Friday, October 30, 2009
Alice in intensiveland
"Alice in intensiveland" is an wonderful article by Bartlett RH which appeared in Chest 1995; 108: 1129-39. This article has commented in an hilarious manner regarding the nonsenses one should not do in ICU. A must read.
Monday, October 19, 2009
Wolff-Parkinson-White Syndrome
WPW Syndrome: Paroxysmal tachycardias mediated by accessory pathways that cross the AV node and electrically link the atria and ventricles, when combined with a short P-R interval (< 0.12 seconds), a wide QRS, and secondary repolarization abnormalities.
Wolff-Parkinson-White pattern or ventricular preexcitation - When this ECG pattern is seen without the tachycardia.
First described in 1930 in an article by Louis Wolff, Sir John Parkinson, and Paul Dudley White in 11 patients.
• Accessory bypass tracts detectable on an ECG - reported in 0.15 to 0.25 %.
• Familial association - 0.55 %.
• 2:1 male: female predominance.
• Tachyarrhythmia - depends on the population studied and varies from 13% in a healthy outpatient population to 80% in the hospital setting.
• Incidence of sudden death in the 0-4% range.
• Approx. 5–10% of patients with documented bypass tracts have concomitant structural heart disease.
o Ebstein anomaly is the most common, accounting for 25–50%,
o Corrected transposition of the great arteries (levo-TGA), and
o Hypertrophic cardiomyopathy.
• Association of right-sided accessory pathways with structural heart disease is strong. 45% of patients with right-sided vs 05% of those with left-sided.
• Most common bypass tract is an accessory atrioventricular (AV) pathway called Kent bundle.
• Another common preexcitation syndrome, Lown-Ganong-Levine (LGL), has an accessory pathway - James fibers, which connect the atria serially to the His bundle.
• Pathways can cross the AV groove anywhere in its course to connect the left or right atrium to its respective ventricle except the region between the aortic and mitral valves. The distribution of accessory pathways,
- 46–60% are located in the left free wall,
- 25% within the posteroseptal space,
- 13–21% in the right free wall, and
- 2% in the anteroseptal space.
ECG
Each location produces a distinct ECG pattern but in the 13% of patients with two or more bypass tracts the ECG tracing can be confounding and show multiple QRS morphologies. During sinus rhythm, an atrial impulse will reach the ventricles via both the AV node and the accessory AV pathway. The latter conducts the atrial impulse to the ventricles before the AV node, resulting in ventricular pre-excitation and a short PR interval. On reaching the ventricles, the pre-excitation impulse is not conducted via the specialised conducting system. Hence, early ventricular activation will be slowed, resulting in a slurred upstroke of the QRS complex, the so-called delta (d) wave.The abnormal ventricular activation also gives rise to secondary S-T segment and T-wave abnormalities. d-wave polarity in a 12-lead ECG may help localise the anatomical position of the accessory pathway.
In type A WPW the accessory pathway is usually situated on the left with pre-excitation of the left ventricle. Positive R waves in the right precordial leads, short PR & a delta wave giving rise to wide QRS complex
Type B WPW has a dominantly negative QRS complex in V1 and the accessory pathway tends to be on the right with pre-excitation of the right ventricle.
CLINICAL - AVRT or AF can occur with WPW.
During AVRT, the re-entry impulse usually travels down the AV node and back up the accessory pathway. Ventricular activation is via the normal conducting pathways and the QRS will be narrow. This is called orthodromic conduction.
Occasionally, the re-entry impulse may pass in the opposite direction (down the accessory pathway and up the AV node), resulting in a wide QRS-complex tachycardia due to abnormal slow ventricular activation. This is antidromic conduction. Treatment is the same as for AVRT.
AF is common in WPW 11-38%, and may be life-threatening. Most impulses are conducted via the accessory pathway, leading to wide QRS complexes. The ECG of WPW with AF usually shows rapid, irregular QRS complexes with variable QRS width. Ventricular response is very rapid, leading to hypotension or cardiogenic shock. This arrhythmia may degenerate to VF.
Symptoms range from palpitations to syncope, episodes of tachycardia may be associated with dyspnea, chest pain, decreased exercise tolerance, anxiety, dizziness, or syncope.
ELECTROPHYSIOLOGIC TESTING
•To confirm the presence of an AP
•To differentiate this condition from other forms of SVT
•To find the pathway participating in the tachycardia and aid in ablative therapy
TREATMENT
Treatment usually involves synchronised DC shock.
