Case Report
Dopamine induced myxedema coma in a patient with Sheehan’s syndrome


    M.E. Jacobs, J.W. Uffen, N.M. van Es, H.S. Moeniralam

    Department of Internal Medicine and Intensive Care, St. Antonius Hospital Nieuwegein, the Netherlands


    H.S. Moeniralam -
    Case Report

    Dopamine induced myxedema coma in a patient with Sheehan’s syndrome


    A 52-year old woman presented at the emergency department with decreased consciousness, hypothermia and hypoglycemia. Months before presentation, yearlong progressive symptoms of apathy, rigidity and lethargy had led to the diagnosis of atypical Parkinsonism and recent initiation of dopamine-agonist therapy. Upon admission, clinical symptoms and extremely low triiodothyronine (<0.30 nmol/L) and thyroxine levels (0.8 pmol/L) led to the diagnosis of myxedema coma. Further hormone level measurements showed a complete anterior pituitary deficiency. In this case, initiation of levodopa triggered the acute presentation through suppression of the remaining thyroid stimulating hormone. The patient was admitted to the ICU for monitoring and IV hormone replacement. The absence of the anterior pituitary lobe on MRI together with a history of postpartum hemorrhage confirmed the diagnosis of Sheehan’s syndrome. After admission, her yearlong symptoms progressively improved with oral replacement therapy. Together, this case emphasizes the importance of recognition of atypical symptoms of pituitary dysfunction.


    Myxedema coma is an extremely rare presentation of decompensated hypothyroidism with an estimated incidence of 0.22 per million persons per year.[1,2] Symptoms include decreased consciousness, hypothermia and less often hypoglycemia, hyponatremia, hypotension and bradycardia.[1,2] Both unrecognized primary and secondary hypothyroidism may result in these severe physical disruptions. Treatment consists of supportive measures, IV hormone suppletion and, in case of deficiencies, electrolyte and glucose suppletion.[2,3] Still, mortality is estimated around 30%.[3] We aim to emphasize the importance of early recognition of pituitary dysfunction in order to prevent severe complications.


    A 52-year old woman with no history of thyroid disease was presented at the emergency department (ED) after being found unresponsive at home. Two months earlier, she had been diagnosed with an atypical form of Parkinsonism with symptoms of lethargy, rigidity and dysarthria. At the time of the diagnosis, the MRI scan of the brain showed no abnormalities. Unfortunately, her chronic symptoms worsened rapidly despite initiation of dopamine replacement therapy.

    On the day of admission, primary survey in the ambulance showed an unresponsive patient with a blood glucose level of 1.7 mmol/L. At the ED, her blood pressure was 128/84 mmHg with a heart rate of 58 beats/minute, a respiratory rate of 14 breaths/minute and a body temperature of 33.6 degree Celsius. Blood glucose levels had risen to 5.7 mmol/L after glucose administration leading to some improvement in her mental status.

    Laboratory results showed a severe hyponatremia of 112 mmol/L with a normal potassium level and low serum osmolality (246 mOsm/kg). Thyroid Stimulating Hormone level (TSH) was within the normal range with an extremely low blood thyroxine level (T4) of 0.8 pmol/L (reference value 12-30 pmol/L). Based on these clinical and laboratory findings, a myxedema coma due to a central hypothyroidism was diagnosed. Further investigation of plasma hormone levels revealed a very low triiodothyronine (T3) level of <0.30nmol/L (reference value 0.9-2.8 nmol/L) together with a total anterior pituitary insufficiency with extremely low adrenocorticotropic hormone and cortisol levels, decreased follicle-stimulating hormone and luteinizing hormone levels and decreased growth factor and insulin-like growth factor levels. Figure 1A summarizes all laboratory values at admission.

    The patient was immediately transferred to the ICU for monitoring and IV suppletion of cortisol, triiodothyronine and thyroxine, sodium and glucose. Respiratory support was not necessary despite her persistently fluctuating consciousness. Hemodynamically, norepinephrine was administered because of fluid unresponsive refractory hypotension. Furthermore, she showed a bradycardia with prolonged QTc intervals. Initial endocrine treatment consisted of 100 mg IV hydrocortisone followed by 200 mg IV levothyroxine and 10 mg IV liothyronine. Supportive measures and hormone suppletion led to rapid improvement of the hemodynamics, mental status and laboratory deficiencies. Within three days, the patient could be transferred to the internal medicine ward for oral levothyroxine and hydrocortisone suppletion. At discharge, mild symptoms of lethargy, apathy and bradykinesia were still present. Fortunately, her functional status kept improving after discharge with complete recovery of initial symptoms of bradykinesia, rigidity and apathy after a few months.

    Retrospectively, the patient suffered from progressive symptoms of endocrine dysfunction ever since a postpartum hemorrhage fifteen years ago. Thereafter, she developed an amenorrhea. During these last fifteen years, her physical condition had slowly gone backwards with a progressive inability to walk and perform everyday activities. The last months prior to presentation, her functional status worsened leading to multiple doctors’ visits and eventually the diagnosis of atypical Parkinsonism. The fact that her father had a rare neurodegenerative disorder might explain why a non-neurological diagnosis was not considered. Initiation of dopamine therapy, however, was in this case accompanied by a severe life-threatening clinical deterioration (figure 1B). After admission, MRI imaging was used to determine the specific cause of pituitary dysfunction (figure 2). The absence of the anterior pituitary lobe on MRI together with the laboratory results on the day of admission and the patient’s history confirmed the diagnosis of Sheehan’ syndrome.

