icuroom.net September 2009 archive

2009-09-30T18:21:00.000-07:00

Wednesday September 30, 2009
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.

See brief review on Serotonin syndrome here 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)

References: Click to get abstract or article

1. Serotonin syndrome. A clinical update - Mills KC - Crit Care Clin. 1997 Oct;13(4):763-83. via pubmed
2. Treatment of the serotonin syndrome with cyproheptadine - J Emerg Med., 1998 Jul-Aug;16(4):615-9. via pubmed
3. The Serotonin Syndrome - NEJM, March 2005 Volume 352:1112-1120

2009-09-29T09:49:00.000-07:00

Tuesday September 29, 2009
Acute A. fib. and Digoxin

Q: 44 year old male with CHF went into Atrial fibrillation with RVR (Rapid Ventricular Rate) of 160 to 180 beats per minute. You ordered Digoxin 0.25 mg IV but after 15 minutes, there is no response?

Answer: Digoxin is an effective medicine for control of Atrial fibrillation associated RVR particularly in patients with congestive heart failure and left ventricular systolic dysfunction. But this is of importance to know that Digoxin is not a treatment for very acute management of A.fib. The onset of action is usually at 30 minutes with a peak effect in 2 - 3 hours.

2009-09-28T16:40:00.000-07:00

Monday September 28, 2009
Bedside tip

Q: Why it is not advisable to draw blood from Cordis (introducer) for blood sampling?

Answer: Given their large diameters, accurate lab draws would be difficult considering the amount of waste that needs to be withdrawn even to get a good blood sample (not visibly diluted) is substantial.

On other hand, Cordis is preferable for resuscitation. The flow rates are incredible. Technically Central line (TLC or PICC line) is not ideal for resuscitation due to longer length and smaller radius. 2 Large bore (say 18 gauge) peripheral IVs or one large bore central IV (cordis) are real placements for aggressive resuscitation, due to bigger radius and shorter length.

Remember as per Hagen-Poiseuille equation just 2 fold increase in radius increase flow by 16 fold but on the other hand, just 2 fold increase in length decrease flow by 50%.

2009-09-27T07:13:00.000-07:00

Sunday September 27, 2009
Ventilator Weaning 3 parts

2009-09-26T06:00:00.000-07:00

Saturday September 26, 2009

Q; 65 year old female admitted to ICU 9 days ago with small bowel obstruction. Pt. is now stable and actually is about to get transferred out of unit. Patient suddenly start complaining of choking sensation with two hands on neck. Monitor shows oxygen desaturation. Patient intubated emergently. No laryngeal or vocal edema seen on laryngoscope but vocal cord paralysis noted.

A; Nasogastric tube syndrome

Nasogastric tube syndrome was described about 25 years ago by Sofferman and coll. It is a life-threatening complication of an indwelling (more than a week) nasogastric tube. The syndrome may present as complete vocal cord abductor paralysis. The syndrome is thought to result from perforation of the NG tube-induced esophageal ulcer and infection of the posterior cricoid region (postcricoid chondritis) with subsequent dysfunction of vocal cord abduction. Unilateral paralysis of cord is also described. Treatment is protection of airway, removal of NG tube and antibiotics. Some advocates antireflux therapy too. Another variant is described with no esophageal ulcer but possibly because of ischemia of the laryngeal abductor muscle secondary to physical compression of the postcricoid blood vessels by NG tube.

References: Please click to get abstract

1. The nasogastric tube syndrome: two case reports and review of the literature. Head Neck. 2001 Jan;23(1):59-63.

2. A variant form of nasogastric tube syndrome. Intern Med. 2005 Dec;44(12):1286-90.

3. Case Report - Nasogastric Tube Syndrome: The Unilateral Variant - Medical Principles and Practice Vol. 12, No. 1, 2003

4. Sofferman, R.A. and Hubbell, R.N., "Laryngeal Complications of Nasogastric Tubes," ANNALS OTOLOGY, RHINOLOGY, AND LARYNGOLOGY, 90:465-468, 1981.

2009-09-25T23:01:00.000-07:00

Friday September 25, 2009
Revisiting Pulmonary Artery Diastolic-Pulmonary Wedge Pressure Gradient

We don't see floatation of pulmonary artery catheter (PAC) as much as we used to see. Lets revisit one important but forgotten value obtained via PAC.

