icuroom.net June 2010 Archive

2010-06-30T11:18:00.000-07:00

Wednesday June 30, 2010

Q: 52 year old male is admitted with unstable angina and going to 'cath. lab' for probable coronary stenting. Cardiologist called you to replace Plavix (Clopidogrel) from protocol to Effient (prasugrel). What would be the replaced dose?

Answer: Loading dose of 60 mg followed by 10 mg per day

Prasugrel (Effient) is a new platelet inhibitor (like Plavix) developed for use in acute coronary syndromes planned for percutaneous coronary intervention (PCI).
It has been said (or claimed) that compared to clopidogrel, 'prasugrel' inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel.

2010-06-29T00:57:00.000-07:00

Tuesday June 29, 2010
Atrial Fibrillation (Medications vs Ablation - 2 parts)

Part-1

Part-2

2010-06-28T07:36:00.000-07:00

Monday June 28, 2010
Picture Diagnosis
(Stages of Sarcoidosis)

Answer: Bilateral hilar enlargement (lymphadenopathy) with clear lung parenchyma. Probable Diagnosis is Sarcoidosis. Frequently, sarcoidosis is diagnosed because of a chest x-ray, taken routinely or for some other reason. A staging system is used to classify chest x-rays taken to detect sarcoidosis.
Stage 0 - normal chest x-ray.

Stage 1 - chest x-ray with enlarged lymph nodes but otherwise clear lungs.

Stage 2 - chest x-ray with enlarged lymph nodes plus infiltrates in the lungs.

Stage 3 - chest x-ray that shows the infiltrates are present but the lymph nodes are no longer seen.

Stage 4 - shows scar tissue in the lung tissue.

X-ray stages do not tell the severity of the disease. However, in general the higher the stage of the x-ray, the worse the person’s symptoms and lung function (PFTs). But there is a lot of individual variation, and persons at Stages 0 through 3 may or may not have symptoms.

2010-06-27T03:46:00.000-07:00

Sunday June 27, 2010
Tracheal temperature as a measurement of body temperature?

Objective: When treating patients with cardiac arrest with mild therapeutic hypothermia, a reliable and easy-to-use temperature probe is desirable. This study was conducted to investigate the accuracy and safety of tracheal temperature as a measurement of body temperature. It was an observational cohort study in emergency department of a tertiary care university hospital.

Patients: Patients successfully resuscitated from cardiac arrest intended for mild hypothermia therapy.

Interventions: Intubation was performed with a newly developed endotracheal tube that contains a temperature sensor inside the cuff surface. During the cooling, mild hypothermia maintenance, and rewarming phases, the temperature was recorded minute by minute. These data were compared with the temperature assessed by esophageal and blood temperature probes. Thereafter, tracheoscopy was performed to evaluate the condition of the tracheal mucosa.

Results: Approximately 2000 measurements per temperature sensor per patient were recorded in 21 patients.

The mean bias between the blood temperature and the tracheal temperature was -0.16[degrees]C (limits of agreement: -0.36[degrees]C to 0.04[degrees]C).
The mean bias between the esophageal and tracheal temperatures was -0.22[degrees]C (limits of agreement: -0.49[degrees]C to 0.07[degrees]C).
Agreement between temperature probes investigated by the Bland-Altman method showed a mean bias of less than -1/4[degrees]C, and time lags assessed graphically by hysteresis plots were negligible.
No clinically relevant injury to the tracheal mucosa was detected.

Conclusion: Temperature monitoring at the cuff surface of an endotracheal tube is safe and provides accurate and reliable data in all phases of therapeutically induced mild hypothermia after cardiac arrest.

Temperature monitored on the cuff surface of an endotracheal tube reflects body temperature - Critical Care Medicine. 38(7):1569-1573, July 2010.

