Sunday August 31, 2008
Venous Air Embolism - VAE - immediate maneuvers

If Venous Air Embolism is suspected during line procedure with symptoms of sudden occurrence of cardiopulmonary dysfunction like hypotension, hypoxia or churning murmur over left sternal border ( "millwheel murmur" ) - following 7 steps are essential:

1. Clamp the line (do not withdraw) - to prevent further air.

2. Rotate patient to left lateral decubitus position - to decrease air leaving through RV outflow tract.

3. Place patient in Trendelenburg position - to help air trap in the apex of the ventricle.

4. Increase oxygen to 100% - Supplemental oxygen reduces the size of embolus. (Avoid High PEEP as it may increase the risk of paradoxical emboli).

5. Advance the catheter little, unclamp the line and aspirate from the 'distal port' to attempt to remove air.

6. If hypotension occurs - start IVF wide open and add pressor if needed (catecholamines are prefered).

7. Continue supportive treatment till air is absorbed or further management like hyperbaric oxygen therapy is planned.


Refrences: Click to get abstract/article.

1. Venous Air Embolism - emedicine.com
2. Gas Embolism - NEJM, feb. 2000, Volume 342:476-482
3. Venous air embolism: a review. J Clin Anesth 1997;9:251-257

Saturday August 30, 2008
Catheter-Directed Embolectomy (CDE), Fragmentation, and Thrombolysis for the Treatment of Massive PE After Failure of Systemic Thrombolysis


Very interesting work from the Department of Radiology, Stanford University Medical Center, Stanford, CA.

A retrospective review was performed on 70 consecutive patients with suspected acute PE over a 10-year period (from 1997 to 2006) who had been referred for pulmonary angiography and/or intervention. The criteria for study inclusion were patients who received CDI due to angiographically confirmed massive PE and hemodynamic shock. CDI involved suction embolectomy and fragmentation with or without catheter thrombolysis.

Results: Twelve patients were treated with CDI. There were seven men and five women (mean age, 56 years; age range, 21 to 80 years). Seven patients (58%) were referred for CDI after failing systemic infusion with 100 mg of tissue plasminogen activator, and five patients (42%) had contraindications to systemic thrombolysis. Catheter-directed fragmentation and embolectomy were performed in all patients (100%). Additionally, catheter-guided thrombolysis was performed in eight patients (67%). Technical success was achieved in 12 of 12 cases (100%). There were no major procedural complications (0%). Significant hemodynamic improvement was observed in 10 of 12 cases (83%). The remaining two patients (17%) died secondary to cardiac arrest within 24 h. Ten of 12 patients (83%) survived and remained stable until hospital discharge.

Conclusion: In the setting of hemodynamic shock from massive PE, catheter-directed intervention (CDI) is potentially a life-saving treatment for patients who have not responded to or cannot tolerate systemic thrombolysis.



Reference: click to get abstract

Catheter-Directed Embolectomy, Fragmentation, and Thrombolysis for the Treatment of Massive Pulmonary Embolism After Failure of Systemic Thrombolysis - Chest. 2008; 134:250-254

Friday August 29, 2008
Propylene Glycol

Being an intensivist it is imperative to understand the dangers of propylene glycol in ICU particularly with Lorazepam drip. Risks are too high if drip is continued beyond 48 hours and dose more than 10 mg/hr. Any unexplained high anion gap metabolic acidosis with elevated osmol gap, should prompt the diagnosis of propylene gylcol toxicity. It may also cause CNS depression, arrhythmias and renal dysfuntion.

Propylene glycol is a viscous, colorless liquid solvent used for many drugs with poor aqueous solubility including lorazepoam, diazepam, esmolol, nitroglycerin, pentobarbital, phenytoin, trimethoprim/sulfamethoxazole and others.

Wednesday August 27, 2008
Vasoconstrictor extravasation

Antidote for vasoconstrictor extravasation in skin and tissues (dopamine, epinephrine, or norepinephrine) is PHENTOLAMINE. Infiltrate 5-15 mg of PHENTOLAMINE in 10 ml of normal saline into the area of extravasation as soon as possible. Treatment may be applied and effective up to 12 hours post extravasation of vasoconstrictor. Keep yourself ready for fluid bolus post treatment.

Mechanism of action: Phentolamine is a nonspecific alpha-adrenergic blocking agent which inhibits vasoconstriction and allow improved blood circulation through the affected area.



References: Click to get abstract or article

1. Drug Monographs - Phentolamine - lhsc.on.ca
2. Treating Extravasation Injuries - extravasation.org
3. The use of phentolamine in the prevention of dopamine-induced tissue extravasation - J Crit Care 1998 Mar;13(1):13-20

Tuesday August 26, 2008

Q: One unit of Fresh Frozen Plasma (FFP) is the plasma taken from a unit of whole blood. How quickly, it should be frozen after collection?