    Figure 1: Laboratory deficiencies leading to the clinical presentation of myxedema coma. A) Laboratory results on the day of admission. B) Presumed course of pituitary dysfunction from the development to the day of admission.
    * Reference values based on morning ACTH and cortisol values; † postmenopausal reference values; ‡ references values adjusted to sex and/or age.
    Abbreviations: ACTH: adrenocorticotropic hormone, FSH: follicle stimulating hormone, IGF-1: insulin-like growth factor 1, LH: luteinizing hormone, T3: triiodothyronine, fT4: free thyroxine, TSH: thyroid stimulating hormone.

    Figure 2: MRI imaging of the pituitary gland shows an absent anterior lobe which, in this case, confirmed the diagnosis of Sheehan’s syndrome. Legend: 1. Corpus callosum, 2. Pons, 3. Cerebrum, 4. Cerebellum, 5. Sella turcica with an absent anterior pituitary lobe.


    This case describes a case of myxedema coma as an uncommon first presentation of Sheehan’s syndrome. Myxedema coma represents an acute hypothyroid crisis, usually in patients with unknown primary hypothyroidism.[2-4] Decompensated hypothyroidism as a consequence of pituitary disease is rare as it includes less than 5% of all myxedema cases.[5] The conversion of hypothyroidism to myxedema coma can be caused by precipitating factors such as infection, cerebrovascular events, congestive heart failure or the use of certain drugs.[3] Moreover, exogenous dopamine administration affects the thyroid axis through suppression of TSH production.[6] In this specific case, we suggest that dopamine agonist therapy for the treatment of atypical Parkinsonism has elicited the myxedema coma through further suppression of the little remaining TSH production (figure 1B). Although the combination of the clinical symptoms, laboratory deficiencies and rapid response to therapy point to hypothyroid crisis as a main diagnosis, the myxedema coma was likely accompanied by a Addisonian crisis through secondary adrenal insufficiency which worsened the mental status, hypotension, hypoglycemia and hyponatremia.

    Patients with myxedema coma are typically women of age 60-85 with symptoms of decreased consciousness, hypothermia, generalized non-pitting edema and delayed deep tendon reflexes.[3] If the patient is still communicative, speech is often slow with a hoarse voice. The incidence of myxedema coma is higher during winter months as cold weather can also act as a precipitating factor.[3] Furthermore, symptoms of hypoxia, hypoglycemia, hypothermia or hyponatremia may either act as precipitating factors or be symptoms of the condition itself .[3]

    Myxedema coma is considered a clinical diagnosis. However, specific laboratory results strengthen the clinical diagnosis and can be used to find the underlying cause of decompensated hypothyroidism .[3] Laboratory test abnormalities include low peripheral thyroid hormones and low blood glucose and sodium levels. Central endocrine deficiencies, such as low TSH levels, may be present dependent on the cause of hypothyroidism (i.e. primary or secondary).[3]  Over the years, few diagnostic scoring systems have been developed to differentiate between severe hypothyroidism or myxedema coma, including both clinical findings and metabolic disturbances. [7,8] Still, the development of diagnostic tools is limited by the low incidence.

    The cornerstone of the treatment includes substitution of both T3 and T4 thyroid hormone as conversion of T4 to T3 is reduced in critically ill patients.[5] ICU monitoring together with supportive measures such as mechanical ventilation, hemodynamic support, warming measures, glucose and electrolyte supplementation are recommended.[2,3] In patients with secondary hypothyroidism, intravenous hydrocortisone should also be administered before thyroid hormone replacement therapy in order to prevent an Addisonian crisis.[5] Meanwhile, it is important to treat underlying precipitating factors leading to the acute hypothyroid decompensation (f.e. infection, heart failure). Despite treatment, mortality remains high and varies between around 30 percent in small cohort studies.[1-3,5]

    As mentioned above, only 5% of all myxedema cases is caused by secondary hypothyroidism. In our case, the cause of secondary hypothyroidism was maternal hypopituitarism, also known as Sheehan’s syndrome. In patients with Sheehan’s syndrome, pituitary infarction after postpartum hemorrhage causes a deficiency in hormone secretion.[9,10] During pregnancy, hyperplasia of the pituitary gland leads to an increased vulnerability to ischemia. Peripartum blood loss and hypovolemic shock may result in hypopituitarism through a temporary decrease in arterial blood flow. Clinical symptoms depend on the severity of hormone deficiency together with the rate in which the pituitary secretion is affected.[9] In most women, first symptoms of Sheehan’s syndrome appear shortly after childbirth and include fatigue, decreased postpartum lactation and amenorrhea. In partial anterior deficiencies, it may also take years for symptoms to develop.[10] In both cases, however, myxedema coma as a first presentation of central hypothyroidism is rarely seen.

    In conclusion, myxedema coma is an uncommon but severe and potentially lethal illness caused by decompensated hypothyroidism. This article emphasizes the importance to recognize postpartum atypical symptoms that could originate from pituitary disease in order to prevent chronic invalidating symptoms, severe metabolic complications and death. Also, it shows the importance to be aware of possible endocrinological deterioration during dopamine treatment.


    All authors declare no conflicts of interest. No funding or financial support was received.

    Written consent was obtained from the patient for the publication of this case report.



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