what does hypophosphatemia mean

What are the signs and symptoms of hypophosphatemia?

Symptoms and Signs of Hypophosphatemia Although hypophosphatemia usually is asymptomatic, anorexia, muscle weakness, and osteomalacia can occur in severe chronic depletion. Serious neuromuscular disturbances may occur, including progressive encephalopathy, seizures, coma, and death.

What are the possible complications of hypophosphatemia?

You’re more likely to get hypophosphatemia if you:

• have a parent or other close family member with the condition
• have the blood infection, sepsis
• have hyperparathyroidism
• are severely malnourished because of starvation or anorexia
• are an alcoholic
• take medications such as steroids, diuretics, or antacids in excess or for long periods of time

What is the prevalence of hypophosphatemia in the US?

XLH is a rare disease. It affects 1 out of every 20,000 people. It’s also inherited. This means a parent with the condition may pass it on to their children. XLH is known by several names. According to the National Organization for Rare Disorders, XLH is also known as: Who gets XLH? XLH is an inherited disease.

What does hyperphosphatemia cause?

Over the short term, it can cause things like subcutaneous tissues, the deposition of calcium and phosphate in bone joints, and chronic kidney disease. Long-term effects can include renal failure; bone, skin and heart complications; organ damage, and damage to the vascular system.

What is the cause of hypophosphatemia?

Hypophosphatemia is a serum phosphate concentration < 2.5 mg/dL (0.81 mmol/L). Causes include alcohol use disorder, burns, starvation, and diuretic use. Clinical features include muscle weakness, respiratory failure, and heart failure; seizures and coma can occur. Diagnosis is by serum phosphate concentration.

What are the signs and symptoms of hypophosphatemia?

Symptoms of hypophosphatemiaConfusion.Appetite loss.Muscle weakness.Feeling tired and upset.Bone pain and fractures.Tooth decay or late baby teeth.Slow growth and short height in children.

What does it mean if you have low phosphate levels?

If your test shows you have low phosphate/phosphorus levels, it may mean you have: Hyperparathyroidism, a condition in which your parathyroid gland produces too much parathyroid hormone. Malnutrition. Alcoholism.

What are the signs and symptoms of hyperphosphatemia?

Signs and symptoms of acute hyperphosphatemia result from the effects of hypocalcemia, with patients occasionally reporting symptoms such as muscle cramps, tetany, and perioral numbness or tingling. Other symptoms include bone and joint pain, pruritus, and rash.

How do you fix hypophosphatemia?

Mild/moderate acute hypophosphatemia usually can be corrected with increased dietary phosphate or oral supplementation, but intravenous replacement generally is needed when significant comorbid conditions or severe hypophosphatemia with phosphate depletion exist.

What is a dangerously low phosphate level?

If your phosphorous levels are below 1.0 mg/dL, your tissues may have more trouble connecting hemoglobin with oxygen - which is critical for breathing. You may become mild to moderately short of breath. The symptoms that you notice, with lowered phosphate levels, are due to the disease that is causing this abnormality.

What diseases cause low phosphorus?

Long-term starvation, malnutrition, and anorexia can deplete the body's stores of phosphorous over time. Acute hypophosphatemia is especially common in hospital patients undergoing refeeding. Additional causes include chronic infections, Crohn's disease, or malignant tumors. Hyperparathyroidism.

What disease is caused by lack of phosphorus?

A reduced concentration of phosphate in the blood serum is a disorder known as hypophosphatemia. Phosphorus deficiency may cause bone diseases such as rickets in children and osteomalacia in adults.

How do I raise my phosphate levels?

Consume Phosphate-Rich FoodsPlain low-fat yogurt: A 6-ounce serving contains 20% of the recommended daily value (DV).2% milk: One cup contains 18% of adult DV.Salmon: A 3-ounce serving contains 17% of adult DV.Chicken: A 3-ounce serving contains 15% of adult DV.Potatoes: 1 medium russet potato has 10% of adult DV.

How serious is hyperphosphatemia?

Outlook. High phosphate levels in your blood can increase your risk for serious medical problems and other complications. Treating hyperphosphatemia with dietary changes and medication as soon as possible can prevent these complications. Getting treated can also slow bone problems linked to chronic kidney disease.

What is the most common cause of hyperphosphatemia?