PADP - PAOP

(Pulmonary Artery Diastolic-Pulmonary Wedge Pressure Gradient)

Most of the literature in regards to this value is 15-30 years old but proven to be very easy to calculate but very vital to follow 1, 3.

Once this gradient starts to exceeds by 6 mm Hg or more, the patient has shown to have a much poorer prognosis particularly in septic patients. Probable explanation is pulmonary venous vasoconstriction induced by endotoxemia in sepsis or postcapillary lekocyte aggregation in development of ARDS 2, 4.

One study suggests that although an initial PAD-PWP gradient in patients with sepsis is associated with a high mortality, a much more sensitive indicator is to follow the trend. There was a 91% mortality in patients with persisting or increasing gradients 2.

References: click to get abstract/artice

1. Pulmonary hypertension in sepsis: Measurement by the pulmonary arterial Diastolic-pulmonary wedge pressure gradient and the influence of passive and active factors. Chest 1978; 73:583-91

2. Significance of the pulmonary artery diastolic-pulmonary wedge pressure gradient in sepsis. Crit Care Med 1982; 10:658-61

3. Pulmonary artery diastolic and wedge pressure relationships in critically and injured patients. Arch Surg 1988; 123:933-6

4. Increased Pulmonary Venous Resistance Contributes to Increased Pulmonary Artery Diastolic-Pulmonary Wedge Pressure Gradient in Acute Respiratory Distress Syndrome - Anesthesiology: Volume 102(3) March 2005 pp 574-580

2009-09-24T10:42:00.000-07:00

Thursday September 24, 2009
"Locked-in" Syndrome (coma vigilante)

"patient is a silent and unresponsive witness to everything that is happening" - from story of Nick Chisholm 1

Patient with Locked-in syndrome is a fully conscious person, but all the voluntary muscles of the body are completely paralyzed, other than those that control eye movement. Term was first introduced about 25 years ago by Plum and Posner with complete occlusion of the basilar artery. 3

Any catastrophy involving ventral pons can cause this syndrome like massive stroke, traumatic head injury, ruptured aneurysm, pontine infarction after prolonged vertebrobasilar ischaemia, haemorrhage, tumor, central pontine myelinolysis, pontine abscess or postinfective polyneuropathy. As all of the nerve tracts responsible for voluntary movement pass through the ventral pons but fortunately or unfortunately, consciousness are above the level of the ventral pons. 2

Only supportive rehabilitation is the answer. Being an intensivist, it is extremely important to educate staff and to protect patient from any physical or psychological harm (like procedure without adequate analgesia), with upmost understanding that it is an "imprisoned mind buried alive in a dead body’’ (as said for character with paralysis like locked-in syndrome in Thérèse Raquin by Emile Zola - 1868).

References: Click to get articles/abstract

1. The patient's journey: Living with locked-in syndrome - BMJ 2005;331:94-97 (9 July)

2. Plum F, Posner JB. The diagnosis of stupor and coma. Philadelphia: FA Davis, 1982; 377

3. Locked-in syndrome: a catastrophic complication after surgery - British Journal of Anaesthesia, 2004, Vol. 92, No. 2 286-288

2009-09-23T12:34:00.000-07:00

Wednesday September 23, 2009

Q: How do you write the drip of soda bicarbonate in preventing contrast induced nephropathy ?

A: Use 154meq/L of sodium bicarbonate (3 amps) in 1 litre of D5W.

Give 3ml/kg/hr one hr prior to the exam.
Give 1ml/kg/hr during the exam and for 6 hours after the exam.

2009-09-22T22:43:00.000-07:00

Tuesday September 22, 2009
Hydroflouric acid exposure

Case: 23 year male while working in the refinery while disconnecting the hose was exposed to hydrofluoric acid. Patient had inhalation of hydrofluoric acid. Patient had no past medical history. Which of the following should be done first?

a. Albuterol nebulizer with 2.5 mg albuterol
b. Albuterol nebulizer with 10mg albuterol
c. Calcium gluconate nebulizer treatment
d. 10% mucomyst treatment

Answer : C

Calcium gluconate should be used after hydrofluoric acid exposure, and if there are any skin lesions it should be applied there too. Patient should be observed for 24-48 for development of pulmonary edema. Ionized calcium should be monitored very closely, and should be supplemented with intravenous calcium gluconate if low.

