem. The life-saving and multi-modal interventions like IABP or ECMO should be initiated earlier in such cases within 24 hours of impending ARDS. Besides, owing to time constraints, brain magnetic resonance imaging (MRI) could not be performed to detect a white matter or profound structural changes missed by CT scan. 


The mortality associated with TCM is sudden and includes a series of irreversible events. Our patient developed TCM with CS and encephalopathy despite exhausting all conventional resuscitative measures. Hyperthyroid states induce multi-organ failure including heart, hepatic, and renal failure along with lactic acidosis. Further studies should be done to evaluate the pathogenesis of TCM leading to the development of the least-invasive, safe, and definitive treatment options. 


  1. Siu CW, Yeung CY, Lau CP, Kung AW, Tse HF: Incidence, clinical characteristics and outcome of congestive heart failure as the initial presentation in patients with primary hyperthyroidism. Heart. 2007, 93:483-7. 10.1136/hrt.2006.100628
  2. Mohananey D, Smilowitz N, Villablanca PA, et al.: Trends in the incidence and in-hospital outcomes of cardiogenic shock complicating thyroid storm. Am J Med Sci. 2017, 354:159-164. 10.1016/j.amjms.2017.04.017
  3. Biondi B: Mechanisms in endocrinology: heart failure and thyroid dysfunction. Eur J Endocrinol. 2012, 167:609-18. 10.1530/EJE-12-0627
  4. Vydt T, Verhelst J, De Keulenaer G: Cardiomyopathy and thyrotoxicosis: tachycardiomyopathy or thyrotoxic cardiomyopathy?. Acta Cardiol. 2006, 61:115-7. 10.2143/AC.61.1.2005149
  5. Khandwala HM: A case of congestive heart failure due to reversible dilated cardiomyopathy caused by hyperthyroidism. South Med J. 2004, 97:1001-3. 10.1097/01.SMJ.0000125100.10857.54
  6. Forfar JC, Muir AL, Sawers SA, Toft AD: Abnormal left ventricular function in hyperthyroidism: evidence for a possible reversible cardiomyopathy. N Engl J Med. 1982, 307:1165-70. 10.1056/NEJM198211043071901
  7. Smit JW, Eustatia-Rutten CF, Corssmit EP, et al.: Reversible diastolic dysfunction after long-term exogenous subclinical hyperthyroidism: a randomized, placebo-controlled study. J Clin Endocrinol Metab. 2005, 90:6041-7. 10.1210/jc.2005-0620
  8. Smit JW, Eustatia-Rutten CF, Corssmit EP, et al.: Thyrotoxicosis induced cardiogenic shock rescued by extracorporeal membrane oxygenation. J Geriatr Cardiol. 2018, 15:203-4. 10.11909/j.issn.1671-5411.2018.02.003
  9. Hsu LM, Ko WJ, Wang CH: Extracorporeal membrane oxygenation rescues thyrotoxicosis-related circulatory collapse. Thyroid. 2011, 21:439-441. 10.1089/thy.2010.0230
Case report

Thyrotoxicosis-Induced Cardiogenic Shock with Encephalopathy and Acute Respiratory Distress: A Case Report and Literature Review

Author Information

Abdul Rana

Internal Medicine, Joan C. Edwards School of Medicine, Marshall University, Huntington, USA

Salman Assad Corresponding Author

Neurology and Neurosurgery, Joan C. Edwards School of Medicine, Marshall University, Huntington, USA

Mahmoud Abuzaid

Internal Medicine, Joan C. Edwards School of Medicine, Marshall University, Huntington, USA

Ashar Farooqi

Neurology, Joan C. Edwards School of Medicine, Marshall University, Huntington, USA

Justin Nolte

Neurology, Joan C. Edwards School of Medicine, Marshall University, Huntington, USA

Ethics Statement and Conflict of Interest Disclosures

Human subjects: Consent was obtained by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Case report

Thyrotoxicosis-Induced Cardiogenic Shock with Encephalopathy and Acute Respiratory Distress: A Case Report and Literature Review

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