Renal failure is the most common cause of hyperphosphatemia. A glomerular filtration rate of less than 30 mL/min significantly reduces the filtration of inorganic phosphate, increasing its serum level. Other less common causes include a high intake of phosphorus or increased renal reabsorption.

Does vitamin D increase phosphorus levels?

Vitamin D functions by stimulating intestinal calcium and phosphorus absorption, by stimulating bone calcium mobilization, and by increasing renal reabsorption of calcium in the distal tubule. These functions on bone and possibly kidney, but not intestine, require the parathyroid hormone.

What causes hypophosphatemia?

Acute hypophosphatemia is usually the more severe and common type of hypophosphatemia seen in clinical settings. Its causes include: 1 Recovery from diabetic ketoacidosis. Diabetic ketoacidosis happens when someone mismanages their diabetes or might not realize they have it. It is a state that the body goes into when it is unable to produce enough insulin. Insulin is what helps your body break fat down and burn it as fuel. When you go into diabetic ketoacidosis, you have a buildup of acids in your bloodstream, leading to loss of consciousness or even death. 2 Chronic Alcoholism. It is believed that over time, alcoholism hampers your kidney’s ability to absorb phosphorus fully. This is one of the most common causes of hypophosphatemia. Fifty percent of people who are hospitalized due to alcoholism develop hypophosphatemia within the first three days of their hospitalization. 3 Burns. Phosphate is a source of intracellular energy, and when someone experiences a severe burn, their phosphate levels dip dangerously low. Therefore, patients must receive supplemental phosphate to stay healthy. 4 Respiratory alkalosis. This is a decreased amount of carbon dioxide pressure without increased bicarbonate. It usually happens when you hyperventilate or simply breathe in and out too quickly. Respiratory alkalosis causes acute hypophosphatemia because your cells naturally begin to shift around the phosphate stores in your bones. This cause of acute hypophosphatemia is different than the other causes because it will immediately return to normal once the hyperventilation stops.#N#‌

Why does respiratory alkalosis cause hypophosphatemia?

Respiratory alkalosis causes acute hypophosphatemia because your cells naturally begin to shift around the phosphate stores in your bones. This cause of acute hypophosphatemia is different than the other causes because it will immediately return to normal once the hyperventilation stops. ‌. Chronic Hypophosphatemia‌.

What causes phosphorus to deplete?

Long-term starvation, malnutrition, and anorexia can deplete the body’s stores of phosphorous over time. Acute hypophosphatemia is especially common in hospital patients undergoing refeeding. Additional causes include chronic infections, Crohn’s disease, or malignant tumors. Hyperparathyroidism.

What is the normal phosphorus level?

Phosphorous is a mineral found in your bones that helps to keep your bones and body healthy. Normal blood phosphorous levels are between 2.5 to 4.5 mg/dL. Hypophosphatemia is a condition in which your blood has a low level of phosphorous. Low levels can cause a host of health challenges, including muscle weakness, respiratory or heart failure, ...

What happens when you go into ketoacidosis?

When you go into diabetic ketoacidosis, you have a buildup of acids in your bloodstream, leading to loss of consciousness or even death. Chronic Alcoholism. It is believed that over time, alcoholism hampers your kidney’s ability to absorb phosphorus fully. This is one of the most common causes of hypophosphatemia.

Why do people need phosphate?

Phosphate is a source of intracellular energy, and when someone experiences a severe burn, their phosphate levels dip dangerously low. Therefore, patients must receive supplemental phosphate to stay healthy. Respiratory alkalosis. This is a decreased amount of carbon dioxide pressure without increased bicarbonate.

Can hypophosphatemia be detected?

Most people with hypophosphatemia don’t immediately present as having hypophosphatemia. Healthcare providers need to pay attention to the patient’s medical history to detect hypophosphatemia.

How to prevent hypophosphatemia?

Manage health conditions that can lead to hypophosphatemia. If you have diabetes, it is important to follow your management plan so you prevent DKA. Ask your healthcare provider for information if you are having problems with alcoholism and need help to stop drinking. Obesity and eating disorders such as bulimia or anorexia can cause malnutrition. This increases your risk for hypophosphatemia. Your provider can help you manage these health conditions or give you information on treatment plans.

What is the difference between hypophosphatemia and chronic hypophosphatemia?