Related article: Medical treatment for Hydroflouric acid exposure (pdf)

2009-09-21T10:16:00.000-07:00

Monday September 21, 2009
Passive Leg Raising or Raising HOB to determine volume status

As we are getting more and more tangled with technology, unfortunately we are losing simple bedside maneuvers which were once integral part of physical examination.

CVP (central venous pressure) is a great way to determine volume status but even before central line get place, simple tricks at bedside may give assessment of volume status and may begin management even earlier. If blood pressure improves by just passively raising legs for 2-4 minutes or blood pressure drop by raising head of bed (HOB) to 45 degree, patient is probably hypovolumic.

See references, where these tests have been validated in clinical trials.

References: click to get abstract/article

1. Changes in BP Induced by Passive Leg Raising Predict Response to Fluid Loading in Critically Ill Patients - Chest. 2002;121:1245-1252.)

2. Passive leg raising predicts fluid responsiveness in the critically ill - Critical Care Medicine. 34(5):1402-1407, May 2006

3. Passive leg raising-induced changes in mean radial artery pressure can be used to assess preload dependence - poster from 27th International Symposium on Intensive Care and Emergency Medicine, Brussels, Belgium. 27–30 March 2007, Critical Care 2007, 11(Suppl 2):P307

2009-09-20T06:54:00.000-07:00

Sunday September 20, 2009
Auto-PEEP

Q; What level of extrinsic PEEP should be applied to counter act (intrinsic) auto-PEEP?

A; 75 - 85% of auto-PEEP.Keeping extrinsic PEEP lower than auto-PEEP not only effectively counter acts auto-PEEP but also any ciruclatory depression or lung hyperinflation is unlikely to occur at extrinsic PEEP slightly lower than intrinsic PEEP value.

Read precise review on auto-peep: Auto-positive end-expiratory pressure: Mechanisms and treatment , M.M. MUGHAL, D.A. CULVER, O.A. MINAI, and A.C. ARROLIGA - CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 72 • NUMBER 9 SEPTEMBER 2005

2009-09-19T08:41:00.000-07:00

Saturday September 19, 2009

Q; Patient with C. Diff. Colitis is having no improvement with PO Flagyl. You ordered PO Vancomycin. Pharmacy informed you that PO Vancomycin is not available. What would be your trick of trade here?

A; Actually, IV Vancomycin can be given via oral route. It works just as well, and a lot cheaper. The ordered dose may be diluted in water and given to the patient to drink. Common flavoring syrups may be added to the solution to improve taste.

2009-09-18T17:48:00.000-07:00

Friday September 18, 2009

Q; In which heart valvular condition, Intra Aortic Balloon Pump (IABP)counterpulsation is contra-indicated for anginal symproms?

A; Severe Aortic valvular insufficiency (Aortic Regrurgitation).

It worsen the the diastolic augmentation of IABP and so the magnitude of regurgitation.

2009-09-17T05:54:00.000-07:00

Thursday September 17, 2009

Q: What is the maximum length of guide-wire is recommended to insert (advance) during subclavian or internal jugular venous catheterization?

A: About 18 cm (may be little less in right IJ)

Beside not to loose control of guide-wire, it is appropriate to know the markings on guidewire in CVC kit. Patient height is less reliable in predicting a safe wire length. 18 cm should be considered the upper limit of guidewire introduced during central catheter placement in adults 1.

Related Previous Pearl: Peres Nomogram to calculate appropriate length of central line depth

Reference: click to get abstract

How much guidewire is too much? Direct measurement of the distance from subclavian and internal jugular vein access sites to the superior vena cava-atrial junction during central venous catheter placement - Critical Care Medicine. 28(1):138-142, January 2000

2009-09-16T09:38:00.001-07:00

Wednesday September 16, 2009
Warning: Ceftriaxone (Rocephin®)—Calcium Interaction

The FDA has warning about Ceftriaxone—Calcium interactions due to potential precipitate/crystalline formation in the IV tubing or vasculature when the two agents are combined. These reactions are potentially lethal. This includes all calcium-containing infusions (e.g. Lactated Ringers, Total Parenteral Nutrition).

Data is not available on interactions between ceftriaxone and oral calcium products or intramuscular ceftriaxone and calcium containing products.

Cases of fatal reactions with calcium-ceftriaxone precipitates in the lungs and kidneys have been reported in both term and premature neonates. Some of these cases occurred even when ceftriaxone and the calcium-containing products were administered by different routes at different times. The use of ceftriaxone with calcium products is now contraindicated in all age groups.