Antiarrhythmic drugs may be used when patients are haemodynamically stable and the ventricular rate is not excessively rapid.
•Drugs that prolong the refractory period of the accessory pathway are useful (e.g. sotalol, amiodarone, flecainide and procainamide).
•Drugs that shorten the refractory period (e.g. digoxin) are contraindicated as they may accelerate ventricular rate.
•Verapamil and lidocaine may increase the ventricular rate during AF, and are also best avoided.
•b-Adrenergic blockers have no effect on the refractory period of the accessory pathway.
Catheter Ablation of APS
In conjunction with a diagnostic EP test. Once the AP is localized to a region of the heart, precise mapping and ablation is performed using a steerable electrode catheter. The largest prospective, multicenter clinical trial to evaluate the safety and efficacy of radiofrequency ablation was reported by Calkins and colleagues. This study involved analysis of 1050 patients, of whom 500 had APs. Overall success curing APs was 93 percent. Following an initially successful procedure, recurrence of AP conduction is found in approximately 5 percent of patients.
Complications
•Obtaining vascular access (hematomas, DVT, perforation of the aorta, AV fistula, PTx),
•Catheter manipulation (valvular damage, microemboli, perforation of the coronary sinus or myocardial wall, coronary dissection and/or thrombosis), or
•Delivery of RF energy (AV block, myocardial perforation, coronary artery spasm or occlusion, transient ischemic attacks, or cerebrovascular accidents).
Calkins and coworkers reported the incidence of
•major complications - 3 %
•minor complications - 8 %.
•procedure-related mortality - 0 - 0.2 %.
The two most common types of major complications reported during catheter ablation of APs are inadvertent complete AV block and cardiac tamponade.
Cryoablation has become available as an alternative energy source for creation of myocardial lesions. The main advantage of cryoenergy, compared to radiofrequency energy, is that the risk of heart block appears to be lower.
Aymptomatic Preexcitaion
Mostly have a good prognosis. Because of the small but real risks associated with invasive procedures, EPS is not routinely recommended for risk stratification and/or ablative therapy. ACC/AHA/ESC Guidelines for Management of Patients With Supraventricular Arrhythmias gives catheter ablation a 2a classification for treatment of patients with asymptomatic preexcitation.
The detection of intermittent preexcitation—which is characterized by an abrupt loss of the delta wave, normalization of the QRS complex, and an increase in the P-R interval during a continuous ECG recording—is evidence that an AP has a relatively long refractory period and is unlikely to precipitate VF. The loss of preexcitation after administration of antiarrhythmic drugs like procainamide has also been used to indicate a low-risk subgroup. These noninvasive tests are generally considered inferior to EPS testing in the assessment of risk of sudden cardiac death. Because of this, they play little role in patient management at present.
Studies have identified markers that identify patients at increased risk –
(1) a short preexcited RR interval <250 msec during spontaneous or induced AF (2) a history of symptomatic tachycardia, (3) multiple APs, and (4) Epstein anomaly.
Wolff-Parkinson-White pattern or ventricular preexcitation - When this ECG pattern is seen without the tachycardia.
First described in 1930 in an article by Louis Wolff, Sir John Parkinson, and Paul Dudley White in 11 patients.
• Accessory bypass tracts detectable on an ECG - reported in 0.15 to 0.25 %.
• Familial association - 0.55 %.
• 2:1 male: female predominance.
• Tachyarrhythmia - depends on the population studied and varies from 13% in a healthy outpatient population to 80% in the hospital setting.
• Incidence of sudden death in the 0-4% range.
• Approx. 5–10% of patients with documented bypass tracts have concomitant structural heart disease.
o Ebstein anomaly is the most common, accounting for 25–50%,
o Corrected transposition of the great arteries (levo-TGA), and
o Hypertrophic cardiomyopathy.
• Association of right-sided accessory pathways with structural heart disease is strong. 45% of patients with right-sided vs 05% of those with left-sided.
• Most common bypass tract is an accessory atrioventricular (AV) pathway called Kent bundle.
• Another common preexcitation syndrome, Lown-Ganong-Levine (LGL), has an accessory pathway - James fibers, which connect the atria serially to the His bundle.
