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.
Monday, September 7, 2009
Assessment and Management Of Airway Burns
The term “inhalational injury” has been used to describe the aspiration of toxic products of combustion, but also more generally any pulmonary insult associated with a burn injury. Patients with cutaneous burns are two to three times more likely to die if they also have lower airway burns. Death may be a direct result of lung injury but is usually due to the systemic consequences of such injury. It may be impossible to distinguish lung injury caused at the time of the burn directly to the lungs by a burn from injury due to the systemic consequences of the burn. Inhalation injury, age, and burn size are the three most commonly cited predictive factors for prolonged ventilator dependence, hospital stay, and death in burn patients. The injuries can generally be divided into three classes:
- thermal injury (restricted to upper airway structures except in cases of blast injury or steam inhalation),
- local chemical irritation throughout the respiratory tract, and
- systemic toxicity (eg, inhalation of toxins such as carbon monoxide or cyanide).
In the clinical setting, diagnosis of inhalation injury is usually a subjective decision based on a combination of history and physical exam, and confirmed by diagnostic studies (eg, fiberoptic bronchoscopy).
History includes -
mechanism of exposure, (eg, flame, electricity, blast injury, steam, or hot liquid)
quality of inhaled irritants (eg, house fire, industrial toxins), and
duration of exposure eg, trapped in an enclosed space or
conditions that limit avoidance behavior such as intoxication, loss of consciousness, or physical disability).
Physical exam can provide
an estimate of the intensity of exposure and includes findings such as
evidence of exposure of the respiratory tract to extreme heat (facial burns or singed facial or nasal hair),
soot deposited on the face or carbonaceous sputum,or
early manifestations of respiratory compromise such as airway obstruction by edema or parenchymal damage.
Defining diagnostic criteria for inhalation injuries is made difficult by the extreme heterogeneity of clinical presentation as evaluated therefore, diagnosis is with a high index of suspicion of airway burns in patients with one or more of the warning signs.
Warning signs of airway burns - Suspect airway burn if:
• Burns occurred in an enclosed space
• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa - Singed nasal hairs; red, tender oral membranes; or obvious intraoral or pharyngeal burns indicate likely airway burn.
• Soot in sputum, nose, or mouth
• Dyspnoea, decreased level of consciousness, or confusion
• Hypoxaemia (low SpO2 or PaO2) or increased carbon monoxide levels (>2%)
Onset of symptoms may be delayed
Mechanisms of pulmonary insult after lower airway burns
• Mucosal inflammation • Ciliary paralysis
• Mucosal burn • Reduced surfactant
• Bronchorrhoea • Obstruction by debris
• Bronchospasm • Systemic inflammatory response
The pathophysiology of airway burns is highly variable, depending on the environment of the burn and the incomplete products of combustion. The clinical manifestations are often delayed for the first few hours but are usually apparent by 24 hours. Airway debris—including secretions, mucosal slough, and smoke residue—can seriously compromise pulmonary function.
Management of Airway burns—key clinical points
• Restricting fluids increases mortality
• If in doubt, intubate
• Give 100% oxygen until carbon monoxide toxicity excluded
• Ventilatory strategies to avoid lung injury (low volume or pressure)
• Aggressive airway toilet
• Early surgical debridement of wounds
• Early enteral feeding
There is no specific treatment for airway burns other than ensuring adequate oxygenation and minimising iatrogenic lung insult. Prophylactic corticosteroids or antibiotics have no role in treatment. Studies on Beta 2 agonists, Nebulized Heparin,Tocopherol, Inhaled NO are also inconclusive or lack sufficient data.
Control of the airway, by endotracheal intubation, is essential before transporting any patient with suspected airway burn. Rapid fluid administration, with inevitable formation of oedema, may lead to life threatening airway compromise if control of the airway is delayed. Endotracheal intubation before oedema formation is far safer and simpler. Oxygen (100%) should be given until the risk of carbon monoxide toxicity has been excluded, since high concentrations of oxygen will clear carbon monoxide from the body more rapidly than atmospheric concentrations. Importantly, carbon monoxide toxicity may result in a falsely elevated pulse oximetry saturation.
Airway burns are associated with a substantially increased requirement for fluid resuscitation. Reducing the fluid volume administered, to avoid fluid accumulation in the lung, results in a worse outcome. Invasive monitoring may be required to guide fluid administration, especially with failure to respond to increasing volumes of fluid. Fluid administration should not be guided by calculated fluid requirements alone.Adequate oxygen delivery to all the tissues of the body is essential to prevent multi-organ failure.
Aggressive airway toilet is essential. Early surgical debridement, enteral feeding, mobilisation of the patient, and early extubation are desirable. Antibiotics should be reserved for established infections and guided by regular microbiological surveillance.
Several ventilatory strategies have been proposed to improve outcome following airway burns. Adequate systemic oxygenation and minimising further alveolar injury is the primary clinical objective. Prolonging survival will permit spontaneous lung recovery.
- thermal injury (restricted to upper airway structures except in cases of blast injury or steam inhalation),
- local chemical irritation throughout the respiratory tract, and
- systemic toxicity (eg, inhalation of toxins such as carbon monoxide or cyanide).
In the clinical setting, diagnosis of inhalation injury is usually a subjective decision based on a combination of history and physical exam, and confirmed by diagnostic studies (eg, fiberoptic bronchoscopy).
History includes -
mechanism of exposure, (eg, flame, electricity, blast injury, steam, or hot liquid)
quality of inhaled irritants (eg, house fire, industrial toxins), and
duration of exposure eg, trapped in an enclosed space or
conditions that limit avoidance behavior such as intoxication, loss of consciousness, or physical disability).
Physical exam can provide
an estimate of the intensity of exposure and includes findings such as
evidence of exposure of the respiratory tract to extreme heat (facial burns or singed facial or nasal hair),
soot deposited on the face or carbonaceous sputum,or
early manifestations of respiratory compromise such as airway obstruction by edema or parenchymal damage.
Defining diagnostic criteria for inhalation injuries is made difficult by the extreme heterogeneity of clinical presentation as evaluated therefore, diagnosis is with a high index of suspicion of airway burns in patients with one or more of the warning signs.
Warning signs of airway burns - Suspect airway burn if:
• Burns occurred in an enclosed space
• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa - Singed nasal hairs; red, tender oral membranes; or obvious intraoral or pharyngeal burns indicate likely airway burn.
• Soot in sputum, nose, or mouth
• Dyspnoea, decreased level of consciousness, or confusion
• Hypoxaemia (low SpO2 or PaO2) or increased carbon monoxide levels (>2%)
Onset of symptoms may be delayed
Mechanisms of pulmonary insult after lower airway burns
• Mucosal inflammation • Ciliary paralysis
• Mucosal burn • Reduced surfactant
• Bronchorrhoea • Obstruction by debris
• Bronchospasm • Systemic inflammatory response
The pathophysiology of airway burns is highly variable, depending on the environment of the burn and the incomplete products of combustion. The clinical manifestations are often delayed for the first few hours but are usually apparent by 24 hours. Airway debris—including secretions, mucosal slough, and smoke residue—can seriously compromise pulmonary function.
Management of Airway burns—key clinical points
• Restricting fluids increases mortality
• If in doubt, intubate
• Give 100% oxygen until carbon monoxide toxicity excluded
• Ventilatory strategies to avoid lung injury (low volume or pressure)
• Aggressive airway toilet
• Early surgical debridement of wounds
• Early enteral feeding
There is no specific treatment for airway burns other than ensuring adequate oxygenation and minimising iatrogenic lung insult. Prophylactic corticosteroids or antibiotics have no role in treatment. Studies on Beta 2 agonists, Nebulized Heparin,Tocopherol, Inhaled NO are also inconclusive or lack sufficient data.
Control of the airway, by endotracheal intubation, is essential before transporting any patient with suspected airway burn. Rapid fluid administration, with inevitable formation of oedema, may lead to life threatening airway compromise if control of the airway is delayed. Endotracheal intubation before oedema formation is far safer and simpler. Oxygen (100%) should be given until the risk of carbon monoxide toxicity has been excluded, since high concentrations of oxygen will clear carbon monoxide from the body more rapidly than atmospheric concentrations. Importantly, carbon monoxide toxicity may result in a falsely elevated pulse oximetry saturation.
Airway burns are associated with a substantially increased requirement for fluid resuscitation. Reducing the fluid volume administered, to avoid fluid accumulation in the lung, results in a worse outcome. Invasive monitoring may be required to guide fluid administration, especially with failure to respond to increasing volumes of fluid. Fluid administration should not be guided by calculated fluid requirements alone.Adequate oxygen delivery to all the tissues of the body is essential to prevent multi-organ failure.
Aggressive airway toilet is essential. Early surgical debridement, enteral feeding, mobilisation of the patient, and early extubation are desirable. Antibiotics should be reserved for established infections and guided by regular microbiological surveillance.
Several ventilatory strategies have been proposed to improve outcome following airway burns. Adequate systemic oxygenation and minimising further alveolar injury is the primary clinical objective. Prolonging survival will permit spontaneous lung recovery.
Saturday, September 5, 2009
Critical Care/Medical Sites of Interest
Hi everyone, I am trying to collect and make list of all useful websites in CRITICAL CARE. Here is the beginning and if you know some, please share for benefit of all.