Ceftriaxone and Calcium containing solutions should not be administered at different times via different infusion lines or within 48 hours of each other in any patient of any age.

http://www.fda.gov/safety/medwatch

2009-09-15T06:39:00.000-07:00

Tuesday September 15, 2009
Tracheostomy

2009-09-14T10:52:00.000-07:00

Monday September 14, 2009
Malignant Hyperthermia: Agent of choice…Dantrolene

Malignant Hyperthermia is a rare, but potentially lethal musculoskeletal disorder associated with exposure to halogenated anesthetic gases or succinylcholine. Some signs/symptoms include tachycardia, hyperthermia, supraventricular and ventricular arrhythmias, and even cardiac arrest.

The mainstay of treatment is Dantrolene. It is a direct-acting skeletal muscle relaxant that blocks calcium release from intracellular stores in the sarcoplasmic reticulum. Dantrolene is dosed 1mg/kg to a maximum cumulative dose of 10 mg/kg. Infuse over approximately 1 hour. Doses may be repeated until signs of malignant hyperthermia are reversed.

It is highly lipophilic, thus poorly soluble in water. Dantrolene is currently available for intravenous use in vials containing 20mg lyophilized dantrolene sodium added to 3 gm mannitol to improve water solubility. The contents in the vial are to be dissolved in 60 mL water, yielding a final concentration of 0.33 mg/mL. The vials are to be protected from light and should be used within 6 hours once reconstituted. Due to the high irritability, it is recommended that dantrolene be infused into a large vein. Dantrolene peaks in 6 hours, and has a half life of 12 hours. It is metabolized by liver microsomes and are excreted mainly via urine and bile.

Reference:

Krause T, et al. Anaesthesia 2004;59:364
Rosenbaum HK, et al. Anesthesiology Clin N Am 2002;20:623

2009-09-13T14:54:00.000-07:00

Sunday September 13, 2009

Q: What is the dosing adjustment of Primaxin (Imipenem/Cilastatin) in Hemdialysis and CVVHD (CRRT)?

Answer: Primaxin (Imipenem/Cilastatin) need to be adjusted in Hemodialysis and CVVHD (CRRT) patients.

DOSING IN HEMODIALYSIS:
250 mg IV q12h with 250 mg post dialysis on dialysis day.

DOSING IN HEMOFILTRATION:
1. CVVHD with dialysis flow rate less than 1.5L/hr: 500 mg IV q12h;
2. CVVHD with dialysis flow rate 2L/hr: 500 mg IV q 8h.

2009-09-12T15:51:00.000-07:00

Saturday September 12, 2009

Q: Kayexalate (Sodium Polystyrene) is a cation exchange resin that enhance potassium clearance across the GI tract. What is the exchange ratio of Na and K?

Answer: For each mEq of potassium removed, 2-3 mEq of sodium is added. So it is important to watch for hypernatremia.

Lasix can be given to enhance removing both sodium and potassium via diuresis.

2009-09-11T10:14:00.001-07:00

Friday September 11, 2009 (pediatric pearl)
Neuron Specific Enolase (NSE) and S-100 as markers of outcomes in pediatric cardiac arrest

NSE is a dimeric glycoprotein found in neurons and neuroectodermal cells. S-100B is a calcium binding protein found primarily in the astroglial and Schwann cells. At nanomolar concentrations it promotes astroglial proliferation and neuronal differentiation, but at micromolar concentrations it induces astroglial and neuronal cell death.

The timing, intensity, and duration of serum NSE and S-100B biomarker concentration patterns are associated with neurologic and survival outcomes following in or out-of-hospital cardiac arrest pediatric cardiac arrest.

For NSE a cutoff level of 51 µg/L at 48 hrs resulted in a sensitivity of only 50% for poor outcome while achieving a specificity of 100%.With these derived cutoffs the posttest probability of NSE for poor outcome is 99%, which is increased from the pretest probability of poor outcome of 54%. The addition of NSE testing may allow clinicians to increase their prediction of poor outcome in this population.

Reference: Click to get abstract

Neuron-specific enolase and S-100B are associated with neurologic outcome after pediatric cardiac arrest - Pediatric Critical Care Medicine 10(4), July 2009, pp 479-490

2009-09-10T09:19:00.000-07:00

Thursday September 10, 2009
Propofol Abuse Growing Problem for Anesthesiologists

"One addict fell asleep at his desk so often that his lolling forehead became a perpetual bruise. Another was so desperate for a fix that he started trolling through sharps bins for discarded needles with traces of drug to inject.