• Pathways can cross the AV groove anywhere in its course to connect the left or right atrium to its respective ventricle except the region between the aortic and mitral valves. The distribution of accessory pathways,
- 46–60% are located in the left free wall,
- 25% within the posteroseptal space,
- 13–21% in the right free wall, and
- 2% in the anteroseptal space.
ECG
Each location produces a distinct ECG pattern but in the 13% of patients with two or more bypass tracts the ECG tracing can be confounding and show multiple QRS morphologies. During sinus rhythm, an atrial impulse will reach the ventricles via both the AV node and the accessory AV pathway. The latter conducts the atrial impulse to the ventricles before the AV node, resulting in ventricular pre-excitation and a short PR interval. On reaching the ventricles, the pre-excitation impulse is not conducted via the specialised conducting system. Hence, early ventricular activation will be slowed, resulting in a slurred upstroke of the QRS complex, the so-called delta (d) wave.The abnormal ventricular activation also gives rise to secondary S-T segment and T-wave abnormalities. d-wave polarity in a 12-lead ECG may help localise the anatomical position of the accessory pathway.
In type A WPW the accessory pathway is usually situated on the left with pre-excitation of the left ventricle. Positive R waves in the right precordial leads, short PR & a delta wave giving rise to wide QRS complex
Type B WPW has a dominantly negative QRS complex in V1 and the accessory pathway tends to be on the right with pre-excitation of the right ventricle.
CLINICAL - AVRT or AF can occur with WPW.
During AVRT, the re-entry impulse usually travels down the AV node and back up the accessory pathway. Ventricular activation is via the normal conducting pathways and the QRS will be narrow. This is called orthodromic conduction.
Occasionally, the re-entry impulse may pass in the opposite direction (down the accessory pathway and up the AV node), resulting in a wide QRS-complex tachycardia due to abnormal slow ventricular activation. This is antidromic conduction. Treatment is the same as for AVRT.
AF is common in WPW 11-38%, and may be life-threatening. Most impulses are conducted via the accessory pathway, leading to wide QRS complexes. The ECG of WPW with AF usually shows rapid, irregular QRS complexes with variable QRS width. Ventricular response is very rapid, leading to hypotension or cardiogenic shock. This arrhythmia may degenerate to VF.
Symptoms range from palpitations to syncope, episodes of tachycardia may be associated with dyspnea, chest pain, decreased exercise tolerance, anxiety, dizziness, or syncope.
ELECTROPHYSIOLOGIC TESTING
•To confirm the presence of an AP
•To differentiate this condition from other forms of SVT
•To find the pathway participating in the tachycardia and aid in ablative therapy
TREATMENT
Treatment usually involves synchronised DC shock.
Antiarrhythmic drugs may be used when patients are haemodynamically stable and the ventricular rate is not excessively rapid.
•Drugs that prolong the refractory period of the accessory pathway are useful (e.g. sotalol, amiodarone, flecainide and procainamide).
•Drugs that shorten the refractory period (e.g. digoxin) are contraindicated as they may accelerate ventricular rate.
•Verapamil and lidocaine may increase the ventricular rate during AF, and are also best avoided.
•b-Adrenergic blockers have no effect on the refractory period of the accessory pathway.
Catheter Ablation of APS
In conjunction with a diagnostic EP test. Once the AP is localized to a region of the heart, precise mapping and ablation is performed using a steerable electrode catheter. The largest prospective, multicenter clinical trial to evaluate the safety and efficacy of radiofrequency ablation was reported by Calkins and colleagues. This study involved analysis of 1050 patients, of whom 500 had APs. Overall success curing APs was 93 percent. Following an initially successful procedure, recurrence of AP conduction is found in approximately 5 percent of patients.
Complications
•Obtaining vascular access (hematomas, DVT, perforation of the aorta, AV fistula, PTx),
•Catheter manipulation (valvular damage, microemboli, perforation of the coronary sinus or myocardial wall, coronary dissection and/or thrombosis), or
•Delivery of RF energy (AV block, myocardial perforation, coronary artery spasm or occlusion, transient ischemic attacks, or cerebrovascular accidents).
Calkins and coworkers reported the incidence of
•major complications - 3 %
•minor complications - 8 %.
•procedure-related mortality - 0 - 0.2 %.
The two most common types of major complications reported during catheter ablation of APs are inadvertent complete AV block and cardiac tamponade.
Cryoablation has become available as an alternative energy source for creation of myocardial lesions. The main advantage of cryoenergy, compared to radiofrequency energy, is that the risk of heart block appears to be lower.