Critical Care Medicine
http://www.ccmtutorials.com
http://www.aic.cuhk.edu.hk/web8/index.htm
http://www.lhsc.on.ca/Health_Professionals/CCTC/edubriefs/index.htm
http://www.uihealthcare.com/vh/
http://cim.ucdavis.edu/
http://www.thoracic.org/sections/clinical-information/critical-care/index.html
http://www.anzics.com.au/
http://www.lhsc.on.ca/programs/critcare/pge/
http://www.dicm.co.uk/papers.htm - Great UK based website, primarily for those doing the UK DICM but a treasure trove of evidence for any intensivist
Evidence Based Medicine
http://www.ebmny.org/">http://www.ebmny.org/">http://www.ebmny.org/
http://www.cche.net/usersguides/ebm.asp
http://www.cebm.utoronto.ca/
http://www.cebm.net/
Anesthesia
http://www.virtual-anaesthesia-textbook.com/vat/main.shtml
Acid Base
Acid Base Tutorial - http://www.acid-base.com/
Acid Base Physiology - http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php
Mechanical Ventilation
http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm
http://www.aic.cuhk.edu.hk/web8/mech%20vent%20intro.htm
Sepsis
http://www.sepsisforum.org/">http://www.sepsisforum.org/">http://www.sepsisforum.org/
http://www.elililly.com/
http://www.ardsfoundation.com/
http://ssc.sccm.org/
http://www.ardsnet.org/
Radiology
http://www.learningradiology.com/
http://www.anatomyatlases.org/
Chest XRay
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/cxr.htm
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/atlas/cxratlas_f.htm
http://www.learningradiology.com/lectures/facultylectures/BASIC%20CXR-mod-Adam_files/v3_document.htm
http://www.usfca.edu/fac-staff/ritter/chestxra.htm
Trauma
http://www.trauma.org/
Pupil assessment
http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm
Delirium
http://www.icudelirium.org/delirium/CAM-ICUTraining.html
Anatomy
http://www.pbs.org/wnet/brain/3d/
http://www.meddean.luc.edu/lumen/MedEd/GrossAnatomy/anatomy.htm
http://msjensen.cehd.umn.edu/webanatomy/
http://www.imaios.com/en/e-Anatomy
IABP
http://www.aic.cuhk.edu.hk/web8/IABP%20pressure%20waveforms.htm
ECHO
http://www.criticalecho.com (By Kishore CMC Vellore)
Brain Herniation
http://rad.usuhs.mil/rad/herniation
Critical Care Medicine
http://www.ccmtutorials.com
http://www.aic.cuhk.edu.hk/web8/index.htm
http://www.lhsc.on.ca/Health_Professionals/CCTC/edubriefs/index.htm
http://www.uihealthcare.com/vh/
http://cim.ucdavis.edu/
http://www.thoracic.org/sections/clinical-information/critical-care/index.html
http://www.anzics.com.au/
http://www.lhsc.on.ca/programs/critcare/pge/
http://www.dicm.co.uk/papers.htm - Great UK based website, primarily for those doing the UK DICM but a treasure trove of evidence for any intensivist
Evidence Based Medicine
http://www.ebmny.org/">http://www.ebmny.org/">http://www.ebmny.org/
http://www.cche.net/usersguides/ebm.asp
http://www.cebm.utoronto.ca/
http://www.cebm.net/
Anesthesia
http://www.virtual-anaesthesia-textbook.com/vat/main.shtml
Acid Base
Acid Base Tutorial - http://www.acid-base.com/
Acid Base Physiology - http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php
Mechanical Ventilation
http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm
http://www.aic.cuhk.edu.hk/web8/mech%20vent%20intro.htm
Sepsis
http://www.sepsisforum.org/">http://www.sepsisforum.org/">http://www.sepsisforum.org/
http://www.elililly.com/
http://www.ardsfoundation.com/
http://ssc.sccm.org/
http://www.ardsnet.org/
Radiology
http://www.learningradiology.com/
http://www.anatomyatlases.org/
Chest XRay
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/cxr.htm
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/atlas/cxratlas_f.htm
http://www.learningradiology.com/lectures/facultylectures/BASIC%20CXR-mod-Adam_files/v3_document.htm
http://www.usfca.edu/fac-staff/ritter/chestxra.htm
Trauma
http://www.trauma.org/
Pupil assessment
http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm
Delirium
http://www.icudelirium.org/delirium/CAM-ICUTraining.html
Anatomy
http://www.pbs.org/wnet/brain/3d/
http://www.meddean.luc.edu/lumen/MedEd/GrossAnatomy/anatomy.htm
http://msjensen.cehd.umn.edu/webanatomy/
http://www.imaios.com/en/e-Anatomy
IABP
http://www.aic.cuhk.edu.hk/web8/IABP%20pressure%20waveforms.htm
ECHO
http://www.criticalecho.com (By Kishore CMC Vellore)
Brain Herniation
http://rad.usuhs.mil/rad/herniation
Tuesday, September 1, 2009
Assessment for extubation
Despite advances in mechanical ventilation and respiratory support, the science of determining if the patient is ready for extubation is still very imprecise. A lot depends on the clinician’s threshold for reduction in ventilatory support, than does the modes of ventilatory wean.
Patients who can be extubated safely can be divided into three phases-
1. Freedom from the primary problem that prompted mechanical ventilation
2. Identifying whether the patient will sustain spontaneous respiration and ventilation and also when the patient is failing the assessment
3. What to look for immediately before extubation.
These assessments are multifaceted and usually include the overall patient condition, hemodynamic stability, neurological and muscular status and adequacy of gas exchange.
Commonly used clinical parameters that predict successful weaning from
mechanical ventilation.
Parameter with Desired value
Respiratory rate Less than 30-38 breaths/minute
Tidal volume 4-6 mL/kg
Minute ventilation 10-15 L/minute
Negative inspiratory force -20 to –30 cm H2O
Maximal inspiratory pressure (MIP) -15 to –30 cm H2O
Mouth occlusion pressure 100 msec after the
onset of inspiratory effort (P0.1) divided by MIP 0.3
Rapid shallow breathing index (RSBI)
(respiratory rate divided by tidal volume) 60-105
Rapid shallow breathing index rate
[(RSBI2 – RSBI1)/RSBI1] x 100 Less than 20%
CROP score (an index including compliance,
rate, oxygenation and pressure) 13
PaO2/FiO2 ratio >150-200
Despite high sensitivity, however, these parameters lack specificity.
All the patients who are deemed fit for extubation should undergo some means of assessment to see if they will tolerate extubation. It is routine to perform Spontaneous breathing trial (SBT), by means of – CPAP of 5 cm of H2O, T –Piece trial, or Pressure support of 7 cm of H2O. Once the patient is on SBT we should watch for indicators of failure, which are –
1. Inadequate gas exchange
Arterial oxygenation saturation (SaO2) <85% - 90% PaO2 <50 – 60 mmHg pH < 7.32 Increase in PaCO2 >10 mmHg
2. Unstable ventilatory/respiratory pattern
Respiratory rate >30 – 35 breaths/minute
Respiratory rate change over 50%
3. Hemodynamic instability
Heart rate >120 – 140 beats/minute
Heart rate change greater than 20%
Systolic blood pressure >180 mmHg or <90 mmHg Blood pressure change greater than 20% Vasopressors required 4. Change in mental status
Agitation
Anxiety
Somnolence
Coma
5. Signs of increased work of breathing
Nasal flaring
Paradoxical breathing movements
Use of accessory respiratory muscles
6. Onset of worsening discomfort ± diaphoresis
Another parameter that is widely used is the Rapid shallow breathing index (RSBI), from which we can calculate the RSBI rate which is the measure of change of RSBI over time, and may offer more predictive value .A RSBI rate of less than 20% is 90 % sensitive and 100% specific for predicting weaning success .It has a positive predictive value of 100% and negative predictive value of over 81 %.
Finally, once it is confirmed that patient can sustain spontaneous breathing , we can extubate the patient provided—
1 .Presence of a patent airway –assessed with “Cuff leak test”( dividing expiratory volume by inspiratory volume and multiplying with 100)
2. Patients’ ability to consistently protect the airway and clear secretions –assessed by the presence of adequate cough and gag reflex.
3. Mental status compatible with maintenance of airway and secretion clearance.
4. Absence of any other reasons for potential post-extubation failure—
- severe pain
- presence of apnea
- poorly controlled seizures
- risk of massive upper GI bleeding.
Thanks to Dr Harjit Mahay for contributing this wonderful article.
Patients who can be extubated safely can be divided into three phases-
1. Freedom from the primary problem that prompted mechanical ventilation
2. Identifying whether the patient will sustain spontaneous respiration and ventilation and also when the patient is failing the assessment
3. What to look for immediately before extubation.
These assessments are multifaceted and usually include the overall patient condition, hemodynamic stability, neurological and muscular status and adequacy of gas exchange.
Commonly used clinical parameters that predict successful weaning from
mechanical ventilation.
Parameter with Desired value
Respiratory rate Less than 30-38 breaths/minute
Tidal volume 4-6 mL/kg
Minute ventilation 10-15 L/minute
Negative inspiratory force -20 to –30 cm H2O
Maximal inspiratory pressure (MIP) -15 to –30 cm H2O
Mouth occlusion pressure 100 msec after the
onset of inspiratory effort (P0.1) divided by MIP 0.3
Rapid shallow breathing index (RSBI)
(respiratory rate divided by tidal volume) 60-105
Rapid shallow breathing index rate
[(RSBI2 – RSBI1)/RSBI1] x 100 Less than 20%
CROP score (an index including compliance,
rate, oxygenation and pressure) 13
PaO2/FiO2 ratio >150-200
Despite high sensitivity, however, these parameters lack specificity.
All the patients who are deemed fit for extubation should undergo some means of assessment to see if they will tolerate extubation. It is routine to perform Spontaneous breathing trial (SBT), by means of – CPAP of 5 cm of H2O, T –Piece trial, or Pressure support of 7 cm of H2O. Once the patient is on SBT we should watch for indicators of failure, which are –
1. Inadequate gas exchange
Arterial oxygenation saturation (SaO2) <85% - 90% PaO2 <50 – 60 mmHg pH < 7.32 Increase in PaCO2 >10 mmHg
2. Unstable ventilatory/respiratory pattern
Respiratory rate >30 – 35 breaths/minute
Respiratory rate change over 50%
3. Hemodynamic instability
Heart rate >120 – 140 beats/minute
Heart rate change greater than 20%
Systolic blood pressure >180 mmHg or <90 mmHg Blood pressure change greater than 20% Vasopressors required 4. Change in mental status
Agitation
Anxiety
Somnolence
Coma
5. Signs of increased work of breathing
Nasal flaring
Paradoxical breathing movements
Use of accessory respiratory muscles
6. Onset of worsening discomfort ± diaphoresis
Another parameter that is widely used is the Rapid shallow breathing index (RSBI), from which we can calculate the RSBI rate which is the measure of change of RSBI over time, and may offer more predictive value .A RSBI rate of less than 20% is 90 % sensitive and 100% specific for predicting weaning success .It has a positive predictive value of 100% and negative predictive value of over 81 %.
Finally, once it is confirmed that patient can sustain spontaneous breathing , we can extubate the patient provided—
1 .Presence of a patent airway –assessed with “Cuff leak test”( dividing expiratory volume by inspiratory volume and multiplying with 100)
2. Patients’ ability to consistently protect the airway and clear secretions –assessed by the presence of adequate cough and gag reflex.
3. Mental status compatible with maintenance of airway and secretion clearance.
4. Absence of any other reasons for potential post-extubation failure—
- severe pain
- presence of apnea
- poorly controlled seizures
- risk of massive upper GI bleeding.
Thanks to Dr Harjit Mahay for contributing this wonderful article.
Thursday, August 27, 2009
Croup Vs Epiglotitis
Croup-Acute Laryngotracheobronchitis: inflammation of the glottic & subglottic region (narrowest part)
1. Viral Croup - parainfluenzae viruses
- occasionally RSV, rhinoviruses, or measles
- coryzal prodrome, low grade fever
- rare < 6/12, consider ? underlying lesion - commonest obstruction at 6/12 to 6 yrs - median age of presentation 18/12 - more common in autumn & winter - <5% require intubation 2. Spasmodic Croup - children with an allergic nature
-? spectrum of asthmatic population
- no coryzal prodrome / fever
3. Bacterial Tracheitis - usually Staph. aureus ± H. influenzae, group A Strep.
- high fever, WCC, purulent secretions
-* risk of sudden obstruction
Varied Clinical Presentation
a. signs of mild croup
- URTI preceding 2-3 days
- loud barking "croupy" cough
- gradual onset inspiratory stridor which is high pitched
- hoarse voice
- no postural preference
- mild fever
- often a past history of croup
b. moderate
- stridor on inspiration & expiration
- tachypnoea
- flaring alar nasae
- suprasternal/intercostal retractions
c. severe - restlessness caused by hypoxia
- exhaustion & listlessness
- deteriorating conscious state
- cyanosis on air
Differential diagnosis
- epiglottitis
- aspiration of foreign body
- bacterial tracheitis
- retropharyngeal abscess
- peritonsillar abscess
Diagnosis
i. history and examination * mainstay of diagnosis
ii. radiology of the larynx (ESS or ICU) ®
"steeple" sign - AP view
widened hypopharynx - lat. view, only ~ 40-50% of cases
iii. direct laryngoscopy under GA
Management
a. minimal disturbance - VM & VO2,nursed by parent
b. adequate hydration,but propensity for pulmonary oedema; hypo-Na+ & convulsions have occurred 2° to SIADH with airway obstruction
c. oxygen therapy ® SpO2 > 90%- hypoxia from parenchymal infection ± increased interstitial water
d. humidification - mainstay for years but studies showing efficacy are lacking now abandoned by many centres but anecdotal evidence ? otherwise
e. steroids - dexamethasone ~ 0.6 mg/kg (= 12 mg) stat., then 0.15 mg/kg q6h.