The addicts were two doctors, an anesthesiologist and a family physician. Their drug of choice: propofol.

If that’s surprising, consider this: One in five academic anesthesiology training programs reported at least one case of abuse by physicians or other healthcare workers over the past decade, new research shows. The incidence of propofol abuse has risen fivefold over the last 10 years"

- CLINICAL ANESTHESIOLOGY - ISSUE: MAY 2007 VOLUME: 33:05 -

www.anesthesiologynews.com/

2009-09-09T11:33:00.000-07:00

Wednesday September 9, 2009

Case: A patient requires anticoagulation for PE. The patient has a history of HIT (Heparin Induced Thrombocytopenia), an allergy to Argatroban (per documentation), with a creatinine clearance less than 30ml/min. What is the best available agent for anticoagulation?

Answer: Heparin and LMWHs should not be used due to the history of HIT. The Argatroban allergy is questionable, may be considered, but would rather not take the chance. Fondaparinux (Arixtra) is contraindicated in patients with a creatinine clearance less than 30 ml/min.

Bivalirudin (Angiomax) would be the best available choice, even though it’s not FDA approved for HIT. Bivalirudin is a specific and reversible direct thrombin inhibitor, binding to circulating and clot-bound thrombin. The dose range is 0.05 – 0.15 mg/kg/hr , titrating to maintain aPTT 1.5 – 3 x baseline. It is eliminated renally and via enzymatic processes. An initial dose adjustment should be made if CrCl less than 50 ml/hr to 0.05 mg/kg/hr. Bivalirudin peaks in 1-2 hours, with a half life of 10-24 minutes. Unlike heparin, there are no reversal agents available. The advantage of Bivalirudin is that it may be used in multiorgan failure patients, and those on CVVHD.

2009-09-08T05:58:00.000-07:00

Tuesday September 8, 2009

Q: Flumazenil can be effective in overdose of which drugs beside benzodiazepines?

Answer: Flumazenil is traditionally use as an antidote in patients with benzodiazepines overdose but it has been found to be effective in overdoses of non-benzodiazepine sleep enhancers, namely zolpidem (ambien) and zaleplon (sonata).

Flumazenil reverses the effects of benzodiazepines by competitive inhibition at the benzodiazepine binding site on the GABA-a receptor.

Also, it has also been used in hepatic encephalopathy.

2009-09-07T09:14:00.000-07:00

Monday September 7, 2009

Scenario: 54 year old female is admitted to ICU with pneumonia. Patient is found to be moderately anemic. To be complete in evaluation and to rule out possible GI bleed, you asked resident to do rectal exam for guaiac stool. Resident performed Guaiac stool via rectal exam with latex free glove and surgilube (surgical lubricant). 10 minutes later patient coded with severe anaphylactic reaction. What could be a reason assuming no new medication administered?

Answer: Possible allergic reaction to Chlorhexidine

Surgilubes (surgical lubricants aka KY Jelly) are usually considered innocuous compound but it contains chlorhexidine. Patients with severe allergy to chlorhexidine may react badly particularly if it enters blood circulation as possible with rectal exam.

References: click to get abstract

1. A Case of Anaphylaxis to Chlorhexidine during Digital Rectal Examination - J Korean Med Sci. 2008 June; 23(3): 526–528.

2. Anaphylaxis to the chlorhexidine component of Instillagel®: a case series - Advance Access published online on November 5, 2008, - British Journal of Anaesthesia

3. Chlorhexidine anaphylaxis in Auckland - Br. J. Anaesth., May 1, 2009; 102(5): 722 - 723.

4. Chlorhexidine anaphylaxis: case report and review of the literature - Contact Dermatitis. 2004 Mar;50(3):113-6

2009-09-06T21:36:00.000-07:00

Sunday September 6, 2009
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

Treating Extravasation Injuries - extravasation.org
The use of phentolamine in the prevention of dopamine-induced tissue extravasation - J Crit Care 1998 Mar;13(1):13-20

2009-09-05T19:25:00.000-07:00

Saturday September 5, 2009
Nosocomial Pneumonia Risk and Stress Ulcer Prophylaxis - Pantoprazole vs Ranitidine

Background: Stress ulcer prophylaxis (SUP) using ranitidine, a histamine H2 receptor antagonist, has been associated with an increased risk of ventilator-associated pneumonia. The proton pump inhibitor (PPI) pantoprazole is also commonly used for SUP. PPI use has been linked to an increased risk of community-acquired pneumonia. The objective of this study was to determine whether SUP with pantoprazole increases pneumonia risk compared with ranitidine in critically ill patients.

