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Shock Thyroid in a Patient with Septic Shock: A Case Report and Literature Review

Shock thyroid is a rare manifestation of the CT hypotension complex and can be diagnosed when thyroid and perithyroidal edemas are observed on CT during the onset of shock. Shock thyroid can be a useful CT sign for decompensated shock. This condition is reversible and recovers rapidly with adequate treatment. We present the case of an 84-year-old female with septic shock, exhibiting CT features consistent with a shock thyroid. We also reviewed the clinical and radiological findings reported in the literature. The present case emphasizes that shock thyroid can be an early indicator of impending hemodynamic instability and has important prognostic and therapeutic implications.


INTRODUCTION
Shock thyroid is an uncommon part of the CT hypotension complex (1,2). Shock thyroid manifests as thyroid and perithyroidal edema, which is incidentally noted in CT of patients with shock conditions (1,2). To our knowledge, only seven cases have been reported in the literature (1,2), and because this disease is largely unknown to radiologists and clinicians, it is frequently underdiagnosed (2). The relationship between shock thyroids and poor prognosis remains unclear. However, shock itself is a life-threatening condition that can lead to multiple organ failure. Prompt diagnosis of shock is very im-J Korean Soc Radiol 2021;82 (5): [1328][1329][1330][1331][1332][1333] portant for proper treatment of the underlying condition. Thus, shock thyroid is a helpful imaging indicator to identify inadequate perfusion in patients with shock (1,2).
Here, we present the case of a female with septic shock secondary to Staphylococcus aureus bacteremia of unknown source, and conduct a comprehensive review of the literature.
Our study emphasizes that shock thyroid is not related to thyroid injury or primary disease, but is related to perfusion alterations. Shock thyroid must be distinguished from other pathologies of the thyroid gland to avoid unnecessary tests and to establish an appropriate treatment plan.

CASE REPORT
An 84-year-old incapacitated female with underlying Alzheimer's dementia presented to our emergency department with a chief complaint of fever. The patient had been admitted to our hospital 39 days previously, due to pulmonary thromboembolism and deep vein thrombosis. Her initial vital signs were as follows: blood pressure, 87/44 mm Hg; heart rate, 105 bpm; and body temperature, 38.2°. Laboratory analyses showed leukocytosis, elevated levels of C-reactive protein, and serum lactate level of 3.57 mmoL/L. Her clinical presentation was characterized by septic shock. Initial blood culture revealed methicillin-resistant Staphylococcus aureus bacteremia.
Approximately 4 hours after arriving at the emergency department, the patient underwent contrast-enhanced chest and abdominal CT to identify the infection focus. Chest CT revealed multiple peripheral nodules in both lungs, indicating septic embolism. Additionally, CT demonstrated mild swelling and heterogeneous enhancement of the thyroid gland with perithyroidal fluid collection (Fig. 1A, B). CT scan obtained at the previous admission due to pulmonary thromboembolism did not show abnormalities in the thyroid gland, except a probable benign hypo-attenuating nodule in the right thyroid gland. The radiologic findings in the thyroid gland were interpreted as shock thyroid. However, there were no accompanying signs of the CT hypotension complex, such as shock bowel, collapse of the inferior vena cava This study was approved by the Institutional Review Board of our institution and the requirement for informed consent was waived (IRB No. 2020-07-033).

DISCUSSION
The CT hypotension complex refers to a spectrum of CT findings with severe hypotension (3,4). It is mainly present in abdominal organs, but multiple organs can exhibit various atypical features (3,4). In 2006, Brochert and Rafoth (1) reported thoracic CT findings of three traumatized patients with hypovolemic shock, showing heterogeneous thyroid contrast enhancement and fluid surrounding the thyroid. They described these CT findings as "shock thyroid" and considered as part of the CT hypotension complex rather than direct traumatic injury (1).
The exact incidence of shock thyroid remains unknown, and to our knowledge, only seven cases have been reported in the literature (Table 1) (1, 2). It is thus certain that shock thyroid is a relatively rare manifestation of the CT hypotension complex. In a previous study involving traumatized or non-traumatized 41 patients with shock bowel on abdominal CT, no shock thyroid cases were found (4). However, because of the low awareness about this disorder, it might be frequently misdiagnosed, as the findings might be attributed to other conditions, such as thyroiditis or traumatic injury (2).
Although the CT hypotension complex was reported for the first time in traumatic patients with hemodynamic instability (5), it may also occur in multiple other hypovolemic conditions, including neurogenic shock from head or spinal injury, blood loss, sepsis, and cardiac arrest (4). Similarly, shock thyroid can be present in patients with hypotension regardless of the underlying etiology (2). One of the seven previously reported patients was a case of shock thyroid secondary to septic shock, as in our patient (2).
The mechanism of the shock thyroid is yet clearly established. The CT hypotension complex is thought to reflect alterations in perfusion secondary to hypotension or hypovolemia affecting sympathetic splanchnic stimulations. Hypoperfusion may affect the thyroid gland, which is a highly vascular organ, resulting in cellular edema or death, as well as intracellular fluid exudation (1,2). Alternatively, severe hypovolemia may trigger shock thyroid since it stimulates transient thyrotoxicosis, which maintains cardiac output by increasing the heart  2). However, in our patient, these morphological changes were not associated with alterations in thyroid function. Although, the results of the thyroid function test showed slightly decreased T3 levels, this finding may be attributed to the normal aging process (6). In the abovementioned previous study, thyroid function tests were performed only in one of the seven patients, and as in our patient, the levels were in the normal range (1).
Typical CT findings of shock thyroid include inhomogeneous enhancement or heterogeneous parenchymal attenuation of the thyroid gland with perithyroidal fluid collection, representing thyroid and perithyroidal edema (1,2). These changes are reversible; however, the recovery time for the shock thyroid remains unknown (1,2). In our patient, follow-up CT tak- The clinical implications of the shock thyroid are unclear. Usually, the CT hypotension complex indicates poor prognosis (3)(4)(5). However, the relationship between poor prognosis and shock thyroid is unclear due to the lack of adequate reports and large studies. Although three out of eight reported patients expired shortly after the diagnosis, it might be dangerous to jump to hasty conclusions due to the limited number of reported cases (1, 2). However, early recognition of shock thyroid is essential because it is a critical condition leading to permanent organ damage and death. Clinicians and radiologists must recognize that shock thyroid is an indicator of hypoperfusion and initiate proper management immediately. We believe that awareness of this disorder will help distinguish shock thyroid from other pathologies.
In conclusion, shock thyroid is a useful early indicator of impending hemodynamic instability and is a reversible phenomenon. It is important for radiologists and clinicians to recognize and report shock thyroid as a manifestation of the CT hypotension complex, rather than a condition resulting from direct injury or other primary thyroid disorders.

Conflicts of Interest
The authors have no potential conflicts of interest to disclose.

Funding
None