2010-06-26T11:48:00.000-07:00

Saturday June 26, 2010
Nomogram for Enoxaparin Treatment

Anti Factor Xa level: less than 0.35 u/ml
Hold Next Dose?: No
Dose Change?: increase by 25%
Repeat Anti Factor Xa level?: 4 hours post next dose

Anti Factor Xa level: 0.35 to 0.69 u/ml
Hold Next Dose?: No
Dose Change?: increase by 15%
Repeat Anti Factor Xa level?: 4 hours post next dose

Anti Factor Xa level: 0.7 to 1.1 u/ml
Hold Next Dose?: No
Dose Change?: 0
Repeat Anti Factor Xa level?: 1 x per week at 4 hours post dose

Anti Factor Xa level: 1.1 to 1.5 u/ml
Hold Next Dose?: No
Dose Change?: decrease by 20%
Repeat Anti Factor Xa level?: 4 hours post next dose

Anti Factor Xa level: 1.6 to 2.0 u/ml
Hold next dose?: No
Dose Change?: decrease by 30%
Repeat Anti Factor Xa level?: 4 hours post next dose

Anti Factor Xa level: more than 2.0 u/ml
For these patients, all further doses should be held, and the anti factor Xa level measured q 12 hours until the anti factor Xa level is less than 0.5 u/ml. Enoxaparin can then be restarted at a dose 40% less than was originally prescribed.

The above nomogram assumes that there is no bleeding.

2010-06-25T20:37:00.000-07:00

Friday June 25, 2010

Q: Is Digoxin and Digitoxin is the same medicine?

Answer: NO

Digoxin, also known as digitalis, is a purified cardiac glycoside extracted from the plant, Digitalis lanata. It is eliminated via kidney.

Digitoxin has similar structure and effects as digoxin. Unlike digoxin it is eliminated via the liver.

2010-06-24T01:44:00.000-07:00

Thursday June 24, 2010
On Prograf 'Trough' level

Prograf (FK 506,Tacrolimus) is a commonly used medicine in transplant patients and its level should be monitored closely. It is important to draw prograf level (preferably written as order) just before dose of next medication (lowest or "trough" blood level). Dosage should be adjusted based on the trough levels of medication. Normal trough level is 5-15 ng/ml.

Important interactions to be aware of in these potentially immunosupressed patients are with antifungals, especially of the azole class (fluconazole, posaconazole). They increase drug levels by competing for degradative enzymes. Diltiazem can also dramatically increase tacrolimus concentrations and result in tacrolimus toxicity. Other drug interactions are common too.

Prograf toxicity may cause blurred vision, liver and renal failure, tremors, hyperkalemia, hypomagnesemia, and neurological problems such as seizure, encephalopathy, cerebral edema, confusion etc.

2010-06-23T05:46:00.000-07:00

Wednesday June 23, 2010
Regarding Ferumoxytol (Feraheme)

Ferumoxytol is a newly approved intravenous iron preparation for treatment of the anemia particularly chronic kidney disease (CKD). Because little free iron is present in the preparation, doses of 510 mg have been administered safely in as little as 20 seconds. The most common adverse events with ferumoxytol are at injection site (bruising, pain, swelling, erythema).

Feraheme injection is an aqueous colloidal product that is formulated with mannitol. It is a black to reddish brown liquid, and is provided in single use vials containing 510 mg of elemental iron.

Intravenous ferumoxytol can be safely and rapidly administered, and is more effective than oral iron therapy in increasing hemoglobin levels. The recommended dose of Feraheme is an initial 510 mg IV injection followed by a second 510 mg intravenous injection 3 to 8 days later.

2010-06-22T06:38:00.000-07:00

Tuesday June 22, 2010

Q: Why it is recommended to perform head imaging (CT or MRI )in patients with severe hypernatremia OR what central complications may occur secondary to severe hypernatremia?

Answer: Head CT scan or MRI is suggested in all patients with severe hypernatremia as traction on dural bridging veins and sinuses caused by movement of water from the brain and brain shrinkage can lead to intracranial hemorrhage, most often in the subdural space. Also, hemoconcentration from total body water loss may lead to dural sinus thrombosis. On other note - imaging studies may reveal a central cause for hypernatremia.

2010-06-21T03:18:00.000-07:00

Monday June 21, 2010
Picture diagnosis

Scenario: As you are intubating a patient you visualize the following picture.