Aymptomatic Preexcitaion
Mostly have a good prognosis. Because of the small but real risks associated with invasive procedures, EPS is not routinely recommended for risk stratification and/or ablative therapy. ACC/AHA/ESC Guidelines for Management of Patients With Supraventricular Arrhythmias gives catheter ablation a 2a classification for treatment of patients with asymptomatic preexcitation.
The detection of intermittent preexcitation—which is characterized by an abrupt loss of the delta wave, normalization of the QRS complex, and an increase in the P-R interval during a continuous ECG recording—is evidence that an AP has a relatively long refractory period and is unlikely to precipitate VF. The loss of preexcitation after administration of antiarrhythmic drugs like procainamide has also been used to indicate a low-risk subgroup. These noninvasive tests are generally considered inferior to EPS testing in the assessment of risk of sudden cardiac death. Because of this, they play little role in patient management at present.
Studies have identified markers that identify patients at increased risk –
(1) a short preexcited RR interval <250 msec during spontaneous or induced AF (2) a history of symptomatic tachycardia, (3) multiple APs, and (4) Epstein anomaly.
Friday, October 9, 2009
Hypophosphatemia
Background
Phosphate is the most abundant intracellular anion and is essential for
- membrane structure,
- transport in all cells.
- production of ATP, which provides energy for nearly all cell functions.
- as an essential component of DNA and RNA.
- production of 2,3-diphosphoglycerate (2,3-DPG) in RBC’s, which facilitates release of oxygen from hemoglobin
Approximately 85% of the body's phosphorus is in bone as hydroxyapatite,
while most of the remainder (15%) is present in soft tissue.
Only 0.1% of phosphorus is present in extracellular fluid, and it is this
fraction that is measured with a serum phosphorus level.
Normal Serum phosphate or phosphorus levels are 0.81-1.45 mmol/L.
Hypophosphatemia is defined as
mild: 0.65-0.81 mmol/L,
moderate: 0.32-0.65 mmol/L,
severe: < 0.32 mmol/L. Mild to moderately severe hypophosphatemia is usually asymptomatic. Major clinical sequelae usually occur only in severe hypophosphatemia.
Pathophysiology
Phosphorus homeostasis is complex and regulated by the actions of several hormones.
- Parathyroid hormone causes phosphate to be released from bone and inhibits renal reabsorption of phosphorus, resulting in phosphaturia
- Vitamin D aids in the intestinal reabsorption of phosphorus.
- Thyroid hormone & growth hormone act to increase renal reabsorption of phosphate.
- Phosphatonins -Factors responsible for inhibition of renal phosphate reabsorption.
Major causes of hypophosphatemia
Internal redistribution
Increased insulin secretion, particularly during refeeding
Acute respiratory alkalosis
Hungry bone syndrome
Decreased intestinal absorption
Inadequate intake
Antacids containing aluminum or magnesium
Steatorrhea and chronic diarrhea
Vitamin D deficiency or resistance
Increased urinary excretion
Primary and secondary hyperparathyroidism
Vitamin D deficiency or resistance
Hereditary hypophosphatemic rickets
Oncogenic osteomalacia
Fanconi syndrome
Other – osmotic diuresis, acetazolamide, acute volume expansion
Internal re-distribution
1) Respiratory alkalosis moves phosphate into cells leading to activation of
phosphofructokinase which stimulates intracellular glycolysis leading to phosphate
consumption as phosphorylated glucose precursors are produced.
Any cause of hyperventilation (eg, sepsis, anxiety, pain, heatstroke, alcohol
withdrawal, diabetic ketoacidosis [DKA], hepatic encephalopathy, salicylate
toxicity) can precipitate hypophosphatemia.
2) Administering carbohydrate lowers serum phosphate by stimulating the release of insulin which moves phosphate and glucose into cells.
The so-called refeeding syndrome occurs when starving or chronically malnourished patients are refed or given intravenous (IV) glucose, and typically produces a hypophosphatemic state by treatment day 3 or 4. In addition, during refeeding cells switch to an anabolic state, resulting in further phosphate depletion as this essential substrate is incorporated into cells and cell products.
3) Catecholamines and beta-receptor agonists also stimulate phosphate uptake into cells.
4) Certain rapidly growing malignancies (eg, acute leukemia, lymphomas) may consume phosphate preferentially, leading to hypophosphatemia.