Methods: The cardiothoracic surgery database at our institution was used to identify retrospectively all patients who had received SUP with pantoprazole or ranitidine, without crossover between agents. From January 1, 2004, to March 31, 2007, 887 patients were identified, with 53 patients excluded (pantoprazole, 30 patients; ranitidine, 23 patients). Our analysis compared the incidence of nosocomial pneumonia in 377 patients who received pantoprazole with 457 patients who received ranitidine.

Results:

Nosocomial pneumonia developed in 35 of the 377 patients (9.3%) who received pantoprazole, compared with 7 of the 457 patients (1.5%) who received ranitidine
Twenty-three covariates were used to estimate the probability of receiving pantoprazole as measured by propensity score (C-index, 0.77). Using this score, pantoprazole and ranitidine patients were stratified according to their probability of receiving pantoprazole. After propensity adjusted, multivariable logistic regression, pantoprazole treatment was found to be an independent risk factor for nosocomial pneumonia (p = 0.034).
Conclusion: The use of pantoprazole for SUP was associated with a higher risk of nosocomial pneumonia compared with ranitidine. This relationship warrants further study in a randomized controlled trial.

Reference

Nosocomial Pneumonia Risk and Stress Ulcer Prophylaxis - A Comparison of Pantoprazole vs Ranitidine in Cardiothoracic Surgery Patients - CHEST August 2009 vol. 136 no. 2 440-447

2009-09-04T02:52:00.000-07:00

Friday September 4, 2009 (pediatric pearl)
Poor Nutritional status in children with hypoplastic left heart syndrome

Infants with hypoplastic left heart syndrome (HLHS) experience a high incidence of growth failure in the postoperative period following stage I palliation. The growth failure in these infants may be related to insufficient nutritional intake, gastrointestinal malabsorption, or high energy expenditure. Clinicians are often reluctant to initiate and advance early enteral feedings in this population because of the increased risk of necrotizing enterocolitis and the high incidence of feeding intolerance and gastroesophageal reflux diseaseThe risk of developing necrotizing enterocolitis in infants with HLHS is significantly higher than in neonates with other forms of congenital heart disease (CHD).

This may be related in part to compromised diastolic flow in the mesenteric circulation in infants undergoing Stage 1 palliation with either a Blalock Taussig shunt or an right ventricle to pulmonary artery conduit. Some studies have also found increased permeability of gut mucosal barrier in children with CHD undergoing cardiopulmonary bypass.

The use of an enteral feeding algorithm (Pediatr Crit Care Med 2009; 10:460–466) is a safe and effective means of initiating and advancing enteral nutrition in infants with HLHS following stage I palliation.

2009-09-03T07:40:00.000-07:00

Thursday September 3, 2009
Finally relief may be coming from Coumadin

In a study by Connolly they studied the effect of Dabigatran versus Warfarin in Patients with Atrial Fibrillation. Dabigatran is a new oral direct thrombin inhibitor.

In this noninferiority trial, they randomly assigned 18,113 patients who had atrial fibrillation and a risk of stroke to receive, in a blinded fashion, fixed doses of dabigatran — 110 mg or 150 mg twice daily — or, in an unblinded fashion, adjusted-dose warfarin. The median duration of the follow-up period was 2.0 years. The primary outcome was stroke or systemic embolism.

Results:

Rates of the primary outcome were 1.69% per year in the warfarin group, as compared with 1.53% per year in the group that received 110 mg of dabigatran and 1.11% per year in the group that received 150 mg of dabigatran.
The rate of hemorrhagic stroke was 0.38% per year in the warfarin group, as compared with 0.12% per year with 110 mg of dabigatran and 0.10% per year with 150 mg of dabigatran.
The rate of major bleeding was 3.36% per year in the warfarin group, as compared with 2.71% per year in the group receiving 110 mg of dabigatran (P=0.003) and 3.11% per year in the group receiving 150 mg of dabigatran (P=0.31).
The mortality rate was 4.13% per year in the warfarin group, as compared with 3.75% per year with 110 mg of dabigatran (P=0.13) and 3.64% per year with 150 mg of dabigatran (P=0.051).