Hypophosphatemia is a low level of phosphate in your blood. Phosphate is an electrolyte (mineral) that works with calcium to help build bones. It also helps produce energy. Hypophosphatemia can be acute or chronic. Acute means the level in your blood drops suddenly. Chronic means the level has been low or drops slowly, over time.

How to increase phosphate levels?

Examples include breads that contain yeast, dairy products, meat, eggs, peas, nuts, and beans. Your provider or a dietitian can tell you how much of these to have each day. Medicine may be given to increase your phosphate level. You may be able to take this as a pill at home. You will need to be admitted to the hospital if you need to get this medicine through an IV. Medicines may also be used to lower your calcium level or to raise other mineral levels.

What medications lower phosphate levels?

Steroid medicine, or use of too many diuretics (water pills) or antacids. Certain cancer medicines can lower your phosphate level. Diabetic ketoacidosis (DKA), hypothyroidism, obesity, or certain lung problems, such as asthma. Severe or chronic diarrhea, or inflammatory bowel disease.

What is used to check phosphate levels?

A blood sample is used to check the level of phosphate. Your calcium, vitamin D, or magnesium levels may also be checked.

How to diagnose hypophosphatemia?

Perform a thorough neuromuscular assessment; assess the patient’s hand grasp and leg strength and note tremors of the extremities. Assess the deep tendon reflexes; often hyporeflexia is found. Neurological deficits include paresthesia, dysarthria, confusion, stupor, seizures, and coma. The patient’s voice may be weak and shaky. Assess the patient’s ability to swallow and the ga g reflex. Auscultate the heart; the pulse may be weak and irregular. Assess the respiratory status, and note if the respirations are rapid and shallow because of impaired diaphragmatic function. Weigh the patient and assess for signs and symptoms of malnutrition, such as pallor, dull hair, poor skin turgor, weight loss, and fatigue.

Why is it difficult to get a history of hypophosphatemia?

With chronic hypophosphatemia, an accurate history may be difficult to obtain because often there is memory loss. The patient may report a history of anorexia, muscle and bone pain, and paresthesia. Hypophosphatemia generally creates neuromuscular, cardiopulmonary, hematological, and GI abnormalities.

What is the name of the disease that results in the inability of the kidney to reabsorb phosphate?

Familial hypophosphatemia (formerly vitamin D–resistant rickets) results in the inability of the kidney to effectively reabsorb phosphate. Low blood levels of phosphate can be seen beginning between 6 and 10 months. In most cases, transmission of the trait follows an X-linked dominant (from PHEX mutations) pattern, although autosomal recessive (via DMP1 mutations), autosomal dominant (from FGF23 mutations), and X-linked recessive transmissions have been reported. About one-third of cases involve a new mutation.

What causes a low phosphorus level?

The many causes of hypophosphatemia include dietary changes, GI abnormalities, drug interactions, hormonal changes, and cellular changes. Changes in the diet as a result of malnutrition or alcoholism can significantly reduce the serum phosphorus levels. Inadequate amounts of phosphorus in total parental nutrition may also lead to hypophosphatemia. GI problems that result in a phosphorus deficit include vomiting, chronic diarrhea, and intestinal malabsorption because of vitamin D deficiency. Two types of medications that most commonly decrease serum phosphorus are aluminum-containing antacids and diuretics. Aluminum binds with phosphorus in the GI tract, and most diuretics promote urinary excretion of phosphorus. Infusion of glucose also leads to phosphate depletion, as do increased levels of PTH, which increase the urinary excretion of phosphorus. Cellular changes in several disorders, such as diabetic ketoacidosis, burns, and acid-base disorders, lead to hypophosphatemia.

What is the phosphorus level in the blood?

Phosphorus is a major anion in the intracellular fluid that is measured in the serum; normal serum phosphorus levels range between 1.7 and 2.6 mEq/L (2.5 and 4.5 mg/dL). In children, the serum phosphorus level is higher, at 4 to 7 mg/dL. Hypophosphatemia occurs when the serum phosphorus levels fall below 1.7 mEq/L (2.5 mg/dL). Patients with moderate hypophosphatemia (1 to 2.5 mg/dL) are usually asymptomatic and require no treatment except to manage the underlying cause; patients with severe hypophosphatemia (< 1 mg/dL) need more aggressive treatment to prevent complications. The possible complications of hypophosphatemia are grave and include dysrhythmias, heart failure, shock, destruction of striated muscles, seizures, and coma. Hypophosphatemia occurs in approximately 1% to 5% of all hospitalized patients, 30% of patients admitted to critical care units, and 40% to 80% of patients with alcohol dependence, diabetic ketoacidosis, sepsis, or septic shock. Severe hypophosphatemia is rare and occurs in less than 1% of all hospitalized patients.

