Monthly Archives: August 2012

Hypocalcemia

Hypocalcemia is the the presence of serum calcium less than 2.1 mmol/L or 9 mg/dl or an ionized calcium level of less than 1.1 mmol/L or 4.5 mg/dL. In the blood, about half of all calcium is bound to proteins such as serum albumin, but it is the unbound, or ionized, calcium that the body regulates. Plasma calcium may be inaccurate for patients with abnormal blood proteins.

For patients with low serum albumin the formula for corrected calcium is:

Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 (4.0 – serum albumin [g/dL]), where 4.0 represents the average albumin level in g/dL.

SI units: Corrected calcium (mmol/L) = measured total Ca (mmol/L) + 0.02 (40 – serum albumin [g/L]), where 40 represents the average albumin level in g/L.

Causes of Hypocalcemia

  1. Major cause is hypoparathyroidism due to underproduction of PTH.
  2. Severe vitamin D deficiency.
  3. Hyperphosphatemia.
  4. Precipitation of calcium from extensive burns, fat emboli, rhabdomyolysis and pancreatitis.
  5. Drugs such as Furosemide and antiepileptic drugs. In the operating room,
  6. Chelation of calcium through massive transfusion of red blood or albumin.

Clinical Signs of Hypocalcemia

  1. Chronic hypocalcemia causes lethargy, muscle cramps, a prolonged QT interval, renal failure, cataracts, dementia, and personality changes.
  2. Acute hypocalcemia produces neuromuscular irritability with muscle cramps and hand, foot, and circumoral paresthesias. Patients may demonstrate facial nerve irritability to percussion (Chvostek sign) or carpal spasm with tourniquet ischemia for 3 minutes (Trousseau sign).
  3. Severe hypocalcemia results in stridor, laryngospasm, tetany, apnea, coagulopathy, hypotension with catecholamine resistance, psychosis/confusion, and seizures unresponsive to conventional treatment.

Treatment  of Hypocalcemia

  1. Severe or symptomatic hypocalcemia should be treated with IV calcium. A 10 mL ampule of calcium gluconate contains 93 mg of elemental calcium; a 10 mL ampule of calcium chloride contains 273 mg of calcium.
  2. Mild to moderate can be treated with oral calcium and vitamin D.

Anesthetic Considerations

  1. Hypocalcemia should be corrected preoperatively.
  2. Patients may have hypotension with insensitivity to β-adrenergic agonists, a prolonged QT interval, advanced atrioventricular block, and digitalis insensitivity.
  3. Responses to NMBA’s are unpredictable and require close monitoring with a nerve stimulator. 

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Filed under Metabolism and Endocrine, Neuromuscular

Hofmann Elimination

Hofmann elimination is defined as a spontaneous chemical breakdown that occurs at physiological pH and temperature. The process is independent of renal, hepatic or enzymatic function. Nondepolarizing muscle relaxants that undergo Hofmann elimination in whole or part are Atricurium and Cisatricurium. 

The chemical reaction is as follows:

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Filed under Neuromuscular

Amniotic Fluid Embolism

Amniotic fluid embolism (AFE) is a rare but catastrophic complication of pregnancy.

  • Affects an estimated  3 to 5 per 100,000 live births.
  • Mortality rate among affected parturients is as high as 85% and accounts for up to 12% of all maternal deaths.
  • Significant and permanent neurologic sequelae are common among survivors.
  • Introduction of fetal cells, amniotic fluid, and inflammatory mediators in the maternal circulation are thought to be the cause.
  • Presents during labor or the immediate postpartum period with acute hypoxia and hypotension.

Clinical Presentation of AFE:

  •  Hypotension is a key feature of the disease and is present in 100% of patients with severe disease.The initial transient physiologic response is pulmonary hypertension resulting in hypoxia and right heart failure. Patients who survive the initial insult develop a left heart failure and pulmonary edema
  • Hypoxia is an early manifestation of AFE and is thought to arise from acute pulmonary hypertension and ventilation/perfusion mismatch. Pulmonary edema develops later in association with left ventricular dysfunction.
  • Disruption of normal clotting cascade occurs in up to two thirds of patients.

Management of AFE: 

  • Oxygenation: Tracheal intubation, mechanical ventilation, and supplemental oxygen.
  • Circulatory support: Fluid resuscitation and pressor support as needed.
  • Lines and monitors: Normal ASA monitors plus invasive BP, and PA catheter and/or TEE to assess ventricular function.
  • Regular lab studies to aggressively treat coagulopathy.

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Filed under Obstetrics and Perinatology

Temperature Monitoring Sites

  1. Skin temperature (forehead): Normally 3°F to 4°F below core temperature. The gradient can increase with further cooling
  2. Axilla:  Common site for noninvasive temperature determination and is usually 1°F below body temperature. The probe needs be placed at the axillary artery with the arm adducted.
  3. Tympanic membrane:  Correlates well with core temperature. Intervening cerumen may enlarge the gradient with respect to core temperature.
  4. Rectal: Changes in temperature can lag behind those of core body temperature. This phenomenon is often noted during rewarming.
  5. Nasopharyngeal:  Measured at the posterior nasopharynx and reflects the brain temperature. Can be associated with epistaxis in coagulopathic or pregnant patients. Discouraged in patients with head trauma or cerebrospinal fluid rhinorrhea.
  6. Esophageal: Reflects the core temperature well. Probe should be located at the lower third of the esophagus.
  7. Blood: Can be obtained with the thermistor of a pulmonary artery catheter (PAC).

 

**Source: Clinical Anesthesia Procedures of the Massachusetts General Hospital (2010)

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Filed under Instrumentation and Monitoring