A: It should be frozen within eight hours of collection.

Each unit of FFP contains approximately 225-250 ml of plasma derived from a single unit of whole blood. It is stored frozen at -18° C or colder to preserve all coagulation factors. FFP is thawed in a 37° C (waterbath) upon request (20-30 minutes) and can be stored after thawing for up to 24 hours at 1-6° C. FFP doesn't require crossmatching.


Related previous pearls:

Ok to fresh frozen plasma but male-donor-only please !!

What if plasma exchange is not available as treatment for TTP

How much FFP?

Some facts about FFP

Monday August 25, 2008
BNP in PE

The relationship between brain natriuretic peptide (BNP) increase in acute pulmonary embolism (PE) and the increase in mortality and morbidity has frequently been suggested in small studies.

Methods: Twelve relevant studies involving a total of 868 patients with acute PE at baseline were included in the meta-analysis using a random-effects model.
Studies were excluded if they were performed in patients without certitude of PE or in a subset of patients with cardiogenic shock.

Results:

• Elevated BNP levels were significantly associated with short-term all-cause mortality,with death resulting from pulmonary embolism, and with serious adverse events.
• The corresponding positive and negative predictive values for death were 14% and 99%, respectively.
  

Conclusions:This meta-analysis indicates that while elevated BNP levels can help to identify patients with acute pulmonary embolism at high risk of death and adverse outcome events, the high negative predictive value of normal BNP levels is certainly more useful for clinicians to select patients with a likely uneventful follow-up.

Reference: click to get abstract

Prognostic Value of Brain Natriuretic Peptide in Acute Pulmonary Embolism - Critical Care 2008, 12:R109

Sunday August 24, 2008
4 stages of Neurocysticercosis

Continuing our pearl from yesterday on neurocysticercosis , here are 4 stages of cyst itself while reviewing brain imaging

A: Vesicular cyst. Note the well-defined scolex, minimal contrast enhancement, and mass effect.

B: MRI of a colloidal cyst. Note ring enhancement, loss of the scolex, and perilesional edema.

C: MRI of the nodular/granular stage. Note nodule with diffuse enhancement and no cystic component.

D: Noncontrast computed tomography showing multiple punctuate calcifications.

Saturday August 23, 2008

Case: 22 year old male recently migrated from mexico, presented with seizure to ER. Following radiological imaging obtained. Your diagnosis?




Answer: Neurocysticercosis

Cysticercosis is a parasitic infection that results from ingestion of eggs from the adult tapeworm, Taenia solium (T. solium). When cysticercosis involves the central nervous system, it is called neurocysticercosis. Neurocysticercosis is a leading parasitic infection of the brain and of epilepsy in the developing world. Because millions of people have immigrated to the United States from Latin America in recent years, neurocysticercosis has become an increasingly important cause of seizures in the United States.

Neurocysticercosis is acquired through consumption of food contaminated with feces of a T. solium carrier (i.e., through fecal–oral contract). Eggs of the tapeworm are shed in stool and contaminate food through poor hygiene. When these eggs are ingested and exposed to gastric acid in the human stomach, they lose their protective capsule and turn into larval cysts, called oncospheres. Oncospheres cross the gastrointestinal tract and migrate via the vascular system to the brain, muscle, eyes, and other structures. Once in the brain, the larval cysts (cysticerci) initially generate a minimal immune response and may remain in the brain as viable cysts for years.

Friday August 22, 2008

Case: 52 year old home bound male with chronic history of seizure presented with hyperreflexia, confusion and nystagmus. You are worried about phenytoin toxicity but level is reported as 18 mcg/mL (normal is 10-20 mcg/mL). You secure ABC (airway, breathing and circulation). You start treating patient with IV Lorazepam. What should be your next step?



Answer: Check free phenytoin level

Its true that the therapeutic range of phenytoin is 10-20 mcg/mL and plasma levels (mcg/mL) have an association with acute neurological symptoms. In individuals with decreased protein binding - nursing home residents, poor diet, chronically ill etc - may have signs of toxicity despite a normal total phenytoin level. Free phenytoin levels should be checked. Free phenytoin levels range from 1-2 mcg/mL and correlate well with clinical evidence of toxicity.

If free phenytoin level is not available, it should be adjusted with albumin level with following formula, called Sheiner-Tozer equation. Its not 100% accurate but give good estimate.