5) Hungry bone syndrome — Parathyroidectomy (for hyperparathyroidism) or rarely thyroidectomy (for hyperthyroidism) in patients with preexisting osteopenia can rarely result in marked deposition of calcium and phosphate in bone in the immediate postoperative period.
In most cases of intracellular phosphate shift, serum phosphate normalizes once the precipitating cause is removed.
Increased urinary excretion
1) Parathyroid hormone stimulates the kidneys to excrete phosphate,hypophosphatemia is a common sequela of primary and secondary hyperparathyroidism.
2) Urinary loss of phosphate occurs with acute volume expansion due to a dilution of serum calcium, which in turn triggers an increase in the release of parathyroid hormone.
3) Osmotic diuresis, such as seen in hyperosmolar hyperglycemic syndrome (HHS)also produces increased urinary excretion of phosphorus. Diuretics, including loop diuretics, thiazides and carbonic anhydrase inhibitors (eg acetazolamide) interfere with the ability of the proximal tubule to reabsorb phosphorus, thus producing hyperphosphaturia and potentially leading to hypophosphatemia.
4) Patients with transplanted kidneys,congenital defects (X-linked hypophosphatemia [XLH] and autosomal dominant hypophosphatemic rickets [ADHR]), or Fanconi syndrome (proximal tubule dysfunction) also may excrete excess urinary phosphate.
Decreased intestinal absorption
Phosphate may be lost via the gut, as in chronic diarrhea, malabsorption syndromes, severe vomiting, or NG suctioning. Phosphate may also be bound in the gut, thereby preventing absorption (eg,chronic use of sucralfate, or phosphate-binding antacids, including aluminum hydroxide, aluminum carbonate, and calcium carbonate).
Decreased dietary intake
This is a rare cause of hypophosphatemia because of the ubiquity of phosphate in foods. Certain conditions such as anorexia nervosa or chronic alcoholism may lead to hypophosphatemia in part via this mechanism.
Manifestations of phosphate deficiency
1) Muscular weakness
2) Rhabdomyolysis via ATP depletion and the consequent inability of muscle cells to maintain membrane integrity. Patients undergoing acute alcohol withdrawal are especially vulnerable to rhabdomyolysis secondary to hypophosphatemia, which is caused by the rapid uptake of phosphate into muscle cells. Rhabdomyolysis occurs more rarely in patients being treated for DKA or being refed after starvation.
3) Respiratory insufficiency
4) Myocardial depression, reduced threshold for ventricular arrhythmias.
5) Impaired neurologic function, manifested by confusion, seizures, and coma. Peripheral neuropathy and ascending motor paralysis, similar to Guillain-Barré syndrome. Extrapontine myelinolysis has also been reported.
6) The hemolytic anemia ,attributed to the inability of erythrocytes to maintain integrity of cell membranes in the face of ATP depletion, leading to their destruction in the spleen.
7) Compromised oxygen delivery to the tissues due to decreases in erythrocyte 2,3-DPG
8) Leukocyte function is affected, which results in impaired chemotaxis and phagocytosis.
Treatment
Treatment of hypophosphatemia is twofold.
o Correct any precipitating causes of hypophosphatemia.
o Replace total body phosphates.
Depending on the clinical situation, replacement options include dietary phosphate, oral phosphate preparations, and IV phosphate.The most important consideration in choosing replacement therapy is whether the patient has signs or symptoms of phosphate depletion.
Mild to moderately severe, asymptomatic hypophosphatemia may require oral phosphate replacement; however, correcting factors that led to the hypophosphatemia usually is sufficient.
Severe/symptomatic Hypophosphatemia -Patients with symptoms of hypophosphatemia or with serum phosphate levels less than 0.32 mmol/L require IV phosphate replacement.
The intracellular nature of phosphate makes interpreting a low serum phosphate level difficult and predicting the amount required to replenish cellular stores nearly impossible.
Phosphate salt
IV preparations are available as sodium phosphate (Na2HPO4 and NAH2PO4)or potassium phosphate (K2HPO4 and KH2PO4).
Response to IV phosphorus supplementation varies widely and may be associated with hyperphosphatemia and hypocalcemia. Rate of infusion and choice of initial dosage should be based on severity of hypophosphatemia and presence of symptoms.
Thanks to Dr Harjit Mahay for contributing this wonderful article.
Phosphate is the most abundant intracellular anion and is essential for
- membrane structure,
- transport in all cells.
