Page 21 - Delaware Medical Journal - February 2018
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A Perfect Storm: Acute Presentation of Thyroid Storm due to Immune Checkpoint Inhibition Therapy
Fazal Ali, DO; Gregory Masters, MD
CASE REPORT
Key Words: Immune check point inhibition therapy, Immunotherapy, Thyroid storm.
BACKGROUND
Thyroid storm is a rare and life threatening disorder which, if untreated, is almost always fatal. Despite current treatments, thyroid storm continues
to have a high mortality rate ranging between 10 – 25 percent.1 Patients require rapid clinical diagnosis, which can be challenging, followed by stabilization
in the intensive care unit to manage the numerous complications of multi-organ failure that can eventually lead to demise. Here we discuss a case of life threating thyroid storm in a patient receiving immune checkpoint inhibition therapy for metastatic melanoma.
A 58-year-old female presented to
the hospital with worsening fatigue, confusion, nausea, vomiting, and abdominal pain. Her medical history was and metastatic melanoma. This was spreading melanoma of the left upper extremity in 2005. At that time, she underwent excision along with sentinel node biopsy, which was negative. The initial melanoma was lentiginous with radial growth phase, Breslow level 5, invasion depth 5.9 mm, associated with dysplastic nevus, and severe atypia with 3 mitosis/mm.2 When a CAT scan of the abdomen for an unrelated reason revealed incidental lung nodules in 2016, the patient underwent screening PET and CT
scans of the head, neck, and chest. She was found to have multiple pulmonary nodules which were concerning for new metastases. Consequently, she underwent a wedge resection and nodal sampling. Pathology was consistent with the initial melanoma from 2005. Subsequently, patient was initiated on immunotherapy with combination of ipilimumab
and nivolumab. Prior to presentation the patient was otherwise healthy, ambulatory, independent, and had no underlying psychological disorders.
CASE PRESENTATION
Three weeks after initiation of immunotherapy patient presented
days of worsening nausea, vomiting, abdominal pain, new onset auditory and visual hallucinations, and increasing confusion and fatigue. On exam, patient was altered, tachycardic, tachypneic,
and diaphoretic. Initial blood work initiated on broad spectrum antibiotics for suspected infection along with diabetic ketoacidosis. Imaging with chest x-ray and CAT scan of the head were unremarkable.
Given her persistent tachycardia, diaphoresis, and altered mentation, thyroid studies were ordered which showed an undetectably low thyroid stimulating hormone (TSH) level with a drastically elevated free thyroxine
(T4). Her outpatient records showed a normal thyroid panel prior to initiation of immunotherapy. Her Burch- Wartofsky Point Scale (BWPS) for thyrotoxicosis was greater than 65, which was highly suggestive of thyroid storm. She was initiated on an esmolol drip to control her tachycardia and excessive adrenergic drive. She was eventually intubated for worsening agitation and inability to protect her airway. Additionally, her cardiac function was severely reduced with global hypokinesis on echocardiogram and she was at high risk for developing cardiogenic shock.
DISCUSSION
Thyroid storm is a clinical diagnosis and is not dependent on the levels of free thyroid hormones or TSH.3 Diagnosis is organ manifestations of thyrotoxicosis. Despite the patient not presenting with hyperpyrexia, she exhibited signs of cardiac, gastrointestinal, and central nervous system involvement. This score. The patient was started on propylthiouracil (PTU) and intravenous corticosteroids for presumptive thyroid storm based on BWPS criteria. PTU works by inhibiting the activity of thyroperoxidase, which is essential in the formation of de novo thyroxine (T4). In addition, both corticosteroids and PTU prevent conversion of free T4 to free triiodothyronine (T3). Based on clinical history and timeframe, the etiology of
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