Thyroid Storm Morning Report pharyngitis

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Thyroid Storm Morning Report pharyngitis Powered By Docstoc
Kimberly Smith
   A 23-year-old woman comes to the office for
    follow-up. The patient has a 5-year history of
    hypothyroidism and has been on a stable dose of
    levothyroxine for the past 3 years. She is now 6
    weeks pregnant with her first child.
   Physical examination findings are noncontributory.
   Results of laboratory studies 1 month ago showed a
    serum thyroid-stimulating hormone (TSH) level of
    2.9 µU/mL (2.9 mU/L) and a free thyroxine level of
    1.4 ng/dL (18.1 pmol/L).
Which of the following is the most appropriate
 A. Add iodine therapy

 B. Measure her free triiodothyronine (T3) level

 C. Recheck her serum TSH level

 D. Continue current management
   The most appropriate next step is to recheck TSH. Because a fetus depends
    on maternal thyroid hormone for the first 10 to 12 weeks, the thyroid should
    be carefully monitored.
   TSH and total thyroxine (T4) levels be monitored throughout pregnancy
    because free T4 levels are not as accurate in pregnant patients. The total T4
    level should be kept stable at approximately 1.5 times the normal range,
    and the TSH level should be kept in the lower range of normal.
   Because of estrogen elevation during pregnancy, TBG levels increase. Free
    T4 levels may decrease as more T4 becomes bound by TBG.
   Pregnant patients may require an increase in their levothyroxine of approx
    35% to 50% as early as the first trimester.
   Measurement of T3 level is not useful in the evaluation of hypothyroidism
    because T3 levels typically remain within the reference range until the point
    of severe hypothyroidism.
The Case…..
40 y/o AAF who presented to the ER with chest pain
  and dyspnea

Additional Questions?
Pertinent HPI
   PTA c/o sore throat, difficulty swallowing, and
    decreased PO intake x 5 days. Initially presented to an
    OSH ER where she received antibiotics for presumed
    strep pharyngitis
   She then re-presented with chest pain and dyspnea and
    received a course of Avelox for presumed CAP
   Symptoms progressed, began experiencing ear pain,
    pleuritic right sided chest pain, shortness of breath,
    cough productive of brown sputum, chills, tremors in
    bilateral hands, N/V
   Upon further questioning she notes ~ 10lb weight loss,
    mood swings, anxiety, decreased appetite, and
    difficulty concentrating over the past month
   PMH
                                   Family History
       None- however patient
        has not been to the          Noncontributory
        doctor in many years
                                   Medications
   PSH
                                     None
       None
   Social History                 Allergies
       Remote history of            NKDA
        smoking Black and Mild's
        and marijuana but she
        quit >1 year ago,
        occasional alcohol,
        denies illicit drugs
Differential Diagnosis
   Pulmonary              Rheum
        Pneumonia             Sarcoid
        PE                    Vasculitis
        Pleuritis         Endocrine
   Cardiovascular             Hyperthyroid
        ACS                   Hypercalcemia
        AS                    Pheochromocytoma
        CHF               Infectious
        Pericarditis          Influenza
        Myocarditis           HIV
   Heme                       EBV
        Malignancy            HiB
   GI                     Upper Airway
        GED                   Thermal injury
        Esophagitis           Foreign body
                               Caustic ingestion
Physical Exam
   38 C, 109, 170/80, 20, 98% RA
   General: Extremely agitated female, tachypnic, writhing in pain
   HEENT: NC, TTP over mastoid sinuses but no erethyma/rash/swelling,
    PERRL, normal conjunctiva, sclera anicteric, no pharyngeal
    erethyma/exudates/swelling, no proptosis
   Neck: supple, thyromegaly- 4 finger widths, no cervical
   Respiratory: coarse breath sounds, wheezes R>L lower lobes
   CV: Tachycardic, normal rhythm, nl S1/S2, no murmurs, no JVD or
    edema, right sided chest wall tenderness
   GI: soft, NTND, + BS, no rebound or guarding
   Neurologic: A x O x 3
   Skin: no C/C/E
Initial Labs

137 109 8.6
                    124                     10.6
3.6 27       0.3                        9          326

 Ck 38
 Mb 0.7
 Troponin <0.07

 UTOX: positive for opiods

 EKG: sinus tachycardia, mild LVH, no
 signs of ischemia
Additional Studies
   TSH <0.03
   Throat Culture: Negative
   Strep Pneumo/Legionella: Negative
   Neck Xray: c/w prevertebral swelling
   CT Neck and chest: Enlarged adenoids, tonsils,
    cervical lymph nodes, thyromegaly, negative for PE
Initial Assessment and Plan
   Initiated therapy with Vancomycin and Zosyn
   Morphine PRN
Patient is still very agitated despite attempting to
  control her pain, remains tachycardic despite IVF
  and initiation of broad spectrum antibiotics, begins
  having multiple episodes of emesis
Diagnostic Criteria for Thyroid Storm

                        Precipitating Event: add 10

                        <25 unlikely
                        25-45 supports diagnosis
                        >45 diagnostic

                              Wartofsky et al
Our Patient
   Temp 38
   Mild agitation
   c/o N/V
   Tachycardic to 104
   Positive Precipitant History

   Total Score 45
Thyroid Storm
   AKA Thyrotoxic crisis
   Incidence 1-2%
   The adult mortality rate is 20-50%
   Mortality rises to 75% with delays in treatment
   More common in females
   Incidence is highest in the third and fourth decades
    of life
Precipitating Events
   Infection
   Surgery
   RAI therapy
   Drugs
       ASA, NSAID’s, chemotherapy, anticholinergics
   Excessive Thyroid Hormone Ingestion
   Withdrawal of thyroid medications
   DKA
   Thyroid Trauma
Initial Therapy
   The therapeutic regimen should include
    B  blocker to control symptoms caused by increased
      adrenergic tone
     Methimazole or PTU to block new hormone synthesis

