Hypocalcemia Presenting as a Code Stroke

Eric C. Katz, M.D.1 and David E. Manthey, M.D.1

Article Table of Contents  
Abstract Introduction Case Report Discussion Conclusion


Cerebrovascular accidents (CVA) present in many ways, and many other pathologies mimic CVAs. This case details a 43-year-old female who presented as a “Code Stroke” due to loss of function of her upper extremity, facial asymmetry, and speech difficulties. After detailed work up, she was found to have hypocalcemia. Her symptoms were muscular tetany interpreted as inability to use her arm, facial changes and slurred speech. Anchoring on the initial data presented, she was assessed for a perfusion abnormality. After careful review of this case, the final diagnosis of hypocalcemia was made. Having heard the description of the patient by emergency medical services (EMS), anchoring bias caused the providers to focus in on CVA and not necessarily consider other causes in the differential. Providers must broaden the differential regardless of how classic the presentation in order to not miss diagnoses and to provide timely and accurate intervention.


“Code Stroke” is a common emergency medical services (EMS) alert in most Emergency Departments (ED), typically indicating that a patient will be arriving to the ED with an acute neurologic deficit that is within a time frame for intervention.1 Many diseases can mimic stroke symptoms, such as metabolic derangements2, intoxications, complex migraines3, post-ictal states of seizures4, intracranial lesions, and psychiatric disorders. An emergency provider must simultaneously determine, in a timely manner, if there is an acute vascular occlusion or hemorrhage upon which one can intervene or if there is another cause of the patient’s presentation.

This process often begins with the EMS providers’ report, and based on that information, the ED provider determines whether to activate a “Code Stroke.” It is not always possible to get a full history from the patient or family for many reasons: patient condition, unknown circumstances, waxing and waning symptoms, and rapidity of the evaluation. Cognitive errors often occur in emergent, fast paced decision making, especially when the “diagnosis” fits. Anchoring early based on limited or misinterpreted information can delay or cause inappropriate treatment. For example, in this case the patient’s symptoms were not caused by the occlusion of a cerebral artery. This patient had hypocalcemia, causing neuromuscular irritability. This metabolic disturbance is capable of causing symptoms that could easily be mistaken or interpreted as stroke-like symptoms.

This case presentation will highlight 1) the cognitive errors that occurred as well as what biases were present and 2) discuss the final diagnosis of hypocalcemia.

Case Report

The patient is a 43-year-old female with a history of hypertension, hyperlipidemia, type 2 diabetes, anxiety, and depression. Her family called EMS for onset of speech trouble, inability to use her left upper extremity, and facial changes. Emergency medical services personnel reported inability to use the left arm, facial asymmetry and slurred speech, as well as tachypnea and a very anxious state. Further history taking on arrival noted that she had gradual onset of symptoms after waking up 2 hours prior. Symptoms included bilateral arm tingling and weakness that eventually progressed to the inability to use the left arm, facial droop, and slurred speech. The symptoms had resolved just before arrival.

Computed tomography (CT) imaging with CT angiography and perfusion studies were unremarkable, point of care glucose was within normal limits, and the patient had a normal neurologic exam with no subjective symptoms upon arrival. While the patient was waiting for her evaluation to be completed, she had another episode of speech difficulty and inability to use her left upper extremity similar to her previous episode. She had return of her symptoms due to the blood pressure cuff inflating, causing tetany, not flaccidity, in that arm and tapping on her facial nerve produced the facial asymmetry due to tetany, not flaccidity of the muscles. An ionized calcium was sent based on the clinical findings, and it was 0.73 (1.00-1.30mM/L). Other laboratory results revealed normal renal and liver function but with a few other electrolyte abnormalities. Her potassium was 3.1 (3.5-5.2mM/L), Magnesium was 0.7 (1.5-2.5mg/dL), and calcium was 7.1 (8.5-10.2mg/dL). The patient’s ECG showed a prolonged QT interval but was otherwise unremarkable. The patient’s electrolytes were replaced, and she was admitted to the Internal Medicine service. All symptoms resolved with correction of her electrolyte abnormalities.


This case illustrates two issues. The first issue is how anchoring and other cognitive biases lead to a belief that the symptoms were from a stroke instead of developing a broad differential for the symptoms. Although it is of paramount importance to evaluate for a stroke rapidly, a detailed history in this case showed that the symptoms were not actually consistent with stroke. The second issue is how a constellation of symptoms known to be caused by hypocalcemia presented as transient stroke-like symptoms. A literature search for similar presentations was only successful in finding reports of how electrolyte derangements predispose patients with cerebrovascular accident (CVA) to worsening outcomes.

