facial percussion sign
Introduction
Introduction A low-calcification physical examination may have a Chvostek's sign. Can go to the hospital's internal medicine, neurology clinic. The related diseases include acute pancreatitis, chronic pancreatitis, hepatolenticular degeneration, hemifacial spasm, spasm, idiopathic facial paralysis, and progressive facial atrophy.
Cause
Cause
Like hypercalcemia, its etiology is also diverse, and the classification methods are also very different. This article also classifies according to the presence or absence of parathyroid hormone abnormalities.
1. Parathyroid dysfunction
(1) Parathyroid hormone release disorder: idiopathic (autoimmune) parathyroid hormone release disorder; parathyroid gene mutation; surgical resection or injury; Wilson's disease; functional parathyroidism Adenosteroid release disorder; hypomagnesemia; postoperative temporary parathyroid hormone release disorder.
(2) Parathyroid hormone dysfunction (hormone resistance).
(3) Pseudohypoparathyroidism.
2. Parathyroid hormone function is normal or increased
(1) Renal failure.
(2) Intestinal malabsorption.
(3) Acute or chronic pancreatitis.
(4) Osteoblastic metastases.
(5) Vitamin D deficiency or resistance.
(two) pathogenesis
The pathogenesis of hypocalcemia is broadly divided into three categories: primary hypoparathyroidism, target organ dysfunction, and other factors. Specifically, it involves the diffusion of calcium from the extracellular fluid and deposition on excessive bones, excessive calcium excretion from the kidneys, and too little calcium absorption in the intestinal mucosa.
The direct action of normal blood TH on the kidneys and bones and the indirect effects on the intestines are maintained. Hypocalcemia is divided into the following three categories according to the pathogenesis:
1. Primary hypoparathyroidism: due to PTH secretion and/or dysfunction, can be seen in congenital parathyroid hypoplasia, autoimmune diseases; can also be secondary to surgery miscut the parathyroid gland, malignant Complications after tumor invasion or radiation therapy. In primary hypoparathyroidism, calcium is reduced from bone mobilization, renal reabsorption of calcium is reduced, urinary phosphorus excretion is reduced, and 1,25-(OH)2D3 production is reduced, and intestinal calcium absorption is reduced. The end result is hypocalcemia and hyperphosphatemia.
2. Target organ dysfunction: such as renal insufficiency, intestinal malabsorption and vitamin D deficiency. In this type, although the secretion of PTH is normal or elevated, the receptor does not feel or the process of conversion of parathyroid hormone to parathyroid hormone, and hypocalcemia can still occur (can be accompanied by secondary thyroid Paragonadergic hyperactivity).
Renal failure and acute phosphorus load (which can occur during chemotherapy in certain tumors) can also cause hypocalcemia and hyperphosphatemia. In the absence of vitamin D, hypophosphatemia occurs with decreased or normal blood phosphorus. Vitamin D deficiency can be seen in inadequate intake, malnutrition or lack of sunlight all year round; also due to malabsorption of vitamin D, such as fatty sputum, gastrectomy, etc.; or seen in vitamin D hydroxylation dysfunction, common in chronic liver disease or chronic renal failure It can also be seen that the decomposition of vitamin D is accelerated. For example, long-term use of phenobarbital or phenytoin can increase liver microsomal oxidase activity and shorten the half-life of vitamin D. When vitamin D is deficient, intestinal calcium and phosphorus absorption are reduced, blood calcium and blood phosphorus are reduced, and it is not able to settle in bone tissue; and further promotes increased secretion of PTH, promotes osteoclast dissolution of bone salt, and finally osteomalacia. Hypocalcemia with reduced blood phosphorus or normal hypocalcemia can also occur in patients with acute pancreatitis and some osteoblastic tumor metastases.
3. Others: such as fluorosis, excessive use of citrate anticoagulation. Hypocalcemia can also occur due to the binding of calcium ions.
Examine
an examination
Related inspection
Facial nerve examination, maxillofacial examination, maxillofacial five-dimensional CT examination
Chvostek sign is a slight deduction of the external nerves of the external auditory canal causing involuntary contraction of the facial muscles. Normal healthy people have 10%. Hypocalcemia (the total calcium in adults is about 1000~1300g, 99% in the form of bone salts in bones and teeth) The rest exist in various soft tissues, extracellular liquid calcium only accounts for 0.1% of total calcium, about 1g), and patients with occult nutritional vitamin D deficiency hand, foot and sputum are often positive.
Diagnosis
Differential diagnosis
Facial muscle atrophy: facial muscle atrophy refers to dystrophy of striated muscle, muscle volume is reduced compared to normal, muscle fibers become thinner or even disappear. Neuromuscular disease is hypertrophy. In addition to the pathological changes of muscle tissue itself, muscle nutrition is closely related to the nervous system. Spinal cord disease often leads to muscular dystrophy and muscle atrophy.
Facial muscle weakness: The facial nerve consists of two parts: the motor fiber and the middle nerve that govern the facial expression muscle. The interneuron is composed of sensory and parasympathetic fibers. The damaged part of the face can be in the brainstem, the skull base, the facial nerve canal and its distal end. The nucleus and the pons are adjacent to the facial nucleus. Therefore, brain stem lesions involving the facial nerve are often accompanied by cross-sectional convulsions composed of ocular abduction or lateral paralysis. Facial nerve injury mainly manifests as peripheral facial spasm or hemifacial spasm.
Facial muscle twitching: facial muscle twitching, also known as hemifacial spasm, the common clinical manifestation of the primary facial muscle twitching patients mostly after the onset of middle-aged, more women. When the disease starts, it is mostly intermittent twitching of the orbicularis muscle, which gradually spreads slowly to other facial muscles on one side of the face. The twitching of the horn muscles is most noticeable, and in severe cases, the platysma can be involved in the same side. The degree of convulsions varies, and can be exacerbated by fatigue, mental stress, and autonomous movement, but cannot be imitated or controlled by oneself. Chvostek sign is a slight deduction of the external nerves of the external auditory canal caused by involuntary contraction of the facial muscles. Normal healthy people have 10%. Patients with hypocalcemia, occult nutritional vitamin D deficiency, hand and foot spasm are often positive.
