Presented by Katie Ohlendorf, MD
History and Physical
CC – Altered mental status
HPI – 88 year old white male presenting to the ED with a history of being found “down” in an apartment which was noted to be in disarray. According to EMS, the pt was unable to provide any history at the time of presentation; however, was noted to exhibit slurred speech. Also, he was unable to ambulate, but was reported to be moving all four extremities equally. EMS found diltazem and synthroid in his medicine cabinet. Landlord and neighbors had not seen him in several days therefore EMS was called.
PMH, surgical history, meds, allergies, social history and family history are unknown.
Vital signs: BP150/100, HR 54 and irregular, RR 22, Temp 90 degrees F (rectal)
HEENT: Normal cephalic, atraumatic. Pupils unequal but reactive bilaterally (L – 3mm, R – 2mm), eyes noted to move past midline bilaterally, no pallor, non-icteric, no papilledema. TM clear bilaterally. Oral mucosa very dry. Gag reflex intact. Neck has nuchal rigidity.
Pulmonary: Tachypneic with Kussmaul-type respirations. Clear to auscultation bilaterally.
Cardiac: Irregularly irregular rhythm with a rate of 54. No murmur, gallop, rub. Capillary refill< 4 seconds.
GI: Abdomen soft, nontender, nondistended. No masses. Positive midline supraumbilical scar. Positive bowel sounds.
Rectal: NST, prostate not enlarged. Positive guiac. Stool was dark in color.
Ext: RLE externally rotated but not shortened, old scar on right hip. No clubbing, cyanosis, or edema. Pulses intact and symmetrical – radial, femoral, and dorsal pedis.
Neuro: Patient is awake making incomprehensible sounds moving all 4 ext. equally. Gag reflex is intact. DTR’s- prolonged hyporeflexia. No clonus. Plantar reflexes down going bilaterally. No obvious facial asymmetry or focal weakness noted. Further neuro testing unable to be performed due to patient’s condition.
Lab Results and Diagnostic Studies
Sodium – 148
Potassium – 4.8
Chloride – 112
Bicarbonate – 18
BUN – 75
Creatnine – 2.3
WBC – 23.2
Hgb – 10.6
Platelets – 252
CPK – 3000
Lactate – 1.5
SDS/UDS – negative
Head CT – negative
CSF – WBC – 0, Glucose – 60, Protein – 76, RBC – 22, Gram stain negative
- What is the likely cause of this patients altered mental status?
- Graves disease
- Myxedema coma
- Adrenal insufficiency
- What will the thyroid studies show in myxedema coma?
|TSH level||Free T4||T3|
3. What drugs should be avoided in hypothyroidism because they are known to exacerbate it?
4. What is the initial ED treatment of myxedema coma?
A. 200-500 mcg T4
B. 200-500 mcg T4 plus 100 mg IV prednisone
C. 100 mg IV prednisone
D. Supportive care
E. BB, PTU, dexamethasone and iodine
- Myxedema coma
- High TSH, low T3 and T4
- Phenytoin, lithium and benzodiazepines
- 200-500 mcg T4 plus 100 mg IV prednisone
This patient has several acute issues that he presented with including atrial fibrillation, GI bleed and myxedema coma. Myxedema coma is a life threatening form of hypothyroidism. It is an uncommon presentation; however mortality rates as high as 80%. These patients usually have a medical history of a chronic thyroid disorder that leads to this state. Myxedema coma is most common in elderly females. Many cases are triggered by cold weather with the majority of patients presenting during the winter. Other causes include infection, medication and trauma preventing access to medications. Medications to avoid in hypothyroidism include phenothiazines, phenobarbital, narcotics, anesthetics, benzodiazepines, lithium, phenytoin, rifampin, amodarone and iodides as they may exacerbate symptoms.
The hypothalamic-pituitary-thyroid axis controls thyroid hormone production via a negative feedback loop. Release of thyroid hormone is regulated by TSH and free T4 acts as a negative feedback inhibiting further TSH release. Thyroid hormones affect many body systems including cardiac, renal, pulmonary and neuromuscular systems.
Approximately 90% of hypothyroidism is primary, where the thyroid itself is affected. It is typically due to an autoimmune process. In the US, the most common autoimmune process is Hashimoto thyroiditis, where anti-TSH antibodies are produced, therefore inhibiting thyroid hormone production. These patients typically have a large goiter. The thyroid destruction is a chronic process, taking months to years. Patients present with nonspecific symptoms of hypothyroidism including weight gain, hair loss, fatigue, etc. These patients should have thyroid studies as well as well as thyroid antibody testing. Treatment includes thyroid hormone replacement.
In undeveloped countries the most common cause of hypothyroidism is iodine deficiency. Other causes include congenital abnormalities, malignancies, infiltrative disorders, as well as iatrogenic causes (thyroid ablation).