Given on admission - decreases intubation rate & duration of stay
Failed extubation rate - administer 24 hrs pre & 12 hrs post-extubation
May also be of use in spasmodic croup
f. nebulized adrenaline - 1:1,000 ~ 0.5 ml/kg £ 5 ml of 0.1% solution, nebulised 2 hrly, this dose is effective, has little systemic effect, and is less than the recommended dose for the racemic solution -subsequent doses ® less effective. The obstruction may be more severe after the effect has worn-off ® rebound phenomenon ? progression of the disease process.
-In Acute LTB - lasts ~ 1-2 hrs,doesn't alter course but may allow secretion expectoration and prior to intubation, enhances induction
-In spasmodic croup - may obviate need for intubation
- Post ETT / endoscopy oedema where effect is often dramatic
- prior to transfer if not for intubation
- prior to anaesthesia & intubation if tolerated
g. Antibiotics - only for proven bacterial infection
h. Intubation ~ 2-5% of cases, nasotracheal,use 1 mm less than "size for age"
Indications for Intubation NB: essentially subjective assessment
a. respiratory rate, HR, and chest wall retractions
b. cyanosis not responsive to oxygen
c. exhaustion and/or confusion
d. increased use of, and failure to respond to, nebulised adrenaline
e. need for transport to another hospital
Method
-spontaneously breathing,
-inhalational anaesthetic induction is prolonged
-ETT ~ 1 size smaller for age to minimise trauma
-most safely passed orally, then changed to a nasal
-small tubes are shorter and may be difficult to secure
-sedation ± arm splints to prevent self extubation
-stomach should be emptied with a nasogastric tube
-CPAP or IPPV with PEEP to maintain oxygenation
- size limited to > 3.0 mm, due to requirement to pass a suction catheter to clear secretions
Extubation
-can be attempted when a leak is present with positive pressure or coughing,
- or when the disease has run its course at 5 to 7 days
Reintubation may be required, but the incidence is reduced by administration of steroids prior to extubation ® prednisolone ~ 2 mg/kg/day.
Prior to steroid therapy intubation duration was average 5 days, but now reduced to 2-3 days.
Bacterial Tracheitis
-results in purulent secretions, pseudomembranes and ulceration of epithelium within the trachea
-death can result from upper airway obstruction, endotracheal tube blockage, and toxic shock
-either a primary bacterial infection or a superinfection on primary viral illness
-the causative organisms are,
a. Staphylococcus aureus
b. Haemophilus influenza type B
c. Streptococcus pneumoniae
d. Branhamella catarrhalis
Clinical Presentation
a. fever & toxaemia
b. respiratory distress
c. similar to epiglottitis except for
- the presence of a cough
- a subjective difference in quality of the stridor
Diagnosis
i. CXR - may show tracheal membranes
- narrowing & "fuzziness" are variable
ii. ETT - absence of epiglotitis
- suction following intubation ® pus and membranes in the trachea
Management - similar to that for epiglottitis (see over)
- if intubation is required, the ETT may block acutely with secretions ® aggressive tracheal suction ± reintubation
- bronchoscopy to clear tracheal pus should be considered where the airway remains compromised after intubation, suction and reintubation
- initially, there may not be a leak around an appropriately sized endotracheal tube
- sputum should be sent for gram stain and culture, and urine for rapid antigen identification
- extubation is best performed when, the fever and secretions have settled, and a leak is present around the endotracheal tube
- initial antibiotic therapy ® cefotaxime ~ 50 mg/kg q6h for 10/7, then by MC&S
Epiglottitis: supraglottic, infective inflammatory lesion, caused almost exclusively by Haemophilus influenzae - type B ± occasionally streptococci, staphlococci, or pneumococci
a. acute onset - short history (hrs) with no preceding URTI
b. high fever & toxaemia
c. stridor - low pitched, inspiratory ± expiratory snore, usually constant in nature
d. absence of cough and reluctance to talk
e. characteristic posture - sitting forward,mouth open, drooling & dysphagia
f. diagnosis
- direct laryngoscopy
- urine latex antigen agglutination
- ~ 80% blood culture (+)'ve
- lateral XRay ® "thumb print"
Most commonly children from 2 to 7 years but the disease can involve adults and infants due to septicaemia. The severity of the illness is often out of proportion to the airway obstruction.Children less than 2 years of age may present with airway obstruction atypically accompanied by apnoea, URTI, low grade fever, and/or cough and sudden total obstruction may be precipitated by,
a. instrumentation of the pharynx
b. painful stimuli - eg. IV insertion
c. supine posture
Management
a. minimal disturbance - nurse in mothers arms, etc.
b. ready access to intubation equipment
c. oxygenation - mask or nasal cannulae, if obstructs ® CPAP/assist by bag
d. antibiotics
- cefotaxime ~ 50 mg/kg q6h ± chloramphenacol ~ 25 mg/kg q6h or
- ampicillin was used but high percentage of resistant strains
e. intubation - all but the mildest cases, average duration ~ 18 hours but may be required for longer in cases with,
- pulmonary oedema
- pneumonia
- cerebral hypoxia
f. racemic adrenaline is of no use in this condition and can precipitate obstruction
Epiglottitis - Intubation Indications
1. severe or progressive respiratory distress
2. prior to transportation to a tertiary centre
3. following diagnosis by direct laryngoscopy under GA
- Patients can be managed without intubation if they remain in an area where appropriate personnel, equipment and supervision is available. Such patients are generally older, co-operative and are seen early in the day with minimal signs of obstruction. Diagnosis in these cases is made by lateral neck XRay
- An IV line can be inserted before anaesthesia, but should be delayed until after induction when the patient is distressed or obstruction is severe in order to avoid sudden obstruction.
- In spontaneously breathing, inhalational GA is best tolerated in the sitting position.
- Agitation and distress at induction may be due to acute hypoxia.
- The patient can be laid flat on loss of awareness, and airway obstruction overcome by application of CPAP or assisted ventilation.
- Laryngospasm may be precipitated if laryngeal stimulation occurs prior to surgical anaesthesia being achieved.
- Copious and persistent pulmonary oedema fluid may obscure the larynx, making intubation difficult.
- An ETT of normal size for age or one size smaller should be inserted orally then changed to the nasal route once the child has settled
- Positive pressure should demonstrate a leak around the tube.
- The patient can be sedated ± restrained to prevent self-extubation.
- Muscle relaxants are not routinely required unless IPPV/PEEP is required to overcome hypoxia and hypoventilation from pulmonary oedema.
Complications
a. respiratory failure / obstruction
b. pulmonary oedema ~ 7-10% of cases and is precipitated by intubation
- hypoxia & SNS discharge - PAP
- vascular - endothelial injury & capillary permeability
- decreased intrathoracic pressure after intubation, augmenting venous return, and increasing transmural pulmonary vascular hydrostatic pressure gradients
c. barotrauma
- pulmonary interstitial emphysema (PIE)
- pneumothorax
- pneumomediastinum
d. septicaemia / pneumonia
Extubation Criteria
a. when the fever has settled
b. signs of inflammation subside ® usually ~ 18 hours
- pain subsided
- able to swallow
- free movement of the larynx
NB: exceptions are where hypoxia and reduced lung compliance persist direct laryngoscopy prior to extubation is not required
Thanks to Dr Anuj Clerk for this wonderful article.
1. Viral Croup - parainfluenzae viruses
- occasionally RSV, rhinoviruses, or measles
- coryzal prodrome, low grade fever
- rare < 6/12, consider ? underlying lesion - commonest obstruction at 6/12 to 6 yrs - median age of presentation 18/12 - more common in autumn & winter - <5% require intubation 2. Spasmodic Croup - children with an allergic nature
-? spectrum of asthmatic population
- no coryzal prodrome / fever
3. Bacterial Tracheitis - usually Staph. aureus ± H. influenzae, group A Strep.
- high fever, WCC, purulent secretions
-* risk of sudden obstruction
Varied Clinical Presentation
a. signs of mild croup
- URTI preceding 2-3 days
- loud barking "croupy" cough
- gradual onset inspiratory stridor which is high pitched
- hoarse voice
- no postural preference
- mild fever
- often a past history of croup
b. moderate
- stridor on inspiration & expiration
- tachypnoea
- flaring alar nasae
- suprasternal/intercostal retractions
c. severe - restlessness caused by hypoxia
- exhaustion & listlessness
- deteriorating conscious state
- cyanosis on air
Differential diagnosis
- epiglottitis
- aspiration of foreign body
- bacterial tracheitis
- retropharyngeal abscess
- peritonsillar abscess
Diagnosis
i. history and examination * mainstay of diagnosis
ii. radiology of the larynx (ESS or ICU) ®
"steeple" sign - AP view
widened hypopharynx - lat. view, only ~ 40-50% of cases
iii. direct laryngoscopy under GA
Management
a. minimal disturbance - VM & VO2,nursed by parent
b. adequate hydration,but propensity for pulmonary oedema; hypo-Na+ & convulsions have occurred 2° to SIADH with airway obstruction
c. oxygen therapy ® SpO2 > 90%- hypoxia from parenchymal infection ± increased interstitial water
d. humidification - mainstay for years but studies showing efficacy are lacking now abandoned by many centres but anecdotal evidence ? otherwise
e. steroids - dexamethasone ~ 0.6 mg/kg (= 12 mg) stat., then 0.15 mg/kg q6h.
Given on admission - decreases intubation rate & duration of stay
Failed extubation rate - administer 24 hrs pre & 12 hrs post-extubation
May also be of use in spasmodic croup
f. nebulized adrenaline - 1:1,000 ~ 0.5 ml/kg £ 5 ml of 0.1% solution, nebulised 2 hrly, this dose is effective, has little systemic effect, and is less than the recommended dose for the racemic solution -subsequent doses ® less effective. The obstruction may be more severe after the effect has worn-off ® rebound phenomenon ? progression of the disease process.