Corrected Dilantin = measured level / [ (0.2 x albumin) + 0.1]

e.g: if measured Dilantin level is 8.2 but albumin is 2.2, the corrected Dilantin level would be 8.2 / { (.2 x 2.2) + .1} = 15.2

In renal patients, If patient CrCl is less than 20, use following formula.

Corrected Dilantin = measured level / [ (0.1 x albumin) + 0.1]

e.g: if measured Dilantin level is 8.2 and albumin is 2.2, the corrected Dilantin level would be 8.2 / { (.1 x 2.2) + .1} = 25.6

Thursday August 21, 2008

Case: 50 year old patient who is Jehovah's Witness by religious belief said that he will not take any blood or even any product from human blood including fresh frozen plasma, platelet etc. Patient hemoglobin is 9.2 and is scheduled to have Coronary artery bypass graft (CABG). You consider Epoetin Alfa as an alternative. What you need to discuss with patient first before writing order?

Answer: Among Erythropoiesis-stimulating agent Epoetin alfa (Procrit and Epogen) contains albumin which is a product from human blood. Beside Epoetin alfa, Darbopoetin alfa (Aranesp) is available in 2 forms: albumin and polysorbate(albumin free). Its important to inform patient about albumin inclusion in given Erythropoiesis-stimulating agent.

Wednesday August 20, 2008
Does Xigris help in ALI ? - 2

I saw your pearl from yesterday "Does Xigris help in ALI" and recalled seeing following article, which has yet to publish. It might make a good counterpoint.

Tony Halat, MD
Clinical Instructor in Medicine
Department of Medicine, The Methodist Hospital
Weill Medical College, Cornell University


Randomized Clinical Trial of Activated Protein C for the Treatment of ALI

Objective: To test the efficacy of activated protein C as a therapy for patients with acute lung injury.

Methods: Eligible subjects were critically ill patients who met the American/European consensus criteria for acute lung injury. Patients with severe sepsis and an APACHE II score 25 were excluded. Participants were randomized to receive activated protein C (24 mcg/kg/hour for 96 hours) or placebo in a double-blind fashion within 72 hours of the onset of acute lung injury.

The primary endpoint was ventilator free days.

Measurements and Main Results:

• Activated protein C increased plasma protein C levels (p=0.002) and decreased pulmonary dead space fraction (p=0.02).
• However, there was no statistically significant difference between patients receiving placebo (n=38) or activated protein C (n=37) in the number of ventilator free days or in 60-day mortality.
• There were no differences in the number of bleeding events between the two groups.

Conclusions: Activated protein C did not improve outcomes from acute lung injury. The results of this trial do not support a large clinical trial of activated protein C for acute lung injury in the absence of severe sepsis and high disease severity.



Reference: Click to get article

Randomized Clinical Trial of Activated Protein C for the Treatment of Acute Lung Injury - Published ahead of print on June 19, 2008 Am. J. Respir. Crit. Care Med. 2008

Tuesday August 19, 2008
Does Xigris help in ALI ?

See this interesting work done on sheeps.

Introduction: Acute lung injury (ALI) often complicates severe sepsis. Recombinant human activated protein C (rhAPC) - Xigris, with its anti-coagulant, anti-inflammatory, fibrinolytic and anti-apoptotic effects, reportedly reduces respirator-dependent days and mortality of patients with severe sepsis.

Methods: Two groups of sheep were exposed to Escherichia coli endotoxin (lipopolysaccharide; LPS) 15 ng/kg/min intravenously from 0 to 24 hours;

• one group received only LPS throughout (n = 8) and
• the other group received LPS in combination with rhAPC 24 mug/kg/hr from 4 to 24 hours (n = 9)

In addition,

• one group received rhAPC as above as the only intervention (n = 4) and
• four sham-operated sheep were used for determination of alpha and epsilon-isoforms of protein kinase C (PKC alpha, epsilon) in pulmonary tissue

Results

• Infusion of endotoxin caused lung injury manifested by increments in pulmonary artery pressure, pulmonary micro-occlusion pressure, pulmonary vascular downstream resistance, pulmonary vascular permeability index, extravascular lung water index (EVLWI) and deterioration of oxygenation that were all attenuated by infusion of rhAPC
• Endotoxemia led to changes in inflammation and coagulation, including pulmonary neutrophil accumulation paralleled by increased tumor necrosis factor-alpha and decreased protein C and fibrinogen in animal plasma, that all improved following infusion of rhAPC
• Moreover, rhAPC prevented the translocation of PKC alpha, epsilon from the cytosolic fraction of lung tissue extracts

Conclusions: In awake sheep, rhAPC alleviates endotoxin-induced lung injury, as characterized by improvements of oxygenation, coagulation and inflammation, as well as by reversal of pulmonary hemodynamic - and volumetric changes.