- production of ATP, which provides energy for nearly all cell functions.
- as an essential component of DNA and RNA.
- production of 2,3-diphosphoglycerate (2,3-DPG) in RBC’s, which facilitates release of oxygen from hemoglobin
Approximately 85% of the body's phosphorus is in bone as hydroxyapatite,
while most of the remainder (15%) is present in soft tissue.
Only 0.1% of phosphorus is present in extracellular fluid, and it is this
fraction that is measured with a serum phosphorus level.
Normal Serum phosphate or phosphorus levels are 0.81-1.45 mmol/L.
Hypophosphatemia is defined as
mild: 0.65-0.81 mmol/L,
moderate: 0.32-0.65 mmol/L,
severe: < 0.32 mmol/L. Mild to moderately severe hypophosphatemia is usually asymptomatic. Major clinical sequelae usually occur only in severe hypophosphatemia.
Pathophysiology
Phosphorus homeostasis is complex and regulated by the actions of several hormones.
- Parathyroid hormone causes phosphate to be released from bone and inhibits renal reabsorption of phosphorus, resulting in phosphaturia
- Vitamin D aids in the intestinal reabsorption of phosphorus.
- Thyroid hormone & growth hormone act to increase renal reabsorption of phosphate.
- Phosphatonins -Factors responsible for inhibition of renal phosphate reabsorption.
Major causes of hypophosphatemia
Internal redistribution
Increased insulin secretion, particularly during refeeding
Acute respiratory alkalosis
Hungry bone syndrome
Decreased intestinal absorption
Inadequate intake
Antacids containing aluminum or magnesium
Steatorrhea and chronic diarrhea
Vitamin D deficiency or resistance
Increased urinary excretion
Primary and secondary hyperparathyroidism
Vitamin D deficiency or resistance
Hereditary hypophosphatemic rickets
Oncogenic osteomalacia
Fanconi syndrome
Other – osmotic diuresis, acetazolamide, acute volume expansion
Internal re-distribution
1) Respiratory alkalosis moves phosphate into cells leading to activation of
phosphofructokinase which stimulates intracellular glycolysis leading to phosphate
consumption as phosphorylated glucose precursors are produced.
Any cause of hyperventilation (eg, sepsis, anxiety, pain, heatstroke, alcohol
withdrawal, diabetic ketoacidosis [DKA], hepatic encephalopathy, salicylate
toxicity) can precipitate hypophosphatemia.
2) Administering carbohydrate lowers serum phosphate by stimulating the release of insulin which moves phosphate and glucose into cells.
The so-called refeeding syndrome occurs when starving or chronically malnourished patients are refed or given intravenous (IV) glucose, and typically produces a hypophosphatemic state by treatment day 3 or 4. In addition, during refeeding cells switch to an anabolic state, resulting in further phosphate depletion as this essential substrate is incorporated into cells and cell products.
3) Catecholamines and beta-receptor agonists also stimulate phosphate uptake into cells.
4) Certain rapidly growing malignancies (eg, acute leukemia, lymphomas) may consume phosphate preferentially, leading to hypophosphatemia.
5) Hungry bone syndrome — Parathyroidectomy (for hyperparathyroidism) or rarely thyroidectomy (for hyperthyroidism) in patients with preexisting osteopenia can rarely result in marked deposition of calcium and phosphate in bone in the immediate postoperative period.
In most cases of intracellular phosphate shift, serum phosphate normalizes once the precipitating cause is removed.
Increased urinary excretion
1) Parathyroid hormone stimulates the kidneys to excrete phosphate,hypophosphatemia is a common sequela of primary and secondary hyperparathyroidism.
2) Urinary loss of phosphate occurs with acute volume expansion due to a dilution of serum calcium, which in turn triggers an increase in the release of parathyroid hormone.
3) Osmotic diuresis, such as seen in hyperosmolar hyperglycemic syndrome (HHS)also produces increased urinary excretion of phosphorus. Diuretics, including loop diuretics, thiazides and carbonic anhydrase inhibitors (eg acetazolamide) interfere with the ability of the proximal tubule to reabsorb phosphorus, thus producing hyperphosphaturia and potentially leading to hypophosphatemia.
4) Patients with transplanted kidneys,congenital defects (X-linked hypophosphatemia [XLH] and autosomal dominant hypophosphatemic rickets [ADHR]), or Fanconi syndrome (proximal tubule dysfunction) also may excrete excess urinary phosphate.