The road to the final diagnosis was filled with many common biases that physicians face routinely. EMS teams gather key information and provide life-saving treatments while transporting patients. However, anchoring too much on the EMS report will inhibit the provider’s ability to develop a wider differential diagnosis list. Anchoring is prematurely keying in on a single diagnosis based on a few important features in the initial presentation. It is easy to hear “cannot use arm,” “slurred speech,” and “facial asymmetry,” and assume stroke. Noting the gradual onset of symptoms which were not timed together, the anxiety with bilateral hand and leg tingling, as well as defining what “cannot use arm” meant would have directed this patient encounter in a different manner, or at least widened the differential. This also might be considered a form of diagnosis momentum in which a diagnostic label has been assigned and it is difficult to view the presentation in another light.

Availability bias is an assumption that the disease that most readily comes to mind is the most relevant. Certainly, stroke is a more common presentation than hypocalcemia for this constellation of symptoms. Keeping a wide differential will help prevent this. Confirmation bias is searching for certain findings that support your original diagnosis, often ignoring findings that do not. Employing an objective way of working through a differential by comparing and contrasting all the findings (signs and symptoms) to the disease process on the differential will help prevent this bias. Finally, premature closure is acceptance of a disease as the diagnosis before it has been fully proven.5 Once the diagnosis of stroke was presumed, all differential thinking stopped and only the workup of stroke continued until it was negative.

Other key learning points involve this patient’s pathology of hypocalcemia. Serum calcium is found in several forms: free (or ionized), bound to proteins, and bound to other organic and inorganic compounds. The majority of calcium is in its free, metabolically active form. The level is primarily regulated by parathyroid hormone (PTH) and Vitamin D.6 Symptoms of hypocalcemia usually do not occur until the calcium level is below 8 mg/dl. Common causes of hypocalcemia include hypoalbuminemia, hypoparathyroidism, hypomagnesemia, and Vitamin D deficiency. Neuromuscular symptoms may occur, including numbness or tingling of the peri-oral area or digits, muscle cramps that may lead to spasm, voice changes due to laryngospasm, and dysphagia.

Hypocalcemia itself will cause muscle tetany secondary to changes in the membrane potential of the axons of nerve cells. Free calcium affects muscles by binding and allowing the actin myosin chains of skeletal muscle to interact and cause contraction.7 Hypocalcemia affects the nerves by putting them in a hyperexcitable state. When calcium drops low enough, the sodium channels become activated, the resting potential is much closer to zero, as opposed to very negative. This makes the cells spontaneously discharge and can cause a prolonged contraction or tetany.8 The Trousseau’s sign elicited in this case, blood pressure cuff inflating causing carpal spasm, was cause by decreased blood flow to the extremity, further worsening neuron excitability and inappropriate firing of motor signals.9 Chvostek Sign, the facial tetany, is caused by external stimulation of the facial nerve.10 These findings can also be exacerbated by hyperventilation.11 Hyperventilation, in this case in the setting of anxiety, can further induce the symptoms of hypocalcemia. Respiratory alkalosis secondary to the hyperventilation raises blood pH. Elevated blood pH increases the binding of free calcium to blood proteins thus transiently lowering ionized calcium.12 This patient had a baseline hypocalcemia, so the hyperventilation served to exacerbate her symptoms.

Diagnosis: Hypocalcemia is diagnosed with laboratory findings and corresponding appropriate exam findings. One can test the serum calcium level as well as the free metabolically active calcium level. Free calcium is often part of a rapid point of care test that can be obtained very quickly. Diagnosing the cause of the hypocalcemia would involve investigating the causes (as listed above).

Treatment: Treatment for hypocalcemia involves initial treatment with calcium supplementation to reverse symptoms and then management of the underlying disease responsible. Correcting other electrolyte derangements may also correct the hypocalcemia when they help maintain calcium homeostasis, such as magnesium. For severe cases, boluses of calcium gluconate/chloride can be given intravenously. If needed to maintain acceptable free calcium levels (~1mM/L) one can chose to start a calcium infusion and then admission to a monitored setting with continuous telemetry is recommended. Finally, physicians should beware of venous injury and dysrhythmia as potential consequences of uncontrolled or rapid infusion of calcium.13


Certainly this case describes a less common mimic for presentation of stroke like symptoms — hypocalcemia causing neuromuscular excitability resulting in tetany. This caused facial spasm during panic and hyperventilation, which was communicated as facial changes and speech difficulty. Inability to use the arm was due to spasm at rest and with the BP cuff inflating. Electrolyte disturbances can have varying effects on the body; in particular calcium has the ability to manifest neuromuscular symptoms. Anchoring, diagnosis momentum, availability bias, and premature closure were cognitive errors and biases that affected the initial evaluation of the patient. Awareness of biases and initiation of cognitive de-biasing strategies may help prevent their influence on patient care.

No financial support given. Authors report no conflicts of interest.