Undiagnosed thyrotoxicosis storm in a patient with perioperative sinus tachycardia and hypertensive crisis after anesthetic induction for emergent hip bipolar hemiarthroplasty after traumatic femoral neck fracture: a case report

Undiagnosed thyrotoxicosis storm in a patient with perioperative sinus tachycardia and hypertensive crisis after anesthetic induction for emergent hip bipolar hemiarthroplasty after traumatic femoral neck fracture: a case report

The clinical presentation of thyrotoxicosis ranges from abnormally elevated serum thyroid hormone levels to severe catabolic crisis with multi-organ failure. In stressful situations, the patient’s ability to maintain adequate metabolic, thermoregulatory, and cardiovascular compensatory mechanisms may be compromised, leading to thyroid crisis or storm. [1]. This makes early diagnosis based on high clinical suspicion crucial, even before confirmatory biochemical tests, as it can easily lead to fatal progression.

A 56-year-old patient presented to the emergency room with a history of tripping and falling on her left hip at home. With the help of relatives, she sat in a wheelchair due to restrictive and painful mobility. On examination, she showed a shortened externally rotated lower extremity. This clinical picture raised the suspension of the femoral neck fracture. The diagnosis was confirmed with a plain radiograph, since the femur diaphysis was displaced.

The patient had a long history of type II diabetes mellitus, complicated by neuropathic arthropathy (Charcot’s joint) of the left foot. Therefore, he requires multiple reconstructive and stabilizing surgeries. After having gastric sleeve surgery 10 years ago, my diabetes was controlled and there was no need to continue anti-diabetic medication. In the last three years, the patient began to experience psychiatric problems in the form of depressive episodes and delusions. Lately, his psychiatrist prescribed quetiapine and olanzapine in addition to low-dose propranolol for his familiar benign tremors. This course of psychiatric illness was accompanied by a loss of appetite, which led to severe weight loss, malnutrition, and cachexia, weighing only 46 kg at presentation with a height of 176 cm (BMI = 15.2 kg). /m2).

The orthopedic team indicated a hip hemiarthroplasty as the optimal surgical management in his case. His blood tests revealed a hemoglobin of 7.8 g/dl on admission. Two packed erythrocytes were transferred to him prior to surgery to optimize his cardiocirculatory situation.

Aside from his cachectic and anxious appearance, he was vitally stable on presentation to the operating room with a mild tachycardia with a heart rate of 95 bpm, a slightly elevated blood pressure of 130/88 mmHg, and a temperature of 36.7 °C. She was premedicated with midazolam. Anesthesia induction was performed with propofol, fentanyl, and rocuronium. Sevoflurane was used for maintenance of anesthesia. After induction of anesthesia, the patient started with tachycardia at 147 bpm and developed severe hypertension of 240/130 mmHg.

With the absence of muscle rigidity, stable partial pressure of carbon dioxide (PaCO2), and multiple uneventful prior exposures to anesthesia for variant surgeries, malignant hyperthermia was low on the list of our differential diagnosis. Neuroleptic malignant syndrome, serotonin release syndrome, and thyroid storm precipitated by surgery could not be excluded in this case. Although this is not the typical presentation of pheochromocytoma, it may present as a first episode under anesthesia in a previously normotensive patient. Support measures and symptomatic management with beta-blockers and antihypertensive medication were performed.

The highly experienced surgeon performed the case in 20 minutes. The patient was immediately extubated in the operating room with no adverse events recorded and transferred to prolonged observation in the recovery room.

In the recovery room, the thyroid panel was sent to the lab and results showed elevated serum thyroid hormone levels (free T3 level: 6.17 pmol/L, serum fT4: 43.31 pmol/L) and Undetectable thyroid-stimulating hormone (TSH) (<0.001 μIU/ml) consistent with thyroid storm.

Although the mechanism is not clearly understood, a thyroid storm exhibits most of its clinical picture due to sympathetic hyperactivity. Many mechanisms have been proposed, including, but not limited to, increased numbers of adrenergic receptors in target organs and a poorly understood post-receptor event that increases sensitivity to catecholamines, ending with the induction of key enzymes that regulate metabolism. [2].

Many patients would come to the operating room with a history of recently developed thyrotoxicosis or already diagnosed and treated, which facilitates the anticipation of a thyroid storm. This was not the case in our patient. In retrospect, it becomes clear that the disease may have had an insidious onset in recent years and played a role in weight loss, osteoporosis, and psychiatric illness. It is worth mentioning that the association between hyperthyroidism and osteoporosis is well established. [3,4].