Decreased intestinal absorption
Phosphate may be lost via the gut, as in chronic diarrhea, malabsorption syndromes, severe vomiting, or NG suctioning. Phosphate may also be bound in the gut, thereby preventing absorption (eg,chronic use of sucralfate, or phosphate-binding antacids, including aluminum hydroxide, aluminum carbonate, and calcium carbonate).
Decreased dietary intake
This is a rare cause of hypophosphatemia because of the ubiquity of phosphate in foods. Certain conditions such as anorexia nervosa or chronic alcoholism may lead to hypophosphatemia in part via this mechanism.
Manifestations of phosphate deficiency
1) Muscular weakness
2) Rhabdomyolysis via ATP depletion and the consequent inability of muscle cells to maintain membrane integrity. Patients undergoing acute alcohol withdrawal are especially vulnerable to rhabdomyolysis secondary to hypophosphatemia, which is caused by the rapid uptake of phosphate into muscle cells. Rhabdomyolysis occurs more rarely in patients being treated for DKA or being refed after starvation.
3) Respiratory insufficiency
4) Myocardial depression, reduced threshold for ventricular arrhythmias.
5) Impaired neurologic function, manifested by confusion, seizures, and coma. Peripheral neuropathy and ascending motor paralysis, similar to Guillain-Barré syndrome. Extrapontine myelinolysis has also been reported.
6) The hemolytic anemia ,attributed to the inability of erythrocytes to maintain integrity of cell membranes in the face of ATP depletion, leading to their destruction in the spleen.
7) Compromised oxygen delivery to the tissues due to decreases in erythrocyte 2,3-DPG
8) Leukocyte function is affected, which results in impaired chemotaxis and phagocytosis.
Treatment
Treatment of hypophosphatemia is twofold.
o Correct any precipitating causes of hypophosphatemia.
o Replace total body phosphates.
Depending on the clinical situation, replacement options include dietary phosphate, oral phosphate preparations, and IV phosphate.The most important consideration in choosing replacement therapy is whether the patient has signs or symptoms of phosphate depletion.
Mild to moderately severe, asymptomatic hypophosphatemia may require oral phosphate replacement; however, correcting factors that led to the hypophosphatemia usually is sufficient.
Severe/symptomatic Hypophosphatemia -Patients with symptoms of hypophosphatemia or with serum phosphate levels less than 0.32 mmol/L require IV phosphate replacement.
The intracellular nature of phosphate makes interpreting a low serum phosphate level difficult and predicting the amount required to replenish cellular stores nearly impossible.
Phosphate salt
IV preparations are available as sodium phosphate (Na2HPO4 and NAH2PO4)or potassium phosphate (K2HPO4 and KH2PO4).
Response to IV phosphorus supplementation varies widely and may be associated with hyperphosphatemia and hypocalcemia. Rate of infusion and choice of initial dosage should be based on severity of hypophosphatemia and presence of symptoms.
Thanks to Dr Harjit Mahay for contributing this wonderful article.
Thursday, October 8, 2009
Management of the pregnant trauma patient
Trauma in 5% of pregnancy, of which greater than 50% are MVAs, and of these 82% of fetal deaths occur during the accident.
*MVA 1/2, Falls 1/5, Assaults 1/5, Burns 1/100
Life threatening trauma results in 50% fetal loss rate.
The most common cause of fetal death after blunt trauma is abruption.
Anterior abdominal penetrating trauma will (unless proven otherwise) injure the fetus >20/40 weeks gestation.
Peri-mortem caesarian has poor prognosis.
Note there are preventive (non-medical) measures which exist are effective when followed. (physical abuse, alcohol, seat-belts)
Principles (on top of basic trauma principles)
Changes in maternal physiology.
Radiation/medication risks greater in early pregnancy.
Fetus viable after 23-24 weeks.
Two-patients: good management of mother is good for fetus usually.
Fetus hates hypoxaemia and hypovolaemia.
Remember the signs of fetal distress (tachycardia, decreased variability, decelerations)
Multi-disciplinarian approach
Trauma surgeon, emergency physician, technicians, obstetricians, neonatologist, many specialist nursing staff.
