Sandbox spinalcord

Risk factors

Common risk factors that can trigger myxedema coma in patients with hypothyroidism include:

• Hypothermia
• CVA
• CHF
• Infections ( pneumonia, influenza, UTI, sepsis)
• Drugs ( Anesthestics, narcotics, amidirone, Lithium carbonate) 6486153
• GI bleeding
• Metabolic disturbances(Hypoglycemia, hyponatremia, acidosis, hypercalcemia, hypoxemia, hypercapneia)

History

• History of antecedent thyroid disease
• History of radioiodine therapy or thyroidectomy
• Discontinuation of medications.

Historical Perspective

• In 874, Gull was the first physician to describe hypothyroidism under the name myxedema due to its characteristics of swollen skin and its mucin content.
• In 1883, Semon was the first to establish a relationship between patients undergoing thyroidectomy and later developing symptoms of myxedema.
• In 1888, Clinical Society of London presented a paper describing that extreme loss of thyroid harmone can lead to cretinism and myxedema.
• In 1891, Murray was the first physician to discover cure for myxedema by using hypodermic injections of sheep thyroid extract.

Pathophysiology

• Myxedema coma occurs as a result of long-standing, undiagnosed, or undertreated hypothyroidism.
• Myxedema coma is usually precipitated by a systemic illness.

Causes

• Myxedema coma can result from any of the causes of hypothyroidism, most commonly chronic autoimmune thyroiditis.
• Myxedema coma can also occur in patients who had thyroidectomy or underwent radioactive iodine therapy for hyperthyroidism.
• Rare causes may include secondary hypothyroidism and medications such as lithium and amiodarone.

Pathogenesis

• Thyroid hormone plays an important role in cell metabolism.
• Long-standing hypothyroidism is associated with reduced metabolic rate and decreased oxygen consumption, which affects all body systems.
• Reduced metabolism results in hypothermia.
• Reduced metabolism and decreased oxygen also results in decreased drug metabolism leading to overdosing of medications particularly sedatives, hypnotics, and anesthetic agents; this can precipitate myxedema coma.
• Even in severe hypothyroidism a balance of metabolic homeostasis is achieved through adaptive neurovascular mechanisms. However in conditions such as respiratory or urinary tract infections, cardiac, acute myocardial infarction or stroke interfere with this adaptive mechanisms by decreasing the blood volume and ventilation triggering myxedema coma.

Treatment

Myxemeda coma is a medical emergency and requires a prompt treatment. All patients must be shifted to ICU.

Supportive Therapy

• Prevention of further heat loss by covering the patient with blankets but avoid external rewarming because it may produce vascular collapse.
• Consider warmed IV fluids.
• Cardiac monitoring of the patient.

Acute Mecial Therapy

• Preffered regimen (1):- Levothyroxine 5 to 8 mcg/kg (200 to 500 mcg) IV infused over 15 min, then 50 to 100 mcg IV q24h until transition to an oral formulation is possible.
• Glucocorticoids should also be empirically administered until coexistent adrenal insufficiency can be ruled out. Hydrocortisone hemisuccinate 100 mg IV bolus is initially given, followed by 100 mg IV q8h until initial plasma cortisol level is confirmed normal.

• IV hydration with D 5 NS is used to correct hypotension and hypoglycemia (if present); avoid overhydration and possible water intoxication because clearance of free water is impaired in these patients. • Rule out and treat precipitating factors (e.g., antibiotics in suspected sepsis).