Reference: Click to get article

Recombinant human activated protein C attenuates endotoxin-induced lung injury in awake sheep Critical Care 2008, 12:R104

Monday August 18, 2008
Choice of first dose of antibiotic makes difference !

A very important article from Barnes-Jewish Hospital, St. Louis, MO

Objective: To identify predictors of 30-day mortality and hospital costs in patients with ventilator-associated pneumonia (VAP) attributed to potentially antibiotic-resistant Gram-negative bacteria (PARGNB) [Pseudomonas aeruginosa, Acinetobacter species, and Stenotrophomonas maltophilia].

Patients: Adult patients requiring hospitalization with microbiologically confirmed VAP attributed to PARGNB.

Results: 76 patients with VAP attributed to PARGNB were identified over a 5-year period. Nineteen patients (25.0%) died during hospitalization.

• Patients receiving their first dose of appropriate antibiotic therapy within 24 hour of BAL sampling had a statistically lower 30-day mortality rate compared to patients receiving the first dose of appropriate therapy after 24 hour after BAL (17.2% vs 50.0%)
• VAP due to Acinetobacter species was most often initially treated with an inappropriate antibiotic regimen, followed by S maltophilia and P aeruginosa (66.7% vs 33.3% vs 17.2%)

Conclusions: These data suggest that inappropriate initial antibiotic therapy of microbiologically confirmed VAP attributed to PARGNB is associated with greater 30-day mortality. High rates of VAP attributed to antibiotic-resistant bacteria (eg, Acinetobacter species) may require changes in the local empiric antibiotic treatment of VAP in order to optimize the prescription of appropriate initial therapy.


Reference: Click to get abstract

Predictors of 30-Day Mortality and Hospital Costs in Patients With Ventilator-Associated Pneumonia Attributed to Potentially Antibiotic-Resistant Gram-Negative Bacteria - Chest. 2008; 134:281-287

Sunday August 17, 2008
PEEP reduces incidence of VAP in nonhypoxemic patients


Very interesting article to analyze the effect on clinical outcomes of prophylactic positive end expiratory pressure in nonhypoxemic ventilated patients. It was a multicenter randomized controlled clinical trial from one trauma and two general ICUs in two university hospitals.

Patients: 132 mechanically ventilated patients with normal chest radiograph and Pao2/Fio2 above 250

Interventions: Patients were randomly allocated to receive mechanical ventilation with

• 5-8 cm H2O of PEEP (PEEP group, n = 66) or
• no-PEEP (control group, n = 65)

Results:

• Hospital mortality rate was similar
• Ventilator-associated pneumonia was detected in 16 (25.4%) patients in the control group and 6 (9.4%) in the PEEP group
• The number of patients who developed hypoxemia was significantly higher in the control group (34 of 63 patients, 54%) than in the PEEP group (12 of 64, 19%) and
• the hypoxemia developed after a shorter period in the control group than in the PEEP group (38 [20-70] hrs vs. 77 [32-164] hrs).
• Groups did not significantly differ in incidence of ARDS (14% in controls vs. 5% in the PEEP group), barotrauma (8% vs. 2%, respectively), or atelectasis (27% vs. 19%, respectively)

Conclusions: These findings indicate that application of prophylactic PEEP in nonhypoxemic ventilated patients reduces the number of hypoxemia episodes and the incidence of ventilator-associated pneumonia.


Reference: Click to get article

Positive-end expiratory pressure reduces incidence of ventilator-associated pneumonia in nonhypoxemic patients - Critical Care Medicine. 36(8):2225-2231, August 2008.

Saturday August 16, 2008
SEROTONIN SYNDROME

Serotonin syndrome is a potentially lethal condition caused by overstimulation of central and peripheral serotonin receptors. SSRI, MAOI and other antidepressants are the biggest culprits. (Everybody seems to be on some type of antidepressant these days!). Mild cases of serotonin syndrome may present with nausea, vomiting, flushing, and diaphoresis. Severe cases may present with hyperreflexia, myoclonus, muscular rigidity, hyperthermia, and autonomic instability. Diagnosis is clinical and no lab tests are available.

Treatment include discontinuation of all serotonergic medications. The initial treatment of serotonin syndrome is with benzodiazepines and cyproheptadine. Cyproheptadine (Periactin) appears to be the most effective antiserotonergic agent in humans. The initial dose is 4 - 8 mg PO. This dose can be repeated in 2 hrs if no response is noted to the initial dose. Periactin therapy should be discontinued if no response is noted after 16 mg has been administered. Patients who respond to cyproheptadine are usually given 4 mg every 6 h for 48 h to prevent recurrences. Dantrolene (0.5-2.5 mg/kg IV every 6 h, maximum 10 mg/kg per 24 h or 50 to 100 mg bid PO) is a nonspecific muscle relaxant that is used occasionally in serotonin syndrome, presenting with hyperthermia.