-In Acute LTB - lasts ~ 1-2 hrs,doesn't alter course but may allow secretion expectoration and prior to intubation, enhances induction
-In spasmodic croup - may obviate need for intubation
- Post ETT / endoscopy oedema where effect is often dramatic
- prior to transfer if not for intubation
- prior to anaesthesia & intubation if tolerated
g. Antibiotics - only for proven bacterial infection
h. Intubation ~ 2-5% of cases, nasotracheal,use 1 mm less than "size for age"
Indications for Intubation NB: essentially subjective assessment
a. respiratory rate, HR, and chest wall retractions
b. cyanosis not responsive to oxygen
c. exhaustion and/or confusion
d. increased use of, and failure to respond to, nebulised adrenaline
e. need for transport to another hospital
Method
-spontaneously breathing,
-inhalational anaesthetic induction is prolonged
-ETT ~ 1 size smaller for age to minimise trauma
-most safely passed orally, then changed to a nasal
-small tubes are shorter and may be difficult to secure
-sedation ± arm splints to prevent self extubation
-stomach should be emptied with a nasogastric tube
-CPAP or IPPV with PEEP to maintain oxygenation
- size limited to > 3.0 mm, due to requirement to pass a suction catheter to clear secretions
Extubation
-can be attempted when a leak is present with positive pressure or coughing,
- or when the disease has run its course at 5 to 7 days
Reintubation may be required, but the incidence is reduced by administration of steroids prior to extubation ® prednisolone ~ 2 mg/kg/day.
Prior to steroid therapy intubation duration was average 5 days, but now reduced to 2-3 days.
Bacterial Tracheitis
-results in purulent secretions, pseudomembranes and ulceration of epithelium within the trachea
-death can result from upper airway obstruction, endotracheal tube blockage, and toxic shock
-either a primary bacterial infection or a superinfection on primary viral illness
-the causative organisms are,
a. Staphylococcus aureus
b. Haemophilus influenza type B
c. Streptococcus pneumoniae
d. Branhamella catarrhalis
Clinical Presentation
a. fever & toxaemia
b. respiratory distress
c. similar to epiglottitis except for
- the presence of a cough
- a subjective difference in quality of the stridor
Diagnosis
i. CXR - may show tracheal membranes
- narrowing & "fuzziness" are variable
ii. ETT - absence of epiglotitis
- suction following intubation ® pus and membranes in the trachea
Management - similar to that for epiglottitis (see over)
- if intubation is required, the ETT may block acutely with secretions ® aggressive tracheal suction ± reintubation
- bronchoscopy to clear tracheal pus should be considered where the airway remains compromised after intubation, suction and reintubation
- initially, there may not be a leak around an appropriately sized endotracheal tube
- sputum should be sent for gram stain and culture, and urine for rapid antigen identification
- extubation is best performed when, the fever and secretions have settled, and a leak is present around the endotracheal tube
- initial antibiotic therapy ® cefotaxime ~ 50 mg/kg q6h for 10/7, then by MC&S
Epiglottitis: supraglottic, infective inflammatory lesion, caused almost exclusively by Haemophilus influenzae - type B ± occasionally streptococci, staphlococci, or pneumococci
a. acute onset - short history (hrs) with no preceding URTI
b. high fever & toxaemia
c. stridor - low pitched, inspiratory ± expiratory snore, usually constant in nature
d. absence of cough and reluctance to talk
e. characteristic posture - sitting forward,mouth open, drooling & dysphagia
f. diagnosis
- direct laryngoscopy
- urine latex antigen agglutination
- ~ 80% blood culture (+)'ve
- lateral XRay ® "thumb print"
Most commonly children from 2 to 7 years but the disease can involve adults and infants due to septicaemia. The severity of the illness is often out of proportion to the airway obstruction.Children less than 2 years of age may present with airway obstruction atypically accompanied by apnoea, URTI, low grade fever, and/or cough and sudden total obstruction may be precipitated by,
a. instrumentation of the pharynx
b. painful stimuli - eg. IV insertion
c. supine posture
Management
a. minimal disturbance - nurse in mothers arms, etc.
b. ready access to intubation equipment
c. oxygenation - mask or nasal cannulae, if obstructs ® CPAP/assist by bag
d. antibiotics
- cefotaxime ~ 50 mg/kg q6h ± chloramphenacol ~ 25 mg/kg q6h or
- ampicillin was used but high percentage of resistant strains
e. intubation - all but the mildest cases, average duration ~ 18 hours but may be required for longer in cases with,
- pulmonary oedema
- pneumonia
- cerebral hypoxia
f. racemic adrenaline is of no use in this condition and can precipitate obstruction
Epiglottitis - Intubation Indications
1. severe or progressive respiratory distress
2. prior to transportation to a tertiary centre
3. following diagnosis by direct laryngoscopy under GA
- Patients can be managed without intubation if they remain in an area where appropriate personnel, equipment and supervision is available. Such patients are generally older, co-operative and are seen early in the day with minimal signs of obstruction. Diagnosis in these cases is made by lateral neck XRay
- An IV line can be inserted before anaesthesia, but should be delayed until after induction when the patient is distressed or obstruction is severe in order to avoid sudden obstruction.
- In spontaneously breathing, inhalational GA is best tolerated in the sitting position.
- Agitation and distress at induction may be due to acute hypoxia.
- The patient can be laid flat on loss of awareness, and airway obstruction overcome by application of CPAP or assisted ventilation.
- Laryngospasm may be precipitated if laryngeal stimulation occurs prior to surgical anaesthesia being achieved.
- Copious and persistent pulmonary oedema fluid may obscure the larynx, making intubation difficult.
- An ETT of normal size for age or one size smaller should be inserted orally then changed to the nasal route once the child has settled
- Positive pressure should demonstrate a leak around the tube.
- The patient can be sedated ± restrained to prevent self-extubation.
- Muscle relaxants are not routinely required unless IPPV/PEEP is required to overcome hypoxia and hypoventilation from pulmonary oedema.
Complications
a. respiratory failure / obstruction
b. pulmonary oedema ~ 7-10% of cases and is precipitated by intubation
- hypoxia & SNS discharge - PAP
- vascular - endothelial injury & capillary permeability
- decreased intrathoracic pressure after intubation, augmenting venous return, and increasing transmural pulmonary vascular hydrostatic pressure gradients
c. barotrauma
- pulmonary interstitial emphysema (PIE)
- pneumothorax
- pneumomediastinum
d. septicaemia / pneumonia
Extubation Criteria
a. when the fever has settled
b. signs of inflammation subside ® usually ~ 18 hours
- pain subsided
- able to swallow
- free movement of the larynx
NB: exceptions are where hypoxia and reduced lung compliance persist direct laryngoscopy prior to extubation is not required
Thanks to Dr Anuj Clerk for this wonderful article.
Monday, August 24, 2009
Perioperative management of the patient with pheochromocytoma
The KEY: Communication between surgeon, anesthesiologist, and internist.
Background:
Pheochromocytoma is an uncommon neuroendocrine tumor of the chromaffin cell.
The most common sign of the tumor is hypertension, which can be paroxysmal.
The tumor’s intermittent catecholamine surges can cause a variety of symptoms,including headache, chest pain, palpitations, diaphoresis, dyspnea, anxiety,and dizziness.
Surgical excision can prevent the life-threatening complications of hypertensive crises, stroke, arrhythmias, and myocardial infarction.Before 1961,surgical mortality ranged from 24–45%. With appropriate medical preparation and an experienced anesthesiologist and surgical team, survival of excision of a pheochromocytoma is 93.3–100%
Preoperative preparation
Catecholamine excess causes --vasoconstriction that leads to both hypertension and hypovolemia.
Pheochromocytoma patients can die intraoperatively from--severe hypertensive crisis or hypotension that leads to cardiovascular collapse.
When tumor veins are ligated during surgery, the sudden drop in circulating catecholamines can lead to vasodilatation. The catecholamine output of the contralateral adrenal may be suppressed from previous catecholamine excess. In the hypovolemic patient, this can lead to hypotension, shock, and death.
Alpha adrenergic blockade is the cornerstone of preoperative preparation
-it treats both hypertension and vasoconstriction
-improves circulating plasma volume prior to surgery.
Phenoxybenzamine[Non selective, non competitive]-start 2 weeks prior to Sx 5-10 mg BID, step up to control BP~140/90 with max. 300 mg per day. Caution Postural hypotension, nasal stuffiness, reflex tachycardia.
Selective Alfa 1 blockers[Prazosin SR 2-20 mg BD ,doxazosin 1-16 mg OD]- do not block NA re uptake- less reflex tachycardia and orthostatic hypotension so better tolerated.
Liberalization of salt in the diet along with alpha blockade should expand plasma volume.
Beta blockade: Propanolol/Atenolol/metoprolol few days after Alfa Blockade[once reflex tachycardia noted] but few days before srgery.[if not contraindicated by heart failure or asthma]. Beta-blockers may also prevent perioperative arrhythmias and cardiac complications.
As calcium ion transport is essential for release of catecholamines from chromaffin cells, calcium channel blockers are used for control of blood pressure and preoperative preparation at some centers Less periop fluid requirement and post op hypotension in one French study.
Metyrosin [(alpha-methyl-p-tyrosine)Tyrosin hydroxylase inhibitor] reserved for refractory cases at doses of 1–4 mg per day -Very Toxic no longer used
Preoperative evaluation of myocardial function MUST.[left ventricular hypertrophy and dysfunction, but chronic catecholamine excess induced cardiomyopathy.]
Pre op Target:
24 BP monitoring, all readings <160/90, HR <100/min, Postural drop in BP with compensatory tachy as sign of adequate alfa blockade. Intraoperative Management:
-Avoid Histamine release causing agents during induction eg. Morphine
-Adrenaline followed by noradrenaline infusion for fluid refractory hypotension [CVP~10-15mmHg].
-Terlipressin 1 mg followed by vasopressin infused can be used.
-Na.nitroprusside infusion better then Phentolamine boluses [due to shorter duration of action] for hypertensive episodes.
-IV Nicardipine and Magnesium can be used to control hypertensive spikes.
-Betablockers for tachyarrhythmia.
Postoperative Management
-12-24 hours HDU/ICU care must.
-patient may remain hypertensive up to 2 weeks after excision.
-urinary catecholamines should be checked to ensure no additional tumor remains.
-hypoglycemia may develop and persist into the postoperative period once the tumor is removed[Catecholamine withdrawal + Beta blockade induced limit to compensation and unawareness]. Glucose should be included in perioperative fluids, and blood sugars should be monitored frequently intraoperatively and postoperatively.
-patients who undergo bilateral adrenalectomy [some with unilateral surgery as well] will need steroid[Hydrocortisone + Fludrocaortisone] replacement.
If catecholamines are normal, the patient may be one of about 25% of pheochromocytoma patients whose hypertension persists after surgical excision caused by other concomitant disease, such as essential or renal hypertension.
Thanks to Dr Anuj Clerk for contributing this wonderful article.
Background:
Pheochromocytoma is an uncommon neuroendocrine tumor of the chromaffin cell.
The most common sign of the tumor is hypertension, which can be paroxysmal.