How to replace phosphorus in a patient with hyperphosphatemia?

Phosphorus is replaced either by dietary intake or by oral administration of phosphate salt tablets or capsules. If hyperphosphatemia inadvertently occurs, hypocalcemia is also likely. Assess for tetany and be sure the patient has an open airway, adequate breathing, normal circulation, and an adequate urine output. Routine serum phosphate and calcium levels are ordered to determine the effectiveness of the replacement. Monitor the IV site for infiltration because potassium phosphate can cause tissue sloughing and necrosis.

Where is phosphorus found in the body?

Approximately 85% of body phosphorus is in bone , and most of the remainder is intracellular. Only 1% is in the extracellular fluid. Phosphorus serves many functions in the body, such as maintenance of the normal nerve and muscle activity; formation and strength of bones and teeth; maintenance of cell membrane structure and function; metabolism of carbohydrates, proteins, and fats; maintenance of oxygen delivery to the tissue; maintenance of acid-base balance; and activation of the B complex vitamins. Phosphorus is excreted by the kidneys (90%) and gastrointestinal (GI) tract (10%). Regulation of phosphorus is controlled by parathyroid hormone (PTH). PTH stimulates a vitamin D derivative (calcitriol) to increase phosphorus absorption by the GI tract. PTH acts on the renal tubules to increase phosphate excretion.

What is hypophosphatemia?

Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. Symptoms may include weakness, trouble breathing, and loss of appetite. Complications may include seizures, coma, rhabdomyolysis, or softening of the bones.

How does hypophosphatemia occur?

Hypophosphatemia is caused by the following three mechanisms: 1 Inadequate intake (often unmasked in refeeding after long-term low phosphate intake) 2 Increased excretion (e.g. in hyperparathyroidism, hypophosphatemic rickets) 3 Shift of phosphorus from the extracellular to the intracellular space. This can be seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g. hungry bone syndrome) and acute respiratory alkalosis.

What causes a low phosphate level in the blood?

Causes include alcohol use disorder, refeeding in those with malnutrition, diabetic ketoacidosis, burns, hyperventilation, and certain medications. It may also occur in the setting of hyperparathyroidism, hypothyroidism, and Cushing syndrome. It is diagnosed based on a blood phosphate concentration of less than 0.81 mmol/L (2.5 mg/dL). When levels are below 0.32 mmol/L (1.0 mg/dL) it is deemed to be severe.

How to diagnose hypophosphatemia?

Hypophosphatemia is diagnosed by measuring the concentration of phosphate in the blood. Concentrations of phosphate less than 0.81 mmol/L (2.5 mg/dL) are considered diagnostic of hypophosphatemia, though additional tests may be needed to identify the underlying cause of the disorder.

How is phosphate given?

Phosphate may be given by mouth or by injection into a vein. Hypophosphatemia occurs in about 2% of people within hospital and 70% of people in the intensive care unit (ICU).

Why does alkalemia occur?

This includes most common respiratory alkalemia (a higher than normal blood pH from low carbon dioxide levels in the blood), which in turn is caused by any hyperventilation (such as may result from sepsis, fever, pain, anxiety, drug withdrawal, and many other causes).

Why do cells need phosphate?

Causes. Refeeding syndrome – This causes a demand for phosphate in cells due to the action of hexokinase, an enzyme that attaches phosphate to glucose to begin metabolism of glucose. Also, production of ATP when cells are fed and recharge their energy supplies requires phosphate.

What causes hypophosphatemia?

As previously stated, hypophosphatemia's most common causes are inadequate phosphate intake, increased phosphate excretion, and shift from extracellular phosphate into the intracellular space. [6][7][8]

What is hypophosphatemia managed by?