     Steroids to reduce T4-T3 conversion
B Blocker
   Propanolol or Esmolol
   Propanolol
    1   mg/min until adequate B Blockade is achieved
   Esmolol
     load  with 250-500 ug/kg followed by an infusion at
      50-100 ug/kg/min
     this regimen allows for more rapid titration of drugs
   Start blocking denovo hormone synthesis within 1-2
    hours after administration
   Have no effect on the release of preformed hormones
    from the thyroid gland
   Methimazole has a longer duration of action
   PTU alone blocks T4-T3 conversion however must be
    given more frequently
   Dosages:
     Methimazole 30mg q6hrs
     PTU 200 mg q4 hours
   Reduce T4-T3 conversion
   Dose
     Hydrocortisone   100mg IV q8
Our Patient
   Esmolol loaded and then started on Esmolol gtt at
   Methimazole 30mg q6hrs
   Hydrocortisone 100mg IV q8
Differential for Hyperthyroidism?
Why is our patient Hyperthyroid?
   Graves disease- autoimmune d/o secondary to TSI which stimulate
    gland growth and hormone synthesis
   Toxic adenoma and toxic multinodular goiter- secondary to focal
    and/or diffuse hyperplasia of the thyroid follicular cells
   Iodine load induced hyperthyroid (CT, amiodarone)
   Trophoblastic disease- hydatidiform mole
   TSH producing pituitary adenomas
   Thyroiditis- inflammation of thyroid, may be 2/2 chemicals
    (amiodarone, sunitinib), radiation, palpation (surgery)
   Factitious ingestion
   Levothyroxine overdose
   Struma ovarii- functioning thyroid tissue in an ovarian neoplasm
Additional Labs
   TSH <0.03 (0.4-5 mu/L)
   TSI 2.4
   Free T3 > 12 (high)
   Free T4 3.55/3.25 (high)
   T3 total 632 (75-195 ng/dl)
   T4 total 20 (4.6-11.2 mcg/dl)
Am Fam Physician
   Our patient could not get the Uptake scan as she
    recently had a CT
Thyroid US
   Enlarged thyroid bilaterally
   Heterogenous with multiple ill defined low density
    nodules throughout
   Increased blood flow
   Most c/w thyroiditis vs multinodular goiter
Radioiodine Uptake Scan
   Essential to evaluate the etiology of hyperthyroid
   Patient is given a dose of radioactive iodine
   The iodine is concentrated into the thyroid or is
    excreted in the urine
   The amount of iodine that the thyroid uptakes is
    evaluated during the thyroid scan
Uptake Scan

Low radioiodine Uptake

                         Hot thryoidol.
Interpreting Results
   Hyperthyroid with high             Hyperthyroid with low
    Radioiodine Uptake                  Radioiodine uptake
       Graves disease
                                           Subacute thyroiditis
       Hashitoxicosis                         Granulomatous thyroiditis,
   Autonomous Thyroid tissue                   lymphocyctic thyroiditis, postpartum,
                                                Amiodarone, radiation, palpation
       Toxic Multinodular goiter
       Toxic Adenoma
                                       Exogenous thyroid hormone
                                           Excessive replacement therapy
   TSH Mediated                           Factitious
       TSH producing pituitary
                                       Ectopic Hyperthyroid
        adenoma                            Struma ovarii
                                           Metastatic follicular thyroid cancer
   HCG Mediated
       Trophoblastic disease
       Hyperemesis gravidum
Back to our patient
 Transitioned from Esmolol gtt to Propanolol PO
 Continued Methimazole

 Tapered Hydrocortisone throughout hospital stay

 Transitioned to Moxifloxacin for treatment of PNA

 d/c on Lisinopril for BP control

 Additional antibodies were ordered and the patient

  was scheduled for Endocrinology appointment but
  failed to follow up
The underlying etiology of our patient’s
  hyperthyroidism remained unclear
Take Home Points
   Thyroid storm is a clinical diagnosis
   Recognize the diagnostic criteria and the severity of
    the presentation
   The Radioiodine uptake scan is a necessary
    diagnostic tool for a complete evaluation of
   Endocrinol Metab Clin North Am. 1993 Jun;22(2):263-77. Life threatening
    thyrotoxicosis. Burch HB;Wartofsky L
   Endocrinol Metab Clin North Am. 2006 Dec;35(4):663-86,
    vii.Thyrotoxicosis and thyroid storm.Nayak B, Burman K.
   Am J Emerg Med 1991 May; 9 (3):232-4. Emergency department
    management of thyrotoxic crisis with esmolol. Brunette DD, Rothong C.
   Thyroid. 2006; 16:691. IV methimazole in the treatment of refractory
    hyperthyroidism. Hodak, SP, Huang, C, Clarke, D.
   Clin Endocrinol 1988;28:305. Comparison of methimazole, methimazole
    and sodium ipodate, and methimazole and saturated solution of potassium
    iodide in the early treatment of hypothyroidism Graves’ disease. Roti, E,
    Robuschi, G, Gardini, E.
   UpToDate. Thyroid Storm. Ross, Douglas.
   Am Fam. Physician. 2005 Aug;72(4):623-630. Hyperthyroidism. Diagnosis
    and Treatment. Reid, Jeri, Wheeler, Stephen.
   Join us Thursdays 2 pm for pathophysiology case
   Held in conference room next to 5th floor workroom
   Open to all residents and interns