Here are 2 review articles for reference

1. Serotonin syndrome from McGill University, Montreal. CMAJ • May 27, 2003; 168 (11) followed with letter Serotonin syndrome: not a benign toxidrome CMAJ • September 16, 2003; 169 (6)
2. The Serotonin Syndrome - NEJM, March 2005 Volume 352:1112-1120

Friday August 15, 2008
Role of High frequency oscillatory ventilation in Trauma

Recent study by Funk in Journal of trauma-injury & critical care helped to shed light on this area.

Background: Severe pulmonary contusions are a common cause of acute respiratory distress syndrome (ARDS) and are associated with significant morbidity. High frequency oscillatory ventilation (HFOV) is a ventilatory mode that employs a lung protective strategy consistent with the ARDSNet low tidal volume ventilation strategy and may result in reduced morbidity. The objective of this report is to examine the impact of HFOV on blunt trauma patients with severe pulmonary contusions who failed or were at a high risk of failing conventional mechanical ventilation.

Methods: We undertook a retrospective chart review of all patients at our institution who received HFOV for severe pulmonary contusions. Patients were placed on HFOV when their mean airway pressure (mPaw) surpassed 30 cm H2O and their FIO2 was greater than 0.6. Serial determinations were made upto 72 hours of

• oxygenation index (OI) and
• the Pao2/FIO2 ratio (P/F)

A linear mixed model was used to analyze the slope ([beta]) of the regression line of P/F versus time and that of OI versus time.

Results: 17 patients were identified who underwent HFOV for ARDS due primarily to pulmonary contusions.

• P/F increased significantly after HFOV was initiated ([beta] = 12.1
• OI significantly decreased after HFOV implementation ([beta] = -1.8
• Mortality rate was 17.6%

Conclusions: The early use of HFOV appears to be safe and efficacious in blunt trauma patients sustaining pulmonary contusions, and results in a rapid improvement in OI and the P/F ratio.



Reference: click to get abstract

Funk D, Lujan E, Moretti EW, Davies J, Young C, Patel M, Vaslef S. A brief report: The use of high-frequency oscillatory ventilation for severe pulmonary contusion. Journal of Trauma-Injury & critical Care 2008; 65(2): 390-395

Thursday August 14, 2008

Q: Citrate is used in continuous renal replacement therapy (CRRT) for extracorporeal anticoagulation. What is the added advantage of using citrate?

Answer: Citrate partially enters the systemic circulation. Apart from being an anticoagulant, citrate is a buffer substrate. The generation of buffer is related to the conversion of sodium citrate to citric acid:

Na3 citrate + 3H2CO3 = citric acid + 3NaHCO3

Citric acid enters the mitochondria and is metabolized in the Krebs cycle, mainly in the liver but also in skeletal muscle and the renal cortex, leaving sodium bicarbonate.

Related Pearl: Citrate in CRRT

Reference: Click to get article

Clinical review: Patency of the circuit in continuous renal replacement therapy- Critical Care 2007, 11:218

Tuesday August 12, 2008

Case: 58 year old male is admitted to ICU with Atrial fibrillation with RVR (rapid ventricular rate). Patient did well with rate control therapy and has been discharged from hospital on metoprolol, aspirin, lisinopril, simvastatin and Amiodarone. Patient presented back after 2 weeks to ED with complain of severe generalized weakness. Patient was found to be in acute renal failure. Beside hyperkalemia and elevated creatinine, patient found to have CPK in 60,000 range. Troponin is normal. Your diagnosis ?



Answer: Acute renal failure secondary to rhabdomyolysis caused by simultaneous use of simvastatin with amiodarone.

Though it has been reported in literature earlier, FDA recently issued warning regarding above drug interaction 1. This risk is dose-related and increases when a dose of simvastatin greater than 20 mg per day is given with amiodarone.

Precise mechanism is not clearly known, but amiodarone inhibits the cytochrome P450 3A4 (CYP3A4) enzyme. This is the same enzyme that metabolizes simvastatin 2.

Use of other statins without relevant CYP metabolism (eg, pravastatin) should be ok.


Reference: click to get abstract

1. Simvastatin (marketed as Zocor and generics), Ezetimibe/Simvastatin (marketed as Vytorin), Niacin extended-release /Simvastatin (marketed as Simcor), used with Amiodarone (Cordarone, Pacerone) - fda.gov

2. Rhabdomyolysis in Association with Simvastatin and Amiodarone - The Annals of Pharmacotherapy: Vol. 38, No. 6, pp. 978-981.