However, the first syndromes that were suspected when the patient began to be tachycardic and hypertensive were serotonin syndrome and neuroleptic malignant syndrome, since the patient had been taking antipsychotic medications in the last three years. With the absence of muscle rigidity, stable PaCO2, and multiple uneventful prior exposures to anesthesia for variant surgeries, malignant hyperthermia was considered less likely to be the causative syndrome. Pheochromocytoma is another important diagnosis that can be triggered by mechanical or psychological stress or after induction of anesthesia, even without stressful manipulation, as reported by Sonntagbauer et al. [5].

Although fever is a defining symptom of neuroleptic malignant syndrome, it may not be evident in cases associated with atypical antipsychotics. [6]. The fulminant form typically includes a high fever ≥40°C and muscle rigidity. Followed by a wide range of mental status changes (from drowsiness to severe delirium and coma with or without seizures), tachycardia and tachypnea, rhabdomyolysis and acute renal failure, elevated lactate and liver function tests, and leukocytosis are all features of the syndrome. [7]. Immediate suspension of the causative agent and supportive measures are the mainstays of treatment. The muscle relaxant dantrolene might help, and restarting an abruptly discontinued dopaminergic agent is recommended. [8].

In serotonin syndrome, the mechanism can be complex and varied. Increasing levels of serotonin at neuronal junctions in the brain cause the release of central catecholamines. [9]. The end result is activation of the sympathetic nervous system through different mechanisms, including stimulation of the anterior hypothalamus and secretion of thyroid hormones and cortisol. [10]. This leads to CNS hyperreflexia, with symptoms ranging from tremors and diarrhea in mild cases and increasing in severity to delirium, muscle rigidity, and hyperthermia in severe cases. [10].

Pheochromocytoma would be diagnosed in the outpatient setting, as patients experience bursts of hypertensive episodes associated with sweating, palpitations, and headache secondary to the abrupt release of catecholamines. [11]. However, and mainly due to the high inter-individual differences in sensitivity to catecholamines, there is a poor correlation between the levels of circulating catecholamines and symptomatic discomfort. About 13% of patients may have normal blood pressure and 48% may only experience paroxysmal episodes of hypertension. [12].

In some case reports, active paragangliomas were described in the literature as an incidental finding. It was mainly in cases where it was planned to remove an abnormal mass. In this case, manipulation of the mass can cause massive hemodynamic instability and cardiovascular fluctuations. [13,14]. However, a pheochromocytoma catecholamine crisis can also occur under anesthesia in a previously normotensive patient. [5]. Exclusion of the diagnosis should be sought with appropriate tests.

As the diagnosis was confirmed as thyroid storm with laboratory tests in the recovery room, the patient was treated accordingly. Treatment of thyroid storm can be categorized into targeting thyroid hormone synthesis and secretion, suppressing peripheral conversion and tissue-level triiodothyronine activity, reversing systemic decompensation, and treating the precipitating factor. [15]. Definitive treatment should follow the acute phase after stabilization. If the patient was previously known to have hyperthyroidism, American Thyroid Association guidelines strongly recommend that the patient be euthyroid prior to the procedure with antithyroid medications with or without a β-blocker combination. If thyroidectomy was planned for the treatment of Graves’ disease, blockade of thyroid iodine uptake with potassium iodide supplementation in the immediate perioperative period was also advised. [15].

The selection of drugs also plays an important role. Selecting propranolol over the other β-blocker could be beneficial as it blocks the enzyme monodeiodinase type I, which transforms T4 into the biologically more functional T3 form of the hormone. [16]. Glucocorticoids also decrease the conversion of T4 to T3 within a couple of hours and belong to the regimen of therapy for thyroid storm. [16].

It is worth mentioning that the treatment of moderate to severe hyperthyroidism prior to urgent surgeries, although it should be attempted to reduce the possibility of developing thyroid storm, does not always prevent it. In a systematic review by de Mul et al., the risk of perioperative storm in hyperthyroid patients was still present even in a cohort treated with a triple drug combination preoperatively. [17]. Therefore, the anesthetist must remain alert and prepared to deal with the situation at any time perioperatively.

We have presented a complicated case of thyroid storm. In the first seconds after induction of anesthesia, when the patient began to be tachycardic, dehydration was suspected given the patient’s malnourished state. As hypertension became apparent, we had to widen our differential to include all causes of sympathetic hyperactivity. We hope to be able to present a case that adds educational value to any member who may face such a scenario in the perioperative period. Preparation and careful review of the deferent diagnosis are critical factors in managing such a crisis.

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