Prehospital issues
History
Beware of the distended abdomen. Also avoid direct pressure on abdomen (e.g. MAST)
Lateral decubitus
Transfusion with O negative
Emergency care issues (on top of ATLS principles)
All investigations (including radiology) and interventions for the mother necessary should be performed (e.g. DPL)
Estimation of gestation from fundal height; any fetus >23 wks should prompt immediate monitoring, which includes tocography and FHS. (umbilicus 20wks) NB 25% of trauma after 2240 wks gestation is complicated by premature labour
Secondary survey includes rectal and vaginal exam (cervical effacement, dilation, blood/amniotic fluid, etc), except in 3rd trim, where there's need to exclude placenta praevia
FAST is useful (intraabdominal bleed sensitivity 83%)
Kleihauer-Betke test, if positive this is relevant to Rhesus negative mothers.
ABG respiratory alkalosis, dilutional anaemia
Intensive care issues
Think pregnancy conditions and post-partum conditions.
DVT, PE prophylaxis
Blunt Trauma
Not as problematic in <13/40 gestation, unless there is pelvic fracture with 25% chance of fetal loss. Placenta is never elastic, even if myometrium is after 20wks: abruptions usually suspected with uterine activity. Think coagulopathy/DIC and fetal loss. Penetrating Trauma after 20wks uterus usually protective. Tetanus toxoid should be given. C-section C-section post trauma for >25/40wks gestation has 45% survival and 72% maternal survival rate.
Peri-mortem c-section is often futile. Consider after 4minutes of CPR to help fetal survival and aid maternal resuscitation.
Reference:
Kenneth L M, Goetzl, L. Trauma in pregnancy. Critical Care Medicine 2005 Vol. 33, No. 10 (Suppl.)
Thnks to William Ng for contributing this wonderful article.
*MVA 1/2, Falls 1/5, Assaults 1/5, Burns 1/100
Life threatening trauma results in 50% fetal loss rate.
The most common cause of fetal death after blunt trauma is abruption.
Anterior abdominal penetrating trauma will (unless proven otherwise) injure the fetus >20/40 weeks gestation.
Peri-mortem caesarian has poor prognosis.
Note there are preventive (non-medical) measures which exist are effective when followed. (physical abuse, alcohol, seat-belts)
Principles (on top of basic trauma principles)
Changes in maternal physiology.
Radiation/medication risks greater in early pregnancy.
Fetus viable after 23-24 weeks.
Two-patients: good management of mother is good for fetus usually.
Fetus hates hypoxaemia and hypovolaemia.
Remember the signs of fetal distress (tachycardia, decreased variability, decelerations)
Multi-disciplinarian approach
Trauma surgeon, emergency physician, technicians, obstetricians, neonatologist, many specialist nursing staff.
Prehospital issues
History
Beware of the distended abdomen. Also avoid direct pressure on abdomen (e.g. MAST)
Lateral decubitus
Transfusion with O negative
Emergency care issues (on top of ATLS principles)
All investigations (including radiology) and interventions for the mother necessary should be performed (e.g. DPL)
Estimation of gestation from fundal height; any fetus >23 wks should prompt immediate monitoring, which includes tocography and FHS. (umbilicus 20wks) NB 25% of trauma after 2240 wks gestation is complicated by premature labour
Secondary survey includes rectal and vaginal exam (cervical effacement, dilation, blood/amniotic fluid, etc), except in 3rd trim, where there's need to exclude placenta praevia
FAST is useful (intraabdominal bleed sensitivity 83%)
Kleihauer-Betke test, if positive this is relevant to Rhesus negative mothers.
ABG respiratory alkalosis, dilutional anaemia
Intensive care issues
Think pregnancy conditions and post-partum conditions.
DVT, PE prophylaxis
Blunt Trauma
Not as problematic in <13/40 gestation, unless there is pelvic fracture with 25% chance of fetal loss. Placenta is never elastic, even if myometrium is after 20wks: abruptions usually suspected with uterine activity. Think coagulopathy/DIC and fetal loss. Penetrating Trauma after 20wks uterus usually protective. Tetanus toxoid should be given. C-section C-section post trauma for >25/40wks gestation has 45% survival and 72% maternal survival rate.
Peri-mortem c-section is often futile. Consider after 4minutes of CPR to help fetal survival and aid maternal resuscitation.
Reference:
Kenneth L M, Goetzl, L. Trauma in pregnancy. Critical Care Medicine 2005 Vol. 33, No. 10 (Suppl.)
Thnks to William Ng for contributing this wonderful article.
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