Rosen & Barkin's 5-Minute Emergency Medicine Consult (371 page)

BASICS

• Excessive thyroid hormone production results in a continuum of disease caused by both the direct physiologic effect of thyroid hormones as well as increased catecholamine sensitivity:
  
  • Subclinical or mild hyperthyroidism
    
  • Thyrotoxicosis
    
  • Thyroid storm or thyrotoxic crisis with life-threatening manifestations:
    
    • 1–2% of patients with hyperthyroidism
      
• Regulation of thyroid hormone:
  
  • Thyrotropin-releasing hormone (TRH) from hypothalamus acts on the anterior pituitary
    
  • Thyroid stimulating hormone (TSH) released by anterior pituitary gland and results in increased T
    ₃
    and T
    ₄
    from the thyroid gland:
    
    • Most of circulating hormone is T
      ₄
      , which is peripherally converted to T
      ₃
      
    • T
      ₃
      is much more biologically active than T
      ₄
      although it has a shorter half-life
      
• Genetics:
  
  • Interplay between genetics and environment
    
  • Graves disease is associated with HLA-B8 and HLA-DR3
    
  • Autosomal dominant inheritance seen in some families with nontoxic goiter
    

• Primary hyperthyroidism:
  
  • Toxic diffuse goiter (Graves disease)
    
  • Toxic multinodular (Plummer disease) or uninodular goiter
    
  • Excessive iodine intake (Jod-Basedow disease)
    
• Thyroiditis:
  
  • Postpartum thyroiditis
    
  • Radiation thyroiditis
    
  • Subacute thyroiditis (de Quervain)
    
  • Chronic thyroiditis (Hashimoto/lymphocytic)
    
• Metastatic thyroid cancer
  
• Ectopic thyroid tissue (struma ovarii)
  
• Pituitary adenoma
  
• Drug induced:
  
  • Amiodarone
    
  • Lithium
    
  • α-interferon
    
  • Interleukin-2
    
  • Iodine (radiographic contrast agents)
    
  • Excessive thyroid hormone (factitious thyrotoxicosis)
    
  • Aspirin overdose
    

DIAGNOSIS

• Signs and symptoms reflect end-organ responsiveness to thyroid hormone:
  
  • Signs:
    
    • Fever
      
    • Tachycardia, wide pulse pressure
      
    • Diaphoresis/sweating
      
    • Congestive heart failure (CHF)
      
    • Shock
      
    • Tremor
      
    • Disorientation/psychosis
      
    • Goiter/thyromegaly
      
    • Thyrotoxic stare/exophthalmos/lid lag
      
    • Hyperreflexia
      
    • Pretibial myxedema
      
  • Symptoms:
    
    • Weight loss despite increased appetite
      
    • Dysphagia or dyspnea secondary to obstruction by a goiter
      
    • Rash/pruritus/hyperhidrosis
      
    • Palpitations/chest pain
      
    • Diarrhea and vomiting
      
    • Myalgias and weakness
      
    • Nervousness/anxiety
      
    • Menstrual irregularities
      
    • Heat intolerance
      
    • Insomnia and fatigue
      
• Thyroid storm involves exaggerated signs and symptoms of thyrotoxicosis:
  
  • Extreme tachycardia/dysrhythmias
    
  • CHF
    
  • Shock
    
  • Disorientation and mental status changes including coma and seizure
    
  • Thromboembolic events
    

Apathetic hyperthyroidism:

• Owing to multinodular goiter, often have history of nontoxic goiter
  
• Subtle clinical findings that often reflect single-organ system dysfunction:
  
  • CHF
    
  • Refractory atrial fibrillation (AFib)
    
  • Weight loss
    
  • Depression, emotional lability, flat affect
    
  • Tremor
    
  • Hyperactivity
    

Gradual onset of aforementioned signs and symptoms

• Vital signs:
  
  • Fever
    
  • Tachycardia
    
  • Elevation of systolic blood pressure
    
  • Widened pulse pressure
    
  • Tachypnea/hypoxia
    
• Alopecia
  
• Exophthalmos or lid lag
  
• Thyromegaly or goiter, thyroid bruit
  
• Fine, thin, diaphoretic skin
  
• Irregularly irregular heartbeat
  
• Lung rales (CHF)
  
• Right upper quadrant tenderness/jaundice
  
• Muscular atrophy/weakness
  
• Tremor
  
• Mental status changes/coma
  

• Find underlying cause/precipitating factors.
  