Conclusions: In patients with atrial fibrillation, dabigatran given at a dose of 110 mg was associated with rates of stroke and systemic embolism that were similar to those associated with warfarin, as well as lower rates of major hemorrhage.

Dabigatran administered at a dose of 150 mg, as compared with warfarin, was associated with lower rates of stroke and systemic embolism but similar rates of major hemorrhage.

Editors note: Unlike Warfarin, Dabigatran acts within hours after ingestion and does not require monitoring

Connolly SJ, Esekowitz MD, Yusuf S, et al. Dabigatran versus Warfarin in Patients with Atrial Fibrillation. N Eng J Med 2009; Published at www.nejm.org August 30, 2009

2009-09-02T03:10:00.000-07:00

Wednesday September 2, 2009
Role of Procalcitonin as prognostic factors in COPD exacerbation

Rammaert et al studied the effects of Procalcitonin as a prognostic factor in severe acute exacerbation of chronic obstructive pulmonary disease. A prospective observational cohort study was conducted of 116 consecutive patients with severe acute exacerbation of COPD requiring intubation and mechanical ventilation with their mean age being 67 years and mean simplified physiological score was 43.

Results: Sixty-five per cent of patients had chronic respiratory insufficiency.

Logistic organ dysfunction score (hazard ratio (95% CI) = 1.19 (1.03–1.37), P = 0.013), rapidly fatal underlying disease (3.33 (1.40–7.87), P = 0.003) and procalcitonin level (1.01 (1–1.03), P = 0.018) were independently associated with increased risk for ICU mortality.
Non-invasive mechanical ventilation use before intubation was independently associated with reduced risk for ICU mortality (0.34 (0.14–0.84), P = 0.020).

Conclusions:

In patients with severe acute exacerbation of COPD requiring intubation and mechanical ventilation, logistic organ dysfunction score, rapidly fatal underlying disease and procalcitonin are independently associated with increased risk for ICU mortality.

Non-invasive mechanical ventilation use before intubation was independently associated with reduced risk for ICU mortality.

Reference:

Rammaert B, Verdier N, Cavestri B, Nseir S. Procalcitonin as a prognostic factor in severe acute exacerbation of chronic obstructive pulmonary disease. Respirology 2009; Published online July 30 2009.

2009-09-01T05:08:00.000-07:00

Tuesday September 1, 2009
Is Plavix going to be History??

Recent study by wallentin et al looked at the Ticagrelor (Brilinta®) versus Clopidogrel (Plavix) in patients with Acute Coronary Syndromes.

Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12 that has a more rapid onset and more pronounced platelet inhibition than clopidogrel.

They studied 18624 patients in double blind randomized trial ticagrelor (180-mg loading dose, 90 mg twice daily thereafter) and clopidogrel (300-to-600-mg loading dose, 75 mg daily thereafter) in patients admitted to the hospital with an acute coronary syndrome, with or without ST-segment elevation.

Results: At 12 months

a composite of death from vascular causes, myocardial infarction, or stroke — had occurred in 9.8% of patients receiving ticagrelor as compared with 11.7% of those receiving clopidogrel.
Secondary end point: Significant differences in the rates of other composite end points, as well as myocardial infarction alone (5.8% in the ticagrelor group vs. 6.9% in the clopidogrel group, P=0.005).
Death from vascular causes (4.0% vs. 5.1%, P=0.001) but not stroke alone (1.5% vs. 1.3%, P=0.22).
Death from any cause was also reduced with ticagrelor (4.5%, vs. 5.9% with clopidogre).
No significant difference in the rates of major bleeding was found between the ticagrelor and clopidogrel groups (11.6% and 11.2%, respectively; P=0.43), but ticagrelor was associated with a higher rate of major bleeding not related to coronary-artery bypass grafting (4.5% vs. 3.8%, P=0.03), including more instances of fatal intracranial bleeding and fewer of fatal bleeding of other types.

Conclusions: In patients who have an acute coronary syndrome with or without ST-segment elevation, treatment with ticagrelor as compared with clopidogrel significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in the rate of overall major bleeding but with an increase in the rate of non–procedure-related bleeding.

Reference:

Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus Clopidogrel in patients with Acute Coronary Syndromes. N Engl J Med 2009; www.nejm.org August 30, 2009