Because of the diverse presentation of hypophosphatemia, the condition is best managed by an interprofessional team that consists of an internist, endocrinologist, intensivist, general surgeon, and nurse practitioner. Specialty trained nurses administer ordered treatments and provide feedback on response to the team. Pharmacists review oral and parenteral treatment, including dosage and drug compatibility. The effects of hypophosphatemia are broad and impact nearly every system. Symptoms of this deficiency become apparent below 0.32 mmol/L. In general, all symptomatic patients need treatment with phosphate; asymptomatic patients may be observed and monitored. The outlook for patients depends on the primary condition causing the hypophosphatemia. If the cause is benign, then treatment outcomes are excellent. [11][12][Level 5]

What does it mean when a phosphate level is less than 100 mg?

A 24-hour urine phosphate excretion less than 100 mg or FEPO4 less than 5% shows decreased phosphate excretion, indicating hypophosphatemia is from a redistribution within the body or decreased intestinal absorption. A 24-hour urine phosphate excretion greater than 100 mg or FEPO4 greater than 5% indicates renal phosphate wasting. Hypophosphatemia in this scenario is likely due to hyperparathyroidism or vitamin D deficiency.

How does hypophosphatemia affect the nervous system?

The effects of hypophosphatemia are broad and impact nearly every system. Symptoms of this deficiency become apparent below 0.32 mmol/L. Effects primarily are due to intracellular depletion; however, chronic effects can be seen in the bone structures. Prolonged hypophosphatemia leads to osteopenia, osteoporosis, rickets, or osteomalacia due to decreased bone mineralization. The central nervous system may manifest with metabolic encephalopathy as a result of ATP depletion and may include altered mental state, irritability, paresthesias, numbness, seizures, or coma.  Cardiac function is impacted by ATP depletion. In addition to possible systolic heart failure, the myocytes become less stable, and arrhythmias are possible. The decreased diaphragmatic function impacts pulmonary function with subsequent hypoventilation. Ventilator-dependent patients have been shown to have longer hospital courses and worse outcomes when hypophosphatemia is present. Gastrointestinal dysfunction occurs as a result of ATP deficiency, also with dysphagia or ileus possible. Generalized muscular weakness can occur. Rhabdomyolysis may occur, resulting in renal injury and increased creatinine phosphokinases; however, this is typically only seen in acute or chronic hypophosphatemia, such as in acutely ill persons with alcohol use disorder. The hematology systems are rarely impacted, but depletion of ATP may result in increased erythrocyte rigidity, predisposing to hemolysis, reduced phagocytosis, and granulocyte chemotaxis by white blood cells, and thrombocytopenia. [9][10]

How does phosphate shift intracellularly?

Refeeding syndrome occurs when a patient who has been starved of nutrition suddenly is replenished with carbohydrates, proteins, and lipids. Insulin and glucose assist in driving phos phate intracellularly. The net body stores of phosphate necessary to perform basic metabolism, such as glycolysis, are depleted. The body begins to process the newfound foods to produce ATP for energy. Cells uptake all available free phosphate, leading to profound hypophosphatemia. The hungry bone syndrome occurs after the correction of hyperparathyroidism, where osteopenic bones begin to reabsorb and store phosphate and calcium. This leads to increased bone demand for these ions and hypophosphatemia. Acute respiratory alkalosis induces hypophosphatemia via changes in cellular pH. Increased pH stimulates phosphofructokinase, thus stimulating glycolysis to produce ATP, thus consuming phosphate from the cellular space. Serum phosphate is shifted intracellularly to meet this demand. While typically mild, extreme hyperventilation with subsequent PCO2 changes to less than 20 mmHg can lower phosphate concentrations to below 0.32 mmol/L. This is thought to be the most common cause of marked hypophosphatemia in hospitalized patients.

What is the normal phosphate level in children?

The normal level of serum phosphate in children is considerably higher and 7 mg/dL for infants. Hypophosphatemia is a relatively common laboratory abnormality and is often an incidental finding. [1][2][3][4][5]

What causes hyperparathyroidism?