The tumor’s intermittent catecholamine surges can cause a variety of symptoms,including headache, chest pain, palpitations, diaphoresis, dyspnea, anxiety,and dizziness.
Surgical excision can prevent the life-threatening complications of hypertensive crises, stroke, arrhythmias, and myocardial infarction.Before 1961,surgical mortality ranged from 24–45%. With appropriate medical preparation and an experienced anesthesiologist and surgical team, survival of excision of a pheochromocytoma is 93.3–100%
Preoperative preparation
Catecholamine excess causes --vasoconstriction that leads to both hypertension and hypovolemia.
Pheochromocytoma patients can die intraoperatively from--severe hypertensive crisis or hypotension that leads to cardiovascular collapse.
When tumor veins are ligated during surgery, the sudden drop in circulating catecholamines can lead to vasodilatation. The catecholamine output of the contralateral adrenal may be suppressed from previous catecholamine excess. In the hypovolemic patient, this can lead to hypotension, shock, and death.
Alpha adrenergic blockade is the cornerstone of preoperative preparation
-it treats both hypertension and vasoconstriction
-improves circulating plasma volume prior to surgery.
Phenoxybenzamine[Non selective, non competitive]-start 2 weeks prior to Sx 5-10 mg BID, step up to control BP~140/90 with max. 300 mg per day. Caution Postural hypotension, nasal stuffiness, reflex tachycardia.
Selective Alfa 1 blockers[Prazosin SR 2-20 mg BD ,doxazosin 1-16 mg OD]- do not block NA re uptake- less reflex tachycardia and orthostatic hypotension so better tolerated.
Liberalization of salt in the diet along with alpha blockade should expand plasma volume.
Beta blockade: Propanolol/Atenolol/metoprolol few days after Alfa Blockade[once reflex tachycardia noted] but few days before srgery.[if not contraindicated by heart failure or asthma]. Beta-blockers may also prevent perioperative arrhythmias and cardiac complications.
As calcium ion transport is essential for release of catecholamines from chromaffin cells, calcium channel blockers are used for control of blood pressure and preoperative preparation at some centers Less periop fluid requirement and post op hypotension in one French study.
Metyrosin [(alpha-methyl-p-tyrosine)Tyrosin hydroxylase inhibitor] reserved for refractory cases at doses of 1–4 mg per day -Very Toxic no longer used
Preoperative evaluation of myocardial function MUST.[left ventricular hypertrophy and dysfunction, but chronic catecholamine excess induced cardiomyopathy.]
Pre op Target:
24 BP monitoring, all readings <160/90, HR <100/min, Postural drop in BP with compensatory tachy as sign of adequate alfa blockade. Intraoperative Management:
-Avoid Histamine release causing agents during induction eg. Morphine
-Adrenaline followed by noradrenaline infusion for fluid refractory hypotension [CVP~10-15mmHg].
-Terlipressin 1 mg followed by vasopressin infused can be used.
-Na.nitroprusside infusion better then Phentolamine boluses [due to shorter duration of action] for hypertensive episodes.
-IV Nicardipine and Magnesium can be used to control hypertensive spikes.
-Betablockers for tachyarrhythmia.
Postoperative Management
-12-24 hours HDU/ICU care must.
-patient may remain hypertensive up to 2 weeks after excision.
-urinary catecholamines should be checked to ensure no additional tumor remains.
-hypoglycemia may develop and persist into the postoperative period once the tumor is removed[Catecholamine withdrawal + Beta blockade induced limit to compensation and unawareness]. Glucose should be included in perioperative fluids, and blood sugars should be monitored frequently intraoperatively and postoperatively.
-patients who undergo bilateral adrenalectomy [some with unilateral surgery as well] will need steroid[Hydrocortisone + Fludrocaortisone] replacement.
If catecholamines are normal, the patient may be one of about 25% of pheochromocytoma patients whose hypertension persists after surgical excision caused by other concomitant disease, such as essential or renal hypertension.
Thanks to Dr Anuj Clerk for contributing this wonderful article.
Sunday, August 23, 2009
Compare and contrast persistent vegetative state, locked-in state & akinetic mutism
Persistent vegetative state
* Loss of cognitive neurological function but retains non cognitive functions- respiration,BP, cardiac function etc.
* Lack of consistency in neuro examination; eg.pt may blink, respiration may quicken to stimulation, lack of constant visual following of objects
* EEG- minimal/no change in EEG activity during & after stimulating the patient(i.e no desynchronization)
* Lesion- diffuse cerebral injury, thalamic injury(medial and ventromedian nuclei) & caudal midbrain lesions
Locked-in state
* De-efferented state- patient is alert & aware of environment + quadriplegia+ lower cranial nerve palsy. The only way the patient responds is by vertical gaze & blinking.
* Lesion- involves motor pathways- CS tract, corticobulbar & cortico pontine pathways with sparing of somatosensory pathways & ARAS. The most common site is the ventral pons
Akinetic mutism
* It is a state of altered behaviour where alert appearing patients are silent, inert & profoundly apathetic. They lack psychiatric drive or impulse to action & are doubly incontinent. They usually lie with eyes opened and retain cycles of self-sustained arousal
* Lesion- B/L anterior frontal lobe- this leaves intact motor & sensory pathways
Thanks to Dr Ishaq M for contributing this wonderful article.
* Loss of cognitive neurological function but retains non cognitive functions- respiration,BP, cardiac function etc.
* Lack of consistency in neuro examination; eg.pt may blink, respiration may quicken to stimulation, lack of constant visual following of objects
* EEG- minimal/no change in EEG activity during & after stimulating the patient(i.e no desynchronization)
* Lesion- diffuse cerebral injury, thalamic injury(medial and ventromedian nuclei) & caudal midbrain lesions
Locked-in state
* De-efferented state- patient is alert & aware of environment + quadriplegia+ lower cranial nerve palsy. The only way the patient responds is by vertical gaze & blinking.
* Lesion- involves motor pathways- CS tract, corticobulbar & cortico pontine pathways with sparing of somatosensory pathways & ARAS. The most common site is the ventral pons
Akinetic mutism
* It is a state of altered behaviour where alert appearing patients are silent, inert & profoundly apathetic. They lack psychiatric drive or impulse to action & are doubly incontinent. They usually lie with eyes opened and retain cycles of self-sustained arousal
* Lesion- B/L anterior frontal lobe- this leaves intact motor & sensory pathways
Thanks to Dr Ishaq M for contributing this wonderful article.
Saturday, August 22, 2009
Management of Acute Variceal Bleeding
* Gastroesophageal variceal bleeding accounts for 10-30% of upper gastrointestinal haemorrhage and is a major cause of death in patients with cirrhosis.
* The prevalence of oesophageal varices in patients with cirrhosis varies from 24-81%.
* At the time of diagnosis of cirrhosis, oesophageal varices are present in about 60% of decompensated and 30% of compensated patients.
* Despite the high occurrence of varices in cirrhotic patients, only 30% of patients with varices will experience variceal haemorrhage.
* The risk of bleeding appears to be greatest within the first year after diagnosis.
* Mortality of the first bleeding episode is high and ranges between 30% and 50% within 6 weeks; mortality from uncontrolled bleeding in the first instance is between 5-8%.
* Risk factors for the 1st episode of variceal bleeding in cirrhotic patients include - the severity of the liver dysfunction,
- the size of the varices (large greater than small), and
- the presence of endoscopic red wale signs.
- the hepatic venous pressure gradient (HVPG).
* Gastric varices account for approximately 20-30% of cases of variceal bleeding. The prevalence of gastric varices in patients with portal hypertension varies from 6-78% and approximately 25% of gastric varices bleed during lifetime.
General management of bleeding
Patients are usually managed in a high-dependency or intensive therapy unit with facilities for central venous pressure and arterial monitoring.
Therapy is aimed at - correcting hypovolumic shock and resuscitation
- achieving haemostasis at the bleeding site.
This include ABC & resuscitation, initially with plasma expanders and subsequently with blood. If coagulation is defective, replace coagulation factors with fresh frozen plasma. Platelet transfusions may also be required for thrombocytopenia.
Local Haemostasis
An emergency endoscopy should be performed to confirm that varices are the source of bleeding, since peptic ulcer disease is also common in cirrhosis. If possible, endoscopic treatment of varices should be undertaken by endoscopic variceal ligation (banding). Where banding is not possible, sclerotherapy may be useful, adverse events such as oesophageal ulceration and stricture were significantly more severe with sclerotherapy. The most commonly used sclerosants are sodium tetradecyl sulphate (thrombovar) and ethanolamine oleate.
Pharmacotherapy
Octreotide: Decrease portal pressure, 50 micrograms IV, immediately, then 25 to 50 micrograms per hour by IV infusion for 5 days.
While control of initial bleeding has been demonstrated with octreotide, no effect on mortality has been shown. Its transient effect is due to tachyphylaxis.
Terlipressin: 2 mg IV, 6-hourly for 2 to 3 days. It reduces splanchnic blood flow and portal pressure. A meta-analysis demonstrated that terlipressin was associated with a 34% relative risk reduction in mortality compared to placebo.
If endoscopic treatment fails/unavailable and bleeding persists despite octreotide or terlipressin, blood loss can usually be controlled with a Sengstaken-Blakemore–type tube for 24 hours. Balloon tamponade is known to have a high re-bleeding rate when the balloon is decompressed and is associated with serious complications such as ulceration, perforation and aspiration pneumonia. Thus, this should only be considered if facilities for endoscopy are not available prior to transfer to a tertiary centre or as a temporary ‘bridge’ for a maximum of 24 hours until definitive treatment can be instituted.
Antibiotics in Acute Variceal Bleeding
Bacterial infections are seen in about 20% of cirrhotics presenting with upper gastrointestinal bleeding within 48 hours. The incidence of sepsis increases to almost 66% at two weeks. Development of bacterial infection is associated with high mortality and variceal re-bleeding. Antibiotic prophylaxis has been shown to reduce the rate of infection, spontaneous bacterial peritonitis and rebleeding. In addition, antibiotic prophylaxis was clearly proven in a meta-analysis to significantly increase the survival rate. Short-term antibiotic prophylaxis for 7 days should be considered the standard of care in cirrhotic patients with upper gastrointestinal bleeding, irrespective of the type of haemorrhage (variceal or nonvariceal) or the presence or absence of ascites. As to the choice of antibiotic, either third generation cephalosporins given intravenously or oral quinolones (norfloxacin/ciprofloxacin) are generally recommended.
Continued bleeding
Continued bleeding is associated with a high mortality. A second course of endoscopic treatment may be undertaken with continued use of a Sengstaken-Blakemore–type tube for up to 24 hours. Adjunctive infusion of octreotide can be given. An emergency transjugular intrahepatic portosystemic shunt (TIPS) or an emergency portosystemic shunt may be considered, depending on available local expertise.
Transjugular intrahepatic portosystemic shunts (TIPS) is effective in the treatment of acute variceal bleeding with a success rate of over 90% in arresting haemorrhage. The main limiting factors to the use of TIPS are the high morbidity and mortality: the 30-day mortality approaches 100% in patients with advanced liver disease, ongoing sepsis and multi-organ failure. Therefore, the most widely accepted indication for TIPS is as a rescue therapy for uncontrolled variceal bleeding after combined pharmacological and endoscopic therapy.