• Plasma TSH is the initial ED test of choice:
  
  • Normal level usually rules out hyperthyroidism:
    
    • TSH may be low with normal T
      ₄
      . Get T
      ₃
      level to rule out T
      ₃
      thyrotoxicosis
      
  • If TSH levels unavailable, clinical suspicion should prompt initiation of therapy
    

• Thyroid function tests for:
  
  • Symptoms of hyperthyroidism
    
  • Elderly patient with new-onset CHF
    
  • New AFib/supraventricular tachycardia (SVT)
    
• TSH (usually decreased)
  
• Free T
  ₄
  (usually elevated):
  
  • If free T
    ₄
    is unavailable, total T
    ₄
    and resin T
    ₃
    uptake
    
  • 5% will have T
    ₃
    thyrotoxicosis, if low TSH with normal T
    ₄
    , send T
    ₃
    to rule out
    
• Lab studies are often not helpful/nonspecific, get as needed to look for underlying precipitants:
  
  • CBC to rule out anemia
    
  • Chemistry panel:
    
    • BUN, creatinine may be elevated secondary to dehydration
      
    • Hypokalemia, hyperglycemia
      
• Liver function tests (increased transaminases)
  
• ABG for hypoxemia and acidosis
  
• Cardiac markers
  

CXR (in CHF or sepsis)

EKG:

• Most commonly sinus tachycardia
  
• Rule out MI as precipitant of thyroid storm
  
• New-onset AFib
  

• Pheochromocytoma
  
• Sepsis
  
• Sympathomimetic ingestion
  
• Psychosis
  
• Heat stroke
  
• Delirium tremens
  
• Malignant hyperthermia
  
• Neuroleptic malignant syndrome
  
• Hypothalamic stroke
  
• Hypothyroidism (may mimic apathetic hyperthyroidism)
  
• Factitious thyrotoxicosis
  

TREATMENT

Stabilization and supportive care

• Airway, breathing, and circulation management
  
• Cardiac monitor
  
• Supplemental oxygen
  
• IV fluids
  
• Initiate cooling measures:
  
  • Acetaminophen for fever:
    
    • Avoid aspirin (displaces thyroid hormone from thyroglobulin, elevates free T
      ₄
      )
      
  • Cooling blanket
    

• Identify and treat the precipitating event
  
• For thyroid storm, initiate treatment sequence outlined below based on clinical suspicion
  
• Inhibit hormone synthesis using thioamides:
  
  • Propylthiouracil (PTU):
    
    • Drug of choice
      
    • Decreases hormone synthesis and reduces peripheral conversion of T
      ₄
      
  • Methimazole (MMI)
    
• Block hormone release using iodine
  only after hormone synthesis is inhibited as above:
  
  • Oral Lugol solution (saturated potassium iodide solution),
    or
    
  • Iopanoic acid (Telepaque)
    
  • Give iodine at least 1 hr after thioamides to prevent increased hormone production
    
  • Consider lithium in patient allergic to iodine
    
• Block peripheral effects of thyroid hormone:
  
  • β-blockade:
    
    • Propranolol is first line as it also inhibits T
      ₄
      conversion to T
      ₃
      
    • Esmolol, β-1 selective so may be used in patient with active CHF, asthma, etc.
      
  • Reserpine, guanethidine
    
  • Albumin solution
    
  • Cholestyramine to reduce enteric reabsorption of thyroid hormone
    
• Dexamethasone/hydrocortisone:
  
  • Prevents peripheral T
    ₄
    to T
    ₃
    conversion
    
• Treatment of thyrotoxicosis, secondary thyroiditis:
  
  • β-blockade
    
  • Anti-inflammatory medications
    
• General thyrotoxicosis support:
  
  • Acetaminophen for hyperpyrexia
    
  • Treat CHF with usual methods
    
  • Manage dehydration with 10% dextrose solution (D 10) to restore depleted hepatic glycogen
    
• Identify and treat associated and underlying conditions (infection, ketoacidosis, pulmonary thromboembolism, stroke, etc.)