Primary or secondary hyperparathyroidism are the most likely causes where primary hyperparathyroidism is due to hypercalcemia, and secondary hyperparathyroidism is induced by any of the causes that lead to vitamin D deficiency. Primary renal phosphate-wasting syndromes also exist where there is a direct failure of the renal system without coexisting systemic failure. These include a wide variety of genetic malformations, leading to faulty sodium-phosphate cotransporters. One of the larger examples of this includes X-linked hypophosphatemic rickets, where a mutation in the PHEX gene leads to increased levels of fibroblast growth factor 23 and directly decreases resorption of phosphate in the proximal renal-collecting tubules. Mutations in the sodium-phosphate cotransporter gene SLC34A3 causes type 2c sodium-phosphate cotransporter failure. The SLC34A1 gene is responsible for encoding the type 2a sodium-phosphate cotransporter and has been associated with mutations. The sodium-hydrogen exchanger regulatory factor 1 is responsible for creating the sodium gradient, which powers most ion reabsorption. Mutations here lead to pan-ionic losses. Fanconi syndrome is another classic cause of renal losses. It is a generalized impairment in proximal tubular function leading to urinary wasting most often due to illnesses such as multiple myeloma where immunoglobulin light chains induce renal tubular damage and Wilson disease with copper accumulation in children. Anything that increases urine production also will lead to increased phosphate loss, including glucosuria, alcohol, lithium, and diuretics such as acetazolamide and thiazides, rapid fluid volume expansion from oral or intravenous fluids. In patients with renal failure, hypophosphatemia can be seen as a result of dialysis therapy removing phosphate in bulk.

What causes hypophosphatemia?

Chronic hypophosphatemia usually is the result of decreased renal phosphate reabsorption. Causes include the following: Increased parathyroid hormone levels, as in primary and secondary hyperparathyroidism. Other hormonal disturbances, such as Cushing syndrome and hypothyroidism. Vitamin D deficiency.

How many hospitalized patients have hypophosphatemia?

Hypophosphatemia occurs in 2% of hospitalized patients but is more prevalent in certain populations (eg, it occurs in up to 10% of hospitalized patients with alcohol use disorder).

Why is sodium phosphate not tolerated?

Oral sodium phosphate or potassium phosphate may be poorly tolerated because of diarrhea. Ingestion of 1 L of low-fat or skim milk provides 1 g of phosphate and may be more acceptable. Removal of the cause of hypophosphatemia may include stopping phosphate-binding antacids or diuretics or correcting hypomagnesemia.

Is potassium phosphate safe to take IV?

It should be administered in any of the following circumstances: IV administration of potassium phosphate (as buffered mix of K2HPO4 and KH2PO4) is relatively safe when renal function is well preserved. Parenteral potassium phosphate contains 93 mg (3 mmol) phosphorus and 170 mg (4.4 mEq) potassium per mL.

Can hypophosphatemia cause anorexia?

Hypophosphatemia is usually asymptomatic, but severe chronic depletion can cause anorexia, muscle weakness, and osteomalacia.

Can hypophosphatemia cause muscle weakness?

Hypophosphatemia is usually asymptomatic, but severe depletion can cause anorexia, muscle weakness, and osteomalacia. Treat the underlying disorder, but some patients require oral, or rarely, IV phosphate replacement.

What is hypophosphatemia in the body?

Hypophosphatemia is an electrolyte disturbance in which there is an abnormally low level of phosphate in the blood. The condition has many causes, but is most commonly seen when malnourished patients are given large amounts of carbohydrates, which creates a high phosphorus demand by cells, removing phosphate from the blood. Because a decrease in phosphate in the blood is sometimes associated with an increase in phosphate in the urine, the terms hypophosphatemia and "phosphaturia" are occasionally used interchangeably; however, this is improper since there exist many causes of hypophosphatemia besides overexcretion and phosphaturia, and in fact the most common causes of hypophosphatemia are not associated with phosphaturia.

What is the numerical value of hypophosphatemia in Pythagorean numerology?

The numerical value of hypophosphatemia in Pythagorean Numerology is: 6

What is a low phosphate level?

A condition of an abnormally low level of PHOSPHATES in the blood. Severe hypophosphatemia (below 1 mg/liter) can affect every organ in the body leading to HEMOLYSIS; LASSITUDE; SEIZURES; and COMA. Chronic hypophosphatemia can lead to MUSCLE WEAKNESS; and bone diseases, such as RICKETS and OSTEOMALACIA.

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• Hypophosphatemia generally creates neuromuscular, cardiopulmonary, hematological, and GI abnormalities. Perform a thorough neuromuscular assessment; assess the patients hand grasp and leg strength and note tremors of the extremities. Assess the deep tendon reflexes; often hyporeflexia is found. Neurological deficits include paresthesia, dysarthria,...

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