Upon reorientation of the head relative to gravity, the cupula is weighted down by the dense particles, thereby inducing an immediate and sustained excitation of semicircular canal afferent nerves. This condition is termed cupulolithiasis.There is evidence in the dental literature that malleting of an osteotome during closed sinus floor elevation, otherwise known as osteotome sinus elevation or lift, transmits percussive and vibratory forces capable of detaching otoliths from their normal location and thereby leading to the symptoms of BPPV.BPPV can be triggered by any action that stimulates the posterior semi-circular canal including:
Looking up or down
Following head injury
Sudden head movement
Rolling over in bed
Tilting the headBPPV may be made worse by any number of modifiers which may vary among individuals:
Changes in barometric pressure – people may feel increased symptoms up to two days before rain or snow
Lack of sleep (required amounts of sleep may vary widely)
StressAn episode of BPPV may be triggered by dehydration, such as that caused by diarrhea. For this reason, it commonly occurs in people with post-operative diarrhea induced by post-operative antibiotics.BPPV is one of the most common vestibular disorders in people presenting with dizziness; a migraine is implicated in idiopathic cases. Proposed mechanisms linking the two are genetic factors and vascular damage to the labyrinth.Although BPPV can occur at any age, it is most often seen in people older than the age of 60.
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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