Monday August 11, 2008

Case: 38 year old female with cervical cancer and undergoing chemotheraphy is admitted with dehydration secondary to chemotherapy-induced nausea and vomiting (CINV). According to patient standard anti nausea medications including zofran (ondansetron), compazine (prochlorperazine) or phenergan doesn't work. Which 'trick' or cocktail usually works in such resistant nausea?

Answer: ABH Cocktail

ABH (Ativan, Benadryl and Haldol) cocktail is effective in resistant nausea particularly in chemotherapy-induced nausea and vomiting (CINV). It is available in capsule, suppository as well as in transdermal gel form. If needed can be given in IV mix over 15 minutes. Extended form is called "ABHR" with addition of Reglan (metoclopramide). Usual IV dose is

• Ativan (lorazepam) = 0.5 mg,
• Benadryl (diphenhydramine) = 12.5 mg,
• Haldol (haloperidol) = 0.5 mg and
• Reglan (metoclopramide)= 5-10 mg

Doses can be escalated in oral and gel form if needed upto lorazepam 4 mg/ diphenhydramine 100 mg/haloperidol 4 mg/metoclopramide 80 mg per ml.

Sunday August 10, 2008

Case: 28 year old male has been brought to ED with possible ethylene glycol toxicity. Osmol gap is greater than 10 mOsm/L and reportedly urinary oxalate crystals are present. Unfortunately, Fomepizole is not available and you decide to treat patient with Ethanol. Before initiating treatment which lab value you would like to see?

Answer: ethanol level itself

Its not uncommon to have both Ethanol and Ethylene Glycol ingestion together. Overly aggressive ethanol administration may cause apnea that required intubation.

Goal is to maintain blood ethanol levels 100-150 mg/dL. Measuring initial blood level is important; if more than 100 mg/dL, loading dose may be unnecessary.

Doses:
IV loading dose: 7-10 mL/kg IV of 10% ethanol (V/V) in dextrose 5% in water over 30 min to achieve blood ETOH concentration of 100-130 mg/dL (21.7-28.2 mmol/L)
Oral loading dose: 1 mL/kg of 95% ethanol mix with orange juice over 30 min
Average maintenance PO dose: 0.15 mL/kg/h of 95% ETOH
Average maintenance IV dose:1.5 mL/kg/h of a 10% solution

Saturday August 9, 2008
3 "NOs" in organophosphate poisoning

Due to their very common usage in ICU, there may be a reflex tendency to use following 3 medications. But its better to avoid them as they may increase the toxicity of the organophosphate exposure.

1. Avoid succinylcholine for intubation *
2. Avoid loop diuretics for increased pulmonary secretions/congestion
3. Avoid morphine for analgesia

* see related previous pearl here

Friday August 8, 2008
Combined milrinone and enteral metoprolol therapy in septic myocardial depression

A very interesting study to counter septic cardiomyopathy.

Methods:This retrospective analysis summarizes preliminary clinical experience with the combined use of milrinone and enteral metoprolol therapy in forty patients with septic shock and cardiac depression. In all study patients, beta blockers were initiated only after stabilization of cardiovascular function in order to decrease heart rate less than 95 bpm. Hemodynamic data and laboratory parameters were extracted from medical charts and documented before, 6, 12, 24, 48, 72, and 96 hours after the first metoprolol dosage. Adverse cardiovascular events were documented.

Patients with other causes of shock or cardiac failure, patients with beta-blocker therapy initiated more than 48 hrs after shock onset and patients with pre-existent decompensated congestive heart failure were excluded.

Results

• Heart rate control (65-95 bpm) was achieved in 97.5% of patients (n=39) within 12.2+/-12.4 hrs.
• Heart rate, central venous pressure, norepinephrine, arginine vasopressin and milrinone dosages decreased.
• Cardiac index and cardiac power index remained unchanged, while stroke volume index increased
• Norepinephrine and milrinone dosages were increased in nine (22.5%) and six (15%) patients, respectively.
• PH increased, while arterial lactate, serum C-reactive protein and creatinine levels decreased during the observation period
• Twenty-eight day mortality was 33%
  

In two patients (5%) metoprolol was discontinued because of asymptomatic bradycardia

Conclusions: Low doses of enteral metoprolol in combination with phosphodiesterase inhibitors are feasible in patients with septic shock and cardiac depression but no overt heart failure.

Reference: click to get article

Combined milrinone and enteral metoprolol therapy in patients with septic myocardial depression - Critical Care 2008, 12:R99 - pdf file

Thursday August 7, 2008
Does Non Invasive ventilation improve short term mortality in patients with acute cardiogenic pulmonary edema??