Surgical Therapy
Surgical options include oesophageal transection with or without devascularisation, portosystemic shunts and liver transplantation. Regardless of the choice of the surgical technique, morbidity and mortality are high: the 30-day mortality associated with emergency surgical procedures is nearly 80%. Similar to TIPS, the role of surgical therapy in the management of acute variceal bleed has been relegated to salvage haemostatic therapy. Liver transplantation is probably only appropriate for liver transplant candidates who bleed while on the waiting list.
Prevention of rebleeding
In patients with cirrhosis who have bled from oesophageal varices, the risk of rebleeding within 12 months is about 60%. Measures to reduce this risk include regular endoscopic banding until varices have largely disappeared. In the longer term, varices recur and may need further banding. In a meta-analysis of clinical trials, therapy with propranolol has been shown to reduce recurrent variceal bleeding and improve survival. In those who rebleed despite the above therapy, TIPS, portosystemic shunt or transplantation should be considered.
* The prevalence of oesophageal varices in patients with cirrhosis varies from 24-81%.
* At the time of diagnosis of cirrhosis, oesophageal varices are present in about 60% of decompensated and 30% of compensated patients.
* Despite the high occurrence of varices in cirrhotic patients, only 30% of patients with varices will experience variceal haemorrhage.
* The risk of bleeding appears to be greatest within the first year after diagnosis.
* Mortality of the first bleeding episode is high and ranges between 30% and 50% within 6 weeks; mortality from uncontrolled bleeding in the first instance is between 5-8%.
* Risk factors for the 1st episode of variceal bleeding in cirrhotic patients include - the severity of the liver dysfunction,
- the size of the varices (large greater than small), and
- the presence of endoscopic red wale signs.
- the hepatic venous pressure gradient (HVPG).
* Gastric varices account for approximately 20-30% of cases of variceal bleeding. The prevalence of gastric varices in patients with portal hypertension varies from 6-78% and approximately 25% of gastric varices bleed during lifetime.
General management of bleeding
Patients are usually managed in a high-dependency or intensive therapy unit with facilities for central venous pressure and arterial monitoring.
Therapy is aimed at - correcting hypovolumic shock and resuscitation
- achieving haemostasis at the bleeding site.
This include ABC & resuscitation, initially with plasma expanders and subsequently with blood. If coagulation is defective, replace coagulation factors with fresh frozen plasma. Platelet transfusions may also be required for thrombocytopenia.
Local Haemostasis
An emergency endoscopy should be performed to confirm that varices are the source of bleeding, since peptic ulcer disease is also common in cirrhosis. If possible, endoscopic treatment of varices should be undertaken by endoscopic variceal ligation (banding). Where banding is not possible, sclerotherapy may be useful, adverse events such as oesophageal ulceration and stricture were significantly more severe with sclerotherapy. The most commonly used sclerosants are sodium tetradecyl sulphate (thrombovar) and ethanolamine oleate.
Pharmacotherapy
Octreotide: Decrease portal pressure, 50 micrograms IV, immediately, then 25 to 50 micrograms per hour by IV infusion for 5 days.
While control of initial bleeding has been demonstrated with octreotide, no effect on mortality has been shown. Its transient effect is due to tachyphylaxis.
Terlipressin: 2 mg IV, 6-hourly for 2 to 3 days. It reduces splanchnic blood flow and portal pressure. A meta-analysis demonstrated that terlipressin was associated with a 34% relative risk reduction in mortality compared to placebo.
If endoscopic treatment fails/unavailable and bleeding persists despite octreotide or terlipressin, blood loss can usually be controlled with a Sengstaken-Blakemore–type tube for 24 hours. Balloon tamponade is known to have a high re-bleeding rate when the balloon is decompressed and is associated with serious complications such as ulceration, perforation and aspiration pneumonia. Thus, this should only be considered if facilities for endoscopy are not available prior to transfer to a tertiary centre or as a temporary ‘bridge’ for a maximum of 24 hours until definitive treatment can be instituted.
Antibiotics in Acute Variceal Bleeding
Bacterial infections are seen in about 20% of cirrhotics presenting with upper gastrointestinal bleeding within 48 hours. The incidence of sepsis increases to almost 66% at two weeks. Development of bacterial infection is associated with high mortality and variceal re-bleeding. Antibiotic prophylaxis has been shown to reduce the rate of infection, spontaneous bacterial peritonitis and rebleeding. In addition, antibiotic prophylaxis was clearly proven in a meta-analysis to significantly increase the survival rate. Short-term antibiotic prophylaxis for 7 days should be considered the standard of care in cirrhotic patients with upper gastrointestinal bleeding, irrespective of the type of haemorrhage (variceal or nonvariceal) or the presence or absence of ascites. As to the choice of antibiotic, either third generation cephalosporins given intravenously or oral quinolones (norfloxacin/ciprofloxacin) are generally recommended.
Continued bleeding
Continued bleeding is associated with a high mortality. A second course of endoscopic treatment may be undertaken with continued use of a Sengstaken-Blakemore–type tube for up to 24 hours. Adjunctive infusion of octreotide can be given. An emergency transjugular intrahepatic portosystemic shunt (TIPS) or an emergency portosystemic shunt may be considered, depending on available local expertise.
Transjugular intrahepatic portosystemic shunts (TIPS) is effective in the treatment of acute variceal bleeding with a success rate of over 90% in arresting haemorrhage. The main limiting factors to the use of TIPS are the high morbidity and mortality: the 30-day mortality approaches 100% in patients with advanced liver disease, ongoing sepsis and multi-organ failure. Therefore, the most widely accepted indication for TIPS is as a rescue therapy for uncontrolled variceal bleeding after combined pharmacological and endoscopic therapy.
Surgical Therapy
Surgical options include oesophageal transection with or without devascularisation, portosystemic shunts and liver transplantation. Regardless of the choice of the surgical technique, morbidity and mortality are high: the 30-day mortality associated with emergency surgical procedures is nearly 80%. Similar to TIPS, the role of surgical therapy in the management of acute variceal bleed has been relegated to salvage haemostatic therapy. Liver transplantation is probably only appropriate for liver transplant candidates who bleed while on the waiting list.
Prevention of rebleeding
In patients with cirrhosis who have bled from oesophageal varices, the risk of rebleeding within 12 months is about 60%. Measures to reduce this risk include regular endoscopic banding until varices have largely disappeared. In the longer term, varices recur and may need further banding. In a meta-analysis of clinical trials, therapy with propranolol has been shown to reduce recurrent variceal bleeding and improve survival. In those who rebleed despite the above therapy, TIPS, portosystemic shunt or transplantation should be considered.
Friday, April 10, 2009
Takotsubo Cardiomyopathy
Recently came across two cases of Takotsubo syndrome. One of them diagnosed during angiography (normal with typical apical balloning. Here is synopsis of this cardiomyopathy, further reading can be done from various resources, however, one good site is http://www.takotsubo.com/
Essentials of Diagnosis
Occurs after a major catecholamine discharge.
Acute chest pain or shortness of breath.
Predominately affects postmenopausal women.
Presents as an acute anterior myocardial infarction, but coronaries normal at cardiac catheterization.
Imaging reveals apical left ventricular ballooning due to anteroapical stunning of the myocardium.
General Considerations
LV apical ballooning can follow a high catecholamine stress. The resulting shape of the LV suggests a rounded ampulla form similar to an octopus pot (takotsubo pot). The acute myocardial injury that occurs is more common in postmenopausal women. It has been described following some stressful event, such as hypoglycemia, lightning strikes, earthquakes, postventricular tachycardia, during alcohol withdrawal, following surgery, during hyperthyroidism, and following emotional stress.
Clinical Findings
Symptoms and Signs
The symptoms are similar to any acute coronary syndrome. Typical angina and dyspnea is usually present. Syncope is rare.
ECG and Chest Radiography
The ECG reveals ST segment elevation as well as deep anterior T wave inversion. The chest radiograph is either normal or reveals pulmonary congestion.
Diagnostic Studies
The echocardiogram reveals LV apical dyskinesia. The urgent cardiac catheterization reveals the LV apical ballooning in association with normal coronaries.
TreatmentImmediate therapy is similar to any acute myocardial infarction. Initiation of long-term therapy depends on whether LV dysfunction persists. Most patients receive aspirin, -blockers, and ACE-inhibitors until the LV fully recovers.
Prognosis
Prognosis is good unless there is a serious complication (such as mitral regurgitation, ventricular rupture, ventricular tachycardia). Recovery is expected in most cases after a period of weeks to months. At times, the LV function recovers in days.
Essentials of Diagnosis
Occurs after a major catecholamine discharge.
Acute chest pain or shortness of breath.
Predominately affects postmenopausal women.
Presents as an acute anterior myocardial infarction, but coronaries normal at cardiac catheterization.
Imaging reveals apical left ventricular ballooning due to anteroapical stunning of the myocardium.
General Considerations
LV apical ballooning can follow a high catecholamine stress. The resulting shape of the LV suggests a rounded ampulla form similar to an octopus pot (takotsubo pot). The acute myocardial injury that occurs is more common in postmenopausal women. It has been described following some stressful event, such as hypoglycemia, lightning strikes, earthquakes, postventricular tachycardia, during alcohol withdrawal, following surgery, during hyperthyroidism, and following emotional stress.
Clinical Findings
Symptoms and Signs
The symptoms are similar to any acute coronary syndrome. Typical angina and dyspnea is usually present. Syncope is rare.
ECG and Chest Radiography
The ECG reveals ST segment elevation as well as deep anterior T wave inversion. The chest radiograph is either normal or reveals pulmonary congestion.
Diagnostic Studies
The echocardiogram reveals LV apical dyskinesia. The urgent cardiac catheterization reveals the LV apical ballooning in association with normal coronaries.
TreatmentImmediate therapy is similar to any acute myocardial infarction. Initiation of long-term therapy depends on whether LV dysfunction persists. Most patients receive aspirin, -blockers, and ACE-inhibitors until the LV fully recovers.
Prognosis
Prognosis is good unless there is a serious complication (such as mitral regurgitation, ventricular rupture, ventricular tachycardia). Recovery is expected in most cases after a period of weeks to months. At times, the LV function recovers in days.
Horners syndrome in ICU
Components
Reason/relevant clinical anatomy
Etiology
Diagnosis
Components- Ptosis, miosis, anhydrosis(classic triad), enophthalmus, chemosis of conjunctiva, nasal stuffiness.
Reason- lesion anywhere in the sympathetic neural pathway supplying the head and neck(oculo sympathetic defect)
Relevant clinical anatomy- ocular sympathetics is a 3 neuron ipsilateral pathway:
1st order neurons- arise from hypothalamus and synapse with
2nd order neurons- pre-ganglionic fibres located in the intermediolateral spinal cord, C8-T2 (cilio spinal centre of Budge)- they exit in the anterior roots and pass over the pulmonary apex to synapse in the superior cervical ganglia (located near the angle of jaw).
