Rifampicin is easily absorbed from the gastrointestinal (GI) tract; its ester functional group is quickly hydrolyzed in bile, and it is catalyzed by a high pH and substrate-specific esterases. After about 6 hours, almost all of the drug is deacetylated. Even in this deacetylated form, rifampicin is still a potent antibiotic; however, it can no longer be reabsorbed by the intestines and is eliminated from the body. Only about 7% of the administered drug is excreted unchanged in urine, though urinary elimination accounts for only about 30% of the drug excretion. About 60% to 65% is excreted through feces.The half-life of rifampicin ranges from 1.5 to 5.0 hours, though hepatic impairment significantly increases it. Food consumption inhibits its absorption from the GI tract, and the drug is more quickly eliminated. When rifampicin is taken with a meal, its peak blood concentration falls by 36%. Antacids do not affect its absorption. The decrease in rifampicin absorption with food is sometimes enough to noticeably affect urine color, which can be used as a marker for whether or not a dose of the drug has been effectively absorbed.Distribution of the drug is high throughout the body, and reaches effective concentrations in many organs and body fluids, including the cerebrospinal fluid. Since the substance itself is red, this high distribution is the reason for the orange-red color of the saliva, tears, sweat, urine, and feces. About 60% to 90% of the drug is bound to plasma proteins.
Diagnosis
Clinical features of myxedema coma:
Cardiovascular
Bradycardia
Bundle branch blocks
Complete heart block and arrhythmias
Cardiomegaly
Elevated diastolic blood pressure—early
Hypotension—late
Low cardiac output
Non-specific ECG findings
Pericardial effusion
Polymorphic ventricular tachycardia (torsades de pointes)
Prolonged QT interval
Respiratory
Hypoxia
Hypercapnia
Hyperventilation
Myxedema of the larynx
Pleural effusion
Gastrointestinal
Abdominal distention
Abdominal pain
Anasarca
Anorexia and nausea
Decreased motility
Fecal impaction and constipation
Gastrointestinal atony or ileus
Myxedema or toxic megacolon—late
Neurogenic oropharyngeal dysphagia
ileus
Neurological
Altered mentation
Coma
Confusion and obtundation
Delayed tendon reflexes
Depression
Poor cognitive function
Psychosis
Seizures
Renal and urinary function
Bladder dystonia and distension
Fluid retention
Appearance and dermatological
Alopecia
Coarse, sparse hair
Dry, cool, doughy skin
Myxedematous face
Generalized swelling
Goiter
Macroglossia
Non-pitting edema
Ptosis
Periorbital edema
Surgical scar from prior thyroidectomy
HypothermiaLaboratory features in myxedema coma:
Anemia
Elevated creatine kinase (CPK)
Elevated creatinine
Elevated transaminases
Hypercapnia
Hypercholesterolemia (elevated LDL)
Hyperlipidemia
Hypoglycemia
Hyponatremia
Hypoxia
Leukopenia
Respiratory acidosis

Epidemiology
Hypothyroidism is four times more common in women than men. The incidence of myxedema coma has been reported to be 0.22 per 1000000 per year but the data is limited and especially lacking in countries outside the western world and countries along the equator. Myxedema coma is most common in people 60 years old and older and is most common in the winter months when hypothermia is more common. See also
Thyroid storm
Euthyroid sick syndrome

References


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