Differential diagnosis for myxedema coma is broad and many conditions can mimic the symptoms. Things to consider are sepsis, hypothermia secondary to environmental exposure, CVA, hypoxia, hyperglycemia, acute MI, ICH, panhypopiuitarism, adrenal insufficiency, hyponatremia, GI bleed and psychiatric disorders.
Emergency center care is focused on stabilizing the patient and initial resuscitation focuses on ABC’s – cardiac monitoring, pulse oximetry, airway management, and IV access.
The history is important to obtain especially regarding previous thyroid disease, medication changes, and symptoms of hypothyroidism (weight gain, hair loss, fatigue, dry skin, voice changes, depression, constipation and menstrual changes). Also ask about history of cold exposure, trauma (may prevent access to medications), infections or other life stressors.
On physical exam, vital signs are essential. The temperature is often less then 35.5 degrees C. Patients are hypotesive and bradycardic. A thyroidectomy scar can provide a clue to diagnosis. Look for myxedema, a nonpitting edema present in the hands, face and pretibial areas. The GI exam may have abdominal distension secondary to constipation and decreased gut motility. The neuro exam may include parasthesia (especially median nerve) and pseudomytonic reflexes (prolonged relaxation phase).
Diagnostic studies will help confirm your clinical diagnosis. Check CBC, electrolytes, BNP, troponin, lactate, UA, pregnancy test (treatment is different in pregnancy), ABG as well as thyroid studies including TSH, T3 and T4 (total and free). The thyroid studies will reflect the chronic thyroid state. In the chronic hypothyroid patient the TSH will be high and the patient will have low T3 and free T4. An EKG will show sinus bradycardia as the most common dysrhythmia in those with hypothyroidism. Chest x-ray is useful to look for pneumonia, cardiomegaly and effusions (pleural and pericardial). A CT head may be done to look for intracranial pathology. A lumbar puncture may be done to look for an infectious cause. Also check a random cortisol level to evaluate for adrenal insufficiency, which may mimic myxedema coma. If suspecting adrenal causes a ACTH stimulation test may be done, but do not delay treatment.
Treatment includes airway and cardiovascular support as well as treating the cause for myxedema coma (infection, hypothermia, etc.). IV fluids must be used with caution. Although patients are typically dehydrated, bradycardia and underlying cardiac disease may tip the patients into a hypervolemic state. Therefore invasive cardiac monitoring as well as frequent physical exams are required with fluid resuscitation. If a patient requires vasopressors, dopamine is first line. Treatment for myxedema coma is IV thyroxine. T4 is classically used and dosed at 200-500 mcg IV. Glucocorticoids are also recommended as adrenal insufficiency may mimic this condition. Stress does hydrocortisone is recommended (100 mg IV).
Patients will be admitted to the ICU for further evaluation and management. Clinical improvement is seen within 24-36 hours of thyroid hormone replacement. Even with medical treatment, mortality rates exceed 20%.
On the opposite end of the spectrum are the hyperthyroid states. Graves disease is the most common form of hyperthyroidism, accounting for 50-60% of the cases. It is an autoimmune state where antibodies stimulate the TSH receptor and causes thyroid hormone production and release. Symptoms include heat intolerance, tremor, palpitations, weight loss, anxiety, nervousness, or hyperactivity. On physical exam the thyroid is often enlarged, ocular abnormalities such as proptosis and periorbital edema may be seen, and signs of thyrotoxicosis may be present including sinus tachycardia, atrial fibrillation, systolic hypertension, excessive perspiration, tremor and large muscle weakness. Lab studies include TSH (low), T3 (usually normal), and free T4 (high). Thyroid antibodies can also be measured. Imaging studies include nuclear medicine imaging using radioactive iodine; in graves disease the thyroid will have increased uptake as compared to normal. Treatment includes symptomatic relief with beta blockers as well as antithyroid drugs (PTU), radioactive iodine ablation or surgical removal.
Thyroid storm is the extreme state of hypothyroidism. Like myxedema coma the mortality rate is high with 90% mortality if not diagnosed and treated quickly. The patient may have a known history of hyperthyroidism. Thyroid storm is usually precipitated by infection. Patients have fever, tachycardia, and hypertension. They may have GI complaints such as nausea, vomiting, diarrhea or abdominal pain. Patients may present with seizures, coma, or anxiety. Thyroid storm is a clinical diagnosis but thyroid studies will show elevated T3 and T4 with low TSH levels. If thyroid storm is suspected, treatment is a three step process involving first beta blockers (to block effects of thyroid hormone), followed by PTU (to stop thyroid hormone production) and iodidine (to inhibit thyroid hormone release). Patients should be admitted to the ICU and clinical improvement seen within 24 hours of treatment.