3rd order neurons- Post ganglionic fibres- run along with the internal carotid artery as sympathetic plexus surrounding it & enter the skull. They exit the skull via orbit in the ophthalmic division of trigemminal nerve and supply the following- Mullers muscle (levator palpebrae superioris) of the upper eyelid, radial muscle of iris (dilator pupilae) and sweat gland of face.
- Horner's syndrome + brain stem/cerebellar signs => suspect a brain stem or cerebellar stroke syndrome affecting the first neuron eg. Wallenberg' syndrome
(* a "central" Horner's syndrome affecting the first neuron does not respond to cocaine and the diagnosis must be made by the associated neurological signs - nearly always associated with pain and temperature loss on the opposite side of the body)
- Horner's syndrome + sensory and/or motor deficit of the limbs => suspect cervical spinal cord pathology affecting the first neuron
- Horner's syndrome + hoarseness => compressive lesion in the chest or neck affecting the second neuron and recurrent laryngeal nerve
- Horner's syndrome + paralysis of the ipsilateral phrenic, vagus and recurrent layngeal nerve => tumor behind the carotid sheath at the C6 level affecting the second neuron
All patients with an unexplained unilateral Horner's syndrome + face/head pain should be presumed to have a carotid artery dissection until proved otherwise
- the sympathetic nerves to the eye travel with the ophthalmic nerve (V1) and a lesion affecting V1 in the region of the orbit is also likely to affect to neighbouring nerves
- Horner's syndrome + cranial nerve 3 and/or 4 and/or 6 and/or V1/V2 dysfunction (and not affecting V3) => suspect cavernous sinus pathology
- Horner's syndrome + cranial nerves 3 and/or 4 and/or 6 and/or V1 (and not affecting V2 and V3) dysfunction => suspect superior orbital fissure pathology
- Horner's syndrome + cranial nerves 2 (optic nerve), 3, and/or 4 and/or 6 and V1 (and not affecting V2 and V3) dysfunction => suspect orbital apex pathology
- Horner's syndrome + optic nerve II dysfunction +/- incomplete cranial nerve 3 dysfunction (and not affecting cranial nerves 3, 4 and 6 and V2 and V3) => suspect posterior orbit pathology
- all patients with an asymptomatic, unexplained Horner's syndrome (especially if they have ipsilateral anhidrosis of the face and neck, which implies a preganglionic Horner's syndrome), who are going to be discharged from the ED for pre-arranged follow-up as an outpatient, should have a chest X-ray performed prior to ED discharge - to exclude a mediastinal or apical lung tumor (Pancoast's tumor) or thoracic aneurysm affecting the second neuron
Etiology-
In general- brain stem lesions (stroke, tumour, trauma), cervical cord lesions, pancoast syndrome & iatrogenic
In ICU- iatrogenic causes are more important (10% of all cases of horners syndrome admitted to hospital)- neck surgery, carotid angiography/endartrectomy/surgeries(are well recognized causes), IJV cannulation and ICC placement. Other causes are- brachial plexus block and thoracic epidural anesthesia. The close proximity of cervical sympathetic trunk to the IJV may result in damage to the trunk by either trauma from the needle or pressure from a hematoma with he development of Horners syndrome. The risk of damaging the sympathetic fibres is increased with a higher approach to the IJV and if the angle between the needle and the skin is great. In the ICU patients with sudden onset of U/L miosis, the d/d is between carotid dissection vs. horners syndrome; the relevant clinical context becomes important to
differentiate.
Clinical Tests for diagnosis-
Dilation lag of miotic pupil- where in dark, the miotic pupil initially fails to dilate increasing the degree of anisocoria- considered specfic test
Cocaine test- Gold std- failure of cocaine drops to dilate the miotic pupil
Differentiation between physiological anisocoria and Horner's syndrome
Thursday, March 5, 2009
Accidental hypothermia – Clinical Effects
Accidental hypothermia is defined as an unintentional decline in core temperature below 35°C (95°F).
•Primary hypothermia occurs because of accidental exposure to cold.
The difference between ambient and core temperature does not have to be great. Since most heat generation occurs through muscle activity, as long as the level of muscle activity required to keep up with heat loss is sustained, the core temperature is maintained. As the ambient temperature remains low, fatigue eventually occurs and muscle activity declines or ceases, and the core temperature falls. Physical conditioning, dehydration, and lack of caloric intake necessary to feed the required muscle activity are examples of factors that exacerbate the problem (this often occurs in recreational situations by accident, misfortune, or stupidity). Medical conditions such as strokes or other injuries may prevent muscle activity or behavioral responses to cold, causing or worsening hypothermia.
•Secondary hypothermia occurs when a disease state causes failure of thermoregulatory function. A high index of suspicion is necessary to accurately diagnose and treat secondary hypothermia since many causes are possible, and treatment is predicated on identification and correction of the underlying abnormality.
At temperatures < 35°C (95°F), the patient becomes less capable of generating heat, and body temperature continues to fall unless some action is taken.
At a core temperature < 30°C (86°F), the body assumes the temperature of the surrounding environment.
Heat is lost or gained through several physical mechanisms, including radiation, conduction, convections, and evaporation. Radiation may account for 55% of loss, evaporation 30%, and conduction 15%, with convection being a relatively minor component. Being wet or immersed in water causes more rapid heat loss.
Air < water (25 X) < ground < Concrete/stone ( 100 X)
A physiologic heat balance is a result of many variables, including the ability to generate heat, body size, age, insulation in the form of clothing, and the temperature of the environment to which the patient is exposed. Heat always flows from a warmer object to a colder object. Under most circumstances the body is warmer than the surrounding environment; thus, the natural flow of heat is out of the body.
3 mechanisms contributing(alone or together) to hypothermia
Reduction in heat production
Endocrine disorders
Myxoedema, Addison’s disease, hypopituitarism, diabetic ketoacidosis, hypoglycaemia, lactic acidosis
Severe infection
Septicaemia, pneumonia, peritonitis, pyelonephritis, meningitis
Malnutrition
Wernicke’s encephalopathy
Uraemia
Cirrhosis
Pancreatitis
Increased heat loss
Cardiovascular accident
Major surgery
Burns, exfoliative dermatitis
Trauma
Massive transfusion
Renal replacement therapy, dialysis
Drugs : ethanol, opiates, barbiturates, benzodiazepines, phenothiazines, tricyclics
Loss of Thermoregulation
Clinical
History
Because hypothermia may accompany a more obvious condition, considering hypothermia in the differential diagnosis in any patient is critical, especially those who present with unexplained symptoms. Remembering that symptoms of a primary condition, such as a stroke, may overshadow the symptoms of hypothermia is also important.
•Symptoms are vague
•Clinical manifestations
•Risk factors include recreational exposure to a cold environment
•Trauma
•Drug use or an overdose
•Inadequate clothing for ambient temperatures
•Hypothermia as a complication of underlying diseases
Physical
Mild hypothermia (32-35°C or 89.6-95°F) : In normal individuals shivering usually occurs when the core temperature is reduced by 0.7°C (increasing the metabolic rate by up to 5 times). When the temperature is reduced to 35°C the patient usually shivers uncontrollably. The reduction in temperature also produces dermal vasoconstriction, tachycardia, elevation of the cardiac output, elevation of plasma catecholamine levels, a ‘cold’ diuresis and hyper-glycaemia. If glycogen stores are depleted, hypo-glycaemia may occur which inhibits shivering. The plasma levels of thyrotropin releasing hormone (TRH), triiodothyronine (T3), L-thyroxine (T4), growth hormone, thyroid-stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH) stimulation tests are normal, suggesting normal pituitary, adrenal and thyroid function during mild hypothermia. other features are Ataxia, Dysarthria, Loss of fine motor coordination, Lethargy, apathy, confusion, impaired judgment
Moderate hypothermia (28-32°C or 82.4-89.6°F) : At temperatures below 33°C, shivering gradually decreases, muscle and joints become stiff and there is a delayed relaxation phase of the stretch reflexes. The patient becomes lethargic, drowsy and often falls asleep. Unconsciousness rarely occurs at temperatures above 28°C, so another cause of coma should be sought if coma exists at levels above this temperature. The pulse, blood pressure and respiratory rate are usually depressed. J waves on ECG and Cold diuresis.
Severe hypothermia (<28°C or 82.4°F) : At a temperature below 30°C, the body loses its ability to spontaneously return to a normal temperature (i.e. the patient becomes poikilothermic); thus active rewarming must be performed. At a temperature below 28°C, the patient is unconscious, areflexic with fixed and dilated pupils, and life may be difficult to detect. Bradycardia and atrial fibrillation occur at temperatures below 30°C and ventricular fibrillation (VF) may occur at temperatures below 28°C. At 20°C asystole is more common than VF. Respiratory frequency maybe reduced to 1 - 2 breaths/min. Bronchorrhoea is common (probably due to deficient ciliary function), whereas pulmonary oedema is rare. Circulatory arrests for 10 min at 30°C, 25 min at 25°C, 45 min at 20°C and 60 min at 16°C are often quoted as being the limits at which cerebral function may return to normal, although case studies indicate that these limits can be extended.The lowest temperature recorded in a person who has subsequently survived is 16.4°C, although under controlled hypothermic conditions for surgical procedures, temperatures down to 10°C are used, and temperatures as low as 6°C have been recorded.
Onset of hypothermia can be triggered by events similar to the generation of primary hypothermia, and primary and secondary hypothermia may exist concurrently. For example, when a patient has a stroke (disruption of thermoregulation due to CNS injury) and falls to a concrete floor (heat loss through conduction) and cannot get up (failure of behavioral adaptations to cold), hypothermia may ensue.
Monday, January 26, 2009
Clinical Pearls - Eye Signs
I just came across some eye signs and the conditions in which they were present and its really fascinating to know their significance.
1. Bilateral Ptosis in a middle aged lady with a recent Right MCA infarct and old Left MCA infarct.
It occurs frequently in patients with hemispheric strokes, especially in association with right hemispheric lesions. Complete bilateral ptosis is usually caused by large infarctions and may be a premonitory sign of an impending herniation.Isolated b/l ptosis has been previously reported in association with midbrain lesions due to subacute encephalitis and midbrain hemorrhage.
Complete ophthalmoplegia, the combination of bilateral ptosis with loss of all extraocular movements, is rarely a consequence of ischemic stroke can be manifestation of bilateral paramedian midbrain-thalamic infarction.
2. Upward Gaze Deviation in a 26 year old man with hypoxic ischaemic brain damage secondary to cardiomyopathy and cardiac arrest.
This deviation is seen in hypoxic brain damage as their is loss of cerebellar Purkinje cells that normally balance vestibular and gaze - holding mechanisms.
In contrast tonic downward gaze deviation with small unreactive pupls is seen in camatose patients due to bilateral thalamic infarction or haemorrhage.
1. Bilateral Ptosis in a middle aged lady with a recent Right MCA infarct and old Left MCA infarct.
It occurs frequently in patients with hemispheric strokes, especially in association with right hemispheric lesions. Complete bilateral ptosis is usually caused by large infarctions and may be a premonitory sign of an impending herniation.Isolated b/l ptosis has been previously reported in association with midbrain lesions due to subacute encephalitis and midbrain hemorrhage.