In a study published in NEJM by Alasdair gray they studied the above issue. A total of 1069 patients were assigned to

• Standard oxygen therapy (367 patients),
• CPAP (346 patients), or
• NIPPV (356 patients)

Standard oxygen therapy, CPAP (5 to 15 cm of water), or NIPPV (inspiratory pressure, 8 to 20 cm of water; expiratory pressure, 4 to 10 cm of water)


Results:

• There was no significant difference in 7-day mortality between patients receiving standard oxygen therapy (9.8%) and those undergoing noninvasive ventilation (9.5%, P=0.87).
• There was no significant difference in the combined end point of death or intubation within 7 days between the two groups of patients undergoing noninvasive ventilation (11.7% for CPAP and 11.1% for NIPPV, P=0.81).
• As compared with standard oxygen therapy, noninvasive ventilation was associated with greater mean improvements at 1 hour after the beginning of treatment in patient-reported dyspne , heart rate, acidosis and hypercapnia.
• There were no treatment-related adverse events

Conclusions: In patients with acute cardiogenic pulmonary edema, noninvasive ventilation induces a more rapid improvement in respiratory distress and metabolic disturbance than does standard oxygen therapy but has no effect on short-term mortality



Reference: click to get abstract

Gray A, Goodacre S, Newby DE, Masson M, Sampson F, Nicholl J. Noninvasive ventilation in acute cardiogenic pulmonary edema. NEJM July 10th 2008; 359: 142-151

Wednesday August 6, 2008

Q; Which condition may mimic pseudo-atrial flutter on EKG and on monitor?


A; Parkinsonian tremor (first reported about 40 years ago 1 and later on many other reports confirmed it).

In literature, cases have been reported of pseudo atrial flutter with use of electronic devices by patient. 2


References:

1. MUSCLE-TREMOR ARTIFACT DUE TO PARKINSON'S SYNDROME. IT STIMULATED ATRIAL FLUTTER AND DISAPPEARED DURING SLEEP - Postgrad Med. 1965 Jun;37:718-20.
2. Atrial flutter simulated by a portable CD player - mayo clinic proceedings - march 2006,82(3), Page 383 -pdf file

Tuesday August 5, 2008
Can we predict who needs ICU admission after Major Lung Resection


Study by Brunelli and his associates helped to address that issue.

Background: We aimed to develop and validate a scoring system to predict intensive care unit (ICU) admission for complications after major lung resection for purposes of optimizing planning of resources for patient care.

Methods: Patients undergoing major lung resections performed between 2000 and 2006 at three thoracic surgery units were analyzed for unplanned admission to the ICU for complications. Variables were initially screened by univariate analysis. Selected variables were used in a stepwise logistic regression analysis that was validated by bootstrap analysis. The scoring system was developed by proportional weighting of the significant and reliable predictors estimates and validated on patients operated on in a different center.

ResuIts: In the derivation set of 1927 patients, 82 had ICU admission for complication, and 30 died (associated mortality rate 36.5%). Predictive variables and their scores were

* 2 points - pneumonectomy; and
* 1 point each for

• age older than 65,
• predicted post operative FEV1 below 65%,
• predicted post operative DLCO below 50%, and
• cardiac comorbidity
  

Patients were grouped into three classes based on their score, which were significantly associated with the incremental risk of ICU admission in the validation set of 349 patients.

Conclusion: It helps us in assessing and preparing for the post operative need for ICU and possible complications.

Reference:

Brunelli A, Ferguson MK, Rocco G, Pieretti P, et al. A Scoring System Predicting the Risk for Intensive Care Unit Admission for Complications After Major Lung Resection: A Multicenter Analysis. Ann Thorac Surg 2008;86:213-218.

Monday August 4, 2008
A randomized controlled trial of conventional versus automated weaning from mechanical ventilation using SmartCare/PS failed to show superiority for SmartCare/PS system

In a study by Lellouche published in 2006 AJRCCM (174;894-900) showed that SmartCare/PS was associated with a substantial reduction in the duration of ventilation and ICU length when compared to physician controlled weaning using local European guidelines.

SmartCare/PS monitors the patient’s respiratory status every 2 to 5 minutes (frequency, tidal volume, and end tidal CO2) and periodically adapts pressure support aiming for a safe efficient weaning process. The computerized SmartCare/PS establishes a respiratory status diagnosis, determines an intervention and then instructs the ventilator to decrease or increase the PS.

In a study by Louise Rose published in Intensive care Medicine they studied 102 patients.