Approach to patients with COMA

• The initial clinical approach to the patient in a state of stupor or coma is based on the principle that all alterations in arousal constitute acute, life-threatening emergencies until vital functions such as blood pressure and oxygenation are stabilized, potentially reversible causes of coma are treated, and the underlying cause of the alteration in arousal is understood.
• Urgent steps may be necessary to avoid or minimize permanent brain damage from reversible causes.
• More than half of all cases of coma are due to diffuse and metabolic brain dysfunction. In Plum and Posner's landmark study (1980, see 2007 revision) of 500 patients initially diagnosed as having coma of unknown cause (in whom the diagnosis was ultimately established), 326 patients had diffuse and metabolic brain dysfunction. Almost half of these had drug poisonings. Of the remaining patients, 101 had supratentorial mass lesions, including 77 hemorrhagic lesions and 9 infarctions; 65 had subtentorial lesions, mainly brainstem infarctions; and 8 had psychiatric coma. A logical decision tree often used in searching for the cause of coma divides the categories of diseases that cause coma into three groups: structural lesions, which may be above or below the tentorium; metabolic and toxic causes; and psychiatric causes. The history and physical examination usually provide sufficient evidence to determine the presence or absence of a structural lesion and quickly differentiate the general categories to decide what further diagnostic tests are needed or to allow for immediate intervention if necessary. Serial examinations are needed, with precise description of the behavioral state at different points in time, to determine whether the patient is improving or—a more ominous finding—worsening, and to decide whether a change in therapy or further diagnostic tests is necessary. Subtle declines in the intermediate states of arousal may herald precipitous changes in brainstem function, which may affect regulation of vital functions such as respiration or blood pressure. The dynamic quality of alterations of consciousness and the need for accurate documentation at different points in time cannot be overemphasized.

Altered level of concoiousness COMA Stupor

Assess ABC Airway Breathing Circulation

Seizure activity

Yes

No

Identity the problem reassess

Diagnostic and therapatic administration of Thiamine 100mg Dextrose 50ml, 50% Nalaoxone 0.4mg

No change in level of conciousness

Improvement in conciousness

Perform labaratory tests CBC,Thyroid studies Blood glucose, CMP,BUN, creatinine LFT's Serum osmolality

Hypoglycemia or Narcotic overdose

Abnormal

Normal

↑TSH ↓T3 and T4

↑WBC

CMP abnormal

Check Head CT/MRI

Myxedema coma

Sepsis Meningitis Encephalitis

Toxic encephalopathy

Abnormal

Normal

Stroke Brain tumor Intracranial bleeding Cerebral edema Brain abscess

Perform lumbar puncture

Abnormal

Normal

Increased ICP Infection

Psyciatric Disorders

Differential diagnosis

Myxedema coma must be differentiated from other diseases that cause hypotension, hypothermia and altered mental status such as hypoglycemia, sepsis, conversion disorder, adrenal insufficiency, hyponatremia, panhypopitutirim, acute myocardial infraction, intracranial hemorrahge .

Diagnostic Scoring System for Myxedema Coma
Component	Variable		Points	Component	Variable	Points
Thermoregulatory dysfunction	>35		0	Gastro-intestinal	Anorexia/abdominal pain/constipation	5
	32-35		10		Decreased intestinal motility	15
	<32		20		Paralytic ileus	20
Central nervous system effects	Somnolent/lethargic		10	Precipitating event	Absent	0
	Obtunded		15		Present	10
	Stupor		20	Metabolic disturbances	Hyponatremia	10
	Coma/seizures		30		Hypoglycemia	10
Cardiovascular	Bradycardia	Absent	0		Hypoxemia	10
		50-59	10		Hypercarbia	10
		40-49	20		Decrease in GFR	10
	EKG changes		10	Others	Pleural effusions	10
	Pericardial effusion		10		Pulmonary edema	15
	Cardiomegaly		15		Hypotension	20
Abbreviations: EKG = electrocardiogram; GFR = glomerular filtration rate. A score of 60 or higher is highly suggestive/diagnostic of myxedema coma A score of 25 to 59 is suggestive of risk for myxedema coma, and a score below 25 is unlikely to indicate myxedema coma. Other EKG changes: QT prolongation, or low voltage complexes, or bundle branch blocks, or nonspecific ST-T changes, or heart blocks