Complete ophthalmoplegia, the combination of bilateral ptosis with loss of all extraocular movements, is rarely a consequence of ischemic stroke can be manifestation of bilateral paramedian midbrain-thalamic infarction.
2. Upward Gaze Deviation in a 26 year old man with hypoxic ischaemic brain damage secondary to cardiomyopathy and cardiac arrest.
This deviation is seen in hypoxic brain damage as their is loss of cerebellar Purkinje cells that normally balance vestibular and gaze - holding mechanisms.
In contrast tonic downward gaze deviation with small unreactive pupls is seen in camatose patients due to bilateral thalamic infarction or haemorrhage.
Friday, January 16, 2009
Intracerebral Haemorrhage
Hello friends, there are two articles on this issue, one in CCM Dec2008 and 2nd in Current opinion of Jan 09(published ahead).
Both articles talk about medical management and emphasis on BP control as obvious to limit size of haematoma. Role of Factor VII is still controversial, associtaed with thromboembolic phenomenon with no survival benefit. Role and protocol of Prothrombinex is well given in both articles for warfarin induced ICH. Various antihypertensives and their doses are given in table form for ready reckoner in CCM article.
Both articles talk about medical management and emphasis on BP control as obvious to limit size of haematoma. Role of Factor VII is still controversial, associtaed with thromboembolic phenomenon with no survival benefit. Role and protocol of Prothrombinex is well given in both articles for warfarin induced ICH. Various antihypertensives and their doses are given in table form for ready reckoner in CCM article.
Thursday, January 15, 2009
Simple way to reduce morbidity and mortality in surgical patients all over the world
WHO has provided a simple checklist which we can apply to our hospitals wherever we work.This is from the current edition of NEJM.
www.nejm.org January 14, 2009 (10.1056/NEJMsa0810119)
A Surgical Safety Checklist to Reduce Morbidity and Mortality in a Global Population
Implementation of the checklist was associated with concomitant reductions in the rates of death and complications among patients at least 16 years of age who were undergoing noncardiac surgery in a diverse group of hospitals.
I suggest that this list should be posted in the surgeons clinic,pre-anaesthetic clinics and most importantly in pre-operative and operating theatres.
It is the simple things in life which when followed religiously lead to amazing results.
M
www.nejm.org January 14, 2009 (10.1056/NEJMsa0810119)
A Surgical Safety Checklist to Reduce Morbidity and Mortality in a Global Population
Implementation of the checklist was associated with concomitant reductions in the rates of death and complications among patients at least 16 years of age who were undergoing noncardiac surgery in a diverse group of hospitals.
I suggest that this list should be posted in the surgeons clinic,pre-anaesthetic clinics and most importantly in pre-operative and operating theatres.
It is the simple things in life which when followed religiously lead to amazing results.
M
Keeping ourselves on track!!
I fully agree with my friend, Anuj, regarding scanning the journals and I can see Harjit already has done some work by scanning Intensive care medicine. I take responsibility of clinics. Let others also come up with ideas. Anuj, you can take care of CCM by SCCM.
Cheers!!
Cheers!!
Wednesday, January 14, 2009
Intensive care medicine recent articles, Dec'08
I have read these two articles and feel that they carry reasonable daily practice importance.
Review - a must read article: Renal replacement therapies: physiological review
Intensive Care Med (2008) 34:2139–2146
Maximizing rates of empiric appropriate
antibiotic therapy with minimized use
of broad-spectrum agents: are surveillance
cultures the key? Intensive Care Med (2008) 34:2130–2133
DOI 10.1007/s00134-008-1249-7
(This is just a summary of the article)E
EDITORIAL
Of the many therapeutic decisions, physicians have to face
in daily ICU practice choosing initial antibiotic therapy in
the patient with suspected severe nosocomial sepsis is one
of the more challenging.
In patients at risk for infection with multidrug
resistant (MDR) pathogens, the clinician has to resort to
broad-spectrum antimicrobials, which are themselves
linked with the emergence of multidrug resistance.
In this respect,appropriate empirical antibiotic therapy should
have a balanced antimicrobial spectrum that includes the
susceptibility of the infectious pathogen, but does not add
unnecessary selection pressure.
As an alternative to empirical combination antibiotic
therapy, a more focused initial antibiotic selection guided
by surveillance cultures (SC) has been reported.
As more reports solidify the clinical usefulness
of SC, cost remains probably the most important factor
prohibiting a general use of systematic SC.
ICUs with a high prevalence of MDR will
benefit the most, as will be patient populations with a high
risk for MDR infection, such as patients with a complex
history, a prolonged hospital stay and numerous previous
antibiotics. To reduce the cost one can consider restricting
surveillance to this ‘difficult’ patient category.
How to keep oneself updated in critcal care?
15th January 2009.
Beginning is Half done.
Lets congratulate Amit for his innovative idea of ongoing virtual meeting of like minded people.
It allows us to solve each other's clinical queries.
Let us set the ball rolling.
How one can keep oneself updated in the rapidly evolving field of critical care.
Yesterday's evidence is disproved today,for example hype of Glycemic control.
We have thought of following system.
I consider following journals have maximum impact on critical care practice all over the world.
1.NEJM
2.Intensive care medicine from ESICM
3.Critical care medicine from SCCM.
4.Critical care clinics.
5.Current opinion on critical care.
6.Critical care [Forum]
To some extant JAMA,LANCET,BMJ,CHEST,AJRCCM.
If we designate one journal each to one or two individual ,whose responsibility is to keep track of what is published in each issue and post summary of suggestions .
The suggestions include...worth reading article,breakthrough article,new idea but poor study etc etc.
This will enable all of us to keep updated but saves time of scanning each journal each month.
I will we very happy to know other ideas to get the same level of updates.
Anuj M. Clerk
M.D, F.N.B., E.D.I.C.
PDCC ISCCM,
Intensive care ,
Westmead ,NSW
Australia.
Beginning is Half done.
Lets congratulate Amit for his innovative idea of ongoing virtual meeting of like minded people.
It allows us to solve each other's clinical queries.
Let us set the ball rolling.
How one can keep oneself updated in the rapidly evolving field of critical care.
Yesterday's evidence is disproved today,for example hype of Glycemic control.
We have thought of following system.
I consider following journals have maximum impact on critical care practice all over the world.
1.NEJM
2.Intensive care medicine from ESICM
3.Critical care medicine from SCCM.
4.Critical care clinics.
5.Current opinion on critical care.
6.Critical care [Forum]
To some extant JAMA,LANCET,BMJ,CHEST,AJRCCM.
If we designate one journal each to one or two individual ,whose responsibility is to keep track of what is published in each issue and post summary of suggestions .
The suggestions include...worth reading article,breakthrough article,new idea but poor study etc etc.
This will enable all of us to keep updated but saves time of scanning each journal each month.
I will we very happy to know other ideas to get the same level of updates.
Anuj M. Clerk
M.D, F.N.B., E.D.I.C.
PDCC ISCCM,
Intensive care ,
Westmead ,NSW
Australia.
Friday, January 9, 2009
HFOV
Dr Vishal Gupta has asked about High Frequency Oscillatory Ventilation, there are some articles available to understand principles. The links are -
1.http://www.med.umich.edu/ccmu/docs/HFOV.pdf
2.http://scalpel.stanford.edu/ICU/HFOV%20Guidelines.pdf
3.High-Frequency Oscillatory Ventilation for Adult Patients With ARDS
Kenneth P. W. Chan, Thomas E. Stewart and Sangeeta Mehta
Chest 2007;131;1907-1916
1.http://www.med.umich.edu/ccmu/docs/HFOV.pdf
2.http://scalpel.stanford.edu/ICU/HFOV%20Guidelines.pdf
3.High-Frequency Oscillatory Ventilation for Adult Patients With ARDS
Kenneth P. W. Chan, Thomas E. Stewart and Sangeeta Mehta
Chest 2007;131;1907-1916
Wednesday, January 7, 2009
Question asked on Renal Failure in ICU
Please see the links -
1. JAMA article: Renal Replacement Therapy in Patients With Acute Renal Failure
JAMA, February 20, 2008—Vol 299, No. 7 793-805
2. www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1661614
Thanks
1. JAMA article: Renal Replacement Therapy in Patients With Acute Renal Failure
JAMA, February 20, 2008—Vol 299, No. 7 793-805
2. www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1661614
Thanks
Sunday, January 4, 2009
AMQ
Its nice Harjit to start something like this. I believe it will help all to understand the facts and principles in critical care.
Ok Harjit, we can start with you, put some question for which you are trying to get answer or some interesting experience in critical care.
Ok Harjit, we can start with you, put some question for which you are trying to get answer or some interesting experience in critical care.
Congratulations!
My sincerest wishes to all on the CCA blog.
It is said that necessity is the mother of all inventions and innovations, and at present the most important need of the hour is to help others with what we have learnt over the years.And what better medium than the Internet to help us achieve this.
Let us spare some time for this ongoing process and hope that we are able to do some service to the mankind and those who need it most.
The simplest way to start any forum is to start asking questions.So, it would be a good idea to start a section on-- ANSWER MY QUERY (AMQ in short).In which we/anybody puts a question/s on the blog and the answer will be provided by some one who either knows the answer or has the time to answer that/those question/s.The questions will come from our everyday practice as we come across the patients/situations/equipment.If we are not able to provide the answer we should at least provide a reference or an authentic link.
To be continued.
It is said that necessity is the mother of all inventions and innovations, and at present the most important need of the hour is to help others with what we have learnt over the years.And what better medium than the Internet to help us achieve this.
Let us spare some time for this ongoing process and hope that we are able to do some service to the mankind and those who need it most.
The simplest way to start any forum is to start asking questions.So, it would be a good idea to start a section on-- ANSWER MY QUERY (AMQ in short).In which we/anybody puts a question/s on the blog and the answer will be provided by some one who either knows the answer or has the time to answer that/those question/s.The questions will come from our everyday practice as we come across the patients/situations/equipment.If we are not able to provide the answer we should at least provide a reference or an authentic link.
To be continued.
Saturday, January 3, 2009
Welcome All!!!!
Happy new year to all of you, we have started this blog to help to uplift the level of Intensive care medicine in India and the rest of world. We intend to do this by-
- Continued medical education by searching the latest developments pertaining to this field
- Discussion and network formation between various critical care specialists and other doctors all over India and abroad
- Helping the formation of group for providing and creating awareness of Basic life support and some knowledge of advanced life support
- Creating the knowledge and referrence bank for doctors
Please feel free to share your experiences and views to help critical care to reach heights for betterment of common man. Looking forward for your support and comments
- Continued medical education by searching the latest developments pertaining to this field
- Discussion and network formation between various critical care specialists and other doctors all over India and abroad
- Helping the formation of group for providing and creating awareness of Basic life support and some knowledge of advanced life support
- Creating the knowledge and referrence bank for doctors
Please feel free to share your experiences and views to help critical care to reach heights for betterment of common man. Looking forward for your support and comments
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