• The median time from the first identified point of suitability for weaning to the state of separation potential using SmartCare/PS was 20 hrs as compared to 8hrs for the Control.
• The median time to successful extubation using SmartCare/PS was 43hrs as compared to 40 hrs with the Control.
• Study showed comparable rate of reintubation, tracheostomy, neuromuscular blockers usage and steroid use.

Conclusion: Substantial reductions in weaning duration with SmartCare/PS as previously demonstrated were not confirmed when compared to weaning managed by experienced critical care specialty nurses using 1:1 nurse to patient ratio. Majority of those nurses held a graduate critical care specialty qualification (Respiratory therapist are not employed in Australian context)



Reference:

Rose L, Presneill JJ, Johnston L, Cade JF. A randomized, controlled trial of conventional versus automated weaning from mechanical ventilation using SmartCare/PS. Intensive Care Med 2008

Sunday August 3, 2008
Interesting website

We try to keep our readers posted with "cool" medical websites. Following is a very well done website. It has

• Clinical Cases by Organ System
• Links to Examination Videos
• Links to Electrocardiograms, X-rays, CT scans
• Procedure Guides Step-by-Step

The web site is Clinical Cases and Images

( http://clinicalcases.blogspot.com/ )

Saturday August 2, 2008


Case: You have been called to ER to consult a critically ill 42 year old male who presented with mental status change and hypotension. Lab shows finding of pre-renal azotemia with acute renal failure (ARF). Wife reports chills and 'very very excessive sweating' since last 3 months, progressively getting worse. Patient was also reported to be hypothermic. Your diagnosis was simple septic shock and you argued about CT scan of head which was done by ER physician. Meanwhile, you received call from radiologist with report of CT head and he strongly recommends MRI of brain to confirm findings. You agreed and it showed agenesis of the corpus callosum. What is your diagnosis?

Diagnosis: Shapiro's Syndrome

Shapiro's Syndrome is characterised by recurrent episodes of hypothermia, hyperhidrosis and agenesis of the corpus callosum. Shapiro syndrome is listed as a "rare disease" by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). Onset is typically in adulthood. Hyperhidrosis can be so severe that it may cause acute renal failure. Different treatments has been described including cyproheptadine, clonidine, glycopyrrolate or topiramate.


*Shapiro's Syndrome was first described by W. R. Shapiro, G.H. Williams and F. Plum in 1969.



References: Click to get abstract/article

1. Agenesis of the corpus callosum associated with paroxysmal hypothermia: Shapiro's syndrome. Neth J Med. 1997 Jan;50(1):29-35.
2. Clonidine therapy for Shapiro's syndrome. Q J Med. 1992 Mar;82(299):235-45.
3. HYPOTHALAMIC DYSFUNCTION IN SHAPIRO'S SYNDROME MAY CAUSE ABNORMALITIES OF THIRST AND APPETITE PERCEPTION Endocrine Abstracts (2002) 4 P24
4. Shapiro's Syndrome: A Renewed Appreciation for Vital Signs Clinical Infectious Diseases 2004;38:e107–e108

Friday August 1, 2008
ICU billing code inconsistency

See this very interesting study titled "Reliability of diagnostic coding in intensive care patients". Is this inconsistency because patients are too sick or we don't know, how to bill?

Introduction: Administrative coding of medical diagnoses in intensive care unit (ICU) patients is mandatory in order to create databases for use in epidemiological and economic studies. We assessed the reliability of coding between different ICU physicians.

Methods: One-hundred medical records selected randomly from 29,393 cases collected between 1998 and 2004 in the French multicenter Outcomerea ICU database were studied. Each record was sent to two senior physicians from independent ICUs who re-coded the diagnoses using the International Classification of Diseases - 10th revision (ICD-10) after being trained according to guidelines developed by two French national intensive care medicine societies, the French Society of Intensive Care Medicine (SRLF) and French Society of Anesthesiology and Intensive Care Medicine (SFAR). These codes were then compared to the original codes, which had been selected by the physician treating the patient. A specific comparison was done for the diagnoses of septicemia and shock.

Results: The ICU physicians coded an average of 4.6+/-3.0 (range 132) diagnoses per patient, with little agreement between the three coders.

• The primary diagnosis was matched by both external coders in 34% of cases, by only one in 35%, and by neither in 31%.
• Only 18% of all codes were selected by all three coders.
• Similar results were obtained for the diagnoses of septicemia and/or shock.

Conclusions: In a multicenter database designed primarily for epidemiological and cohort studies in ICU patients, the coding of medical diagnoses varied between different observers. This could limit the interpretation and validity of research and epidemiological programs using diagnoses as inclusion criteria.


References: Click to get abstract/article

1. Reliability of diagnostic coding in intensive care patients Critical Care 2008, 12:R95