Answer: Vocal Fold Polyp

A vocal fold polyp is a fluid-filled lesion that may occur unilaterally or bilaterally. They may vary in size and may be either "sessile" or pedunculated". They are most commonly thought to be caused by vocal abuse or trauma, cigarette smoking, or vocal fold hemorrhage. Vocal characteristics often include hoarseness, diplophonia (audible perception of two distinct pitches), and stridor (noisy breathing). A vocal fold polyp usually require surgical removal

2010-06-20T02:35:00.000-07:00

Sunday June 20, 2010
Vernakalant - The AVRO Trial

Summary: A Phase III Prospective Randomized Double-Blind Active Controlled, Multicenter Superiority Study of Vernakalant Injection versus Intravenous Amiodarone in Subjects with Recent Onset Atrial Fibrillation. The AVRO Trial.

Study Design: The investigators randomized patients (n= 254) with recent onset sustained (3 -48 hours) atrial fibrillation in a double blind, active controlled, double blind manner to two serial doses of vernakalant (3 mg/kg followed by an additional 2 mg/kg dose if the patient remained in atrial fibrillation) or serial doses of amiodarone (5 mg/kg followed by a 50 mg dose if the patient remained in atrial fibrillation) . The primary endpoint was proportion of patients with conversion to sinus rhythm in 90 minutes. and secondary endpoints included: Time to conversion, proportion of patients without symptoms due to atrial fibrillation at 90 minutes, and change in quality of life.

Results and Conclusions

Vernakalant was significantly more effective than amiodarone for converting atrial fibrillation to sinus rhythm within 90 minutes (vernakalant: 51.7% vs. amiodaone: 5.2%).
Vernakalant was also more effective than amiodaone for eliminating symptoms due to atrial fibrillation within 90 minutes (vernakalant: 53.4 % vs. amiodarone: 32.8%).
Vernakalant was safe and generally well tolerated although patients complained of transient symptoms such as dysgeusia (6.9%), cough (3.4%) and nausea (2.6%). One patient developed nonsustained V.Tach. but no episodes of Torsades de Pointes or sustained ventricular arrhythmias were observed.

* Presented by Dr A John Camm (St George's University, London, UK) during the late-breaking clinical-trials session at the Heart Rhythm Society 2010 Scientific Sessions.

* It is still not approved in the US.

A Phase III Superiority Study of Vernakalant vs Amiodarone in Subjects With Recent Onset Atrial Fibrillation (AVRO) - clinicaltrials.gov

2010-06-19T09:35:00.000-07:00

Saturday June 19, 2010

Q: What is singers' emboli?

Answer: Helium gas emboli in singers

An interesting cause of "Helium emboli" can occur from inhalation of pressurized helium. Some singers intentionally inhale high-pressure helium for entertainment or to produce a change in their voice. Inhaled high-pressure gas can produce high transpulmonary pressure sufficient to rupture alveoli and surrounding blood vessels, introducing gas into the pulmonary veins and allowing systemic embolization through the left heart; particularly in an upright person!

But more common cause of "helium emboli" is from IABP. Intra Aortic Balloon Pump (IABP) Counterpulsation utilizes helium gas to inflate its balloon. As Helium is a low density as well as an inert gas, in case of balloon rupture it is easily absorbed into the bloodstream. But fairly well numbered incidents of "Helium emboli" after balloon rupture have been described in literature.

Major clinical sign of helium embolus is neurological deficit associated with other findings of balloon rupture as blood in the tubing. Treatment is hyperbaric oxygen.

1. Cerebral and coronary gas embolism from the inhalation of pressurized helium Critical Care Medicine: May 2002 - Volume 30 - Issue 5 - pp 1156-1157

2. Cerebral Gas Embolism Resulting From Inhalation of Pressurized Helium - Annals of Emergency Medicine Volume 28, Issue 3, Pages 363-366, September 1996

2010-06-18T08:05:00.000-07:00

Friday June 18, 2010
Differences Between Venoarterial and Venovenous Extracorporeal Membrane Oxygenation

Venoarterial ECMO

Higher PaO2 is achieved
Lower perfusion rates are needed.
Bypasses pulmonary circulation
Decreases pulmonary artery pressures
Provides cardiac support to assist systemic circulation
Requires arterial cannulation

Venovenous ECMO

Lower PaO2 is achieved.
Higher perfusion rates are needed.
Maintains pulmonary blood flow
Elevates mixed venous PO2
Does not provide cardiac support to assist systemic circulation
Requires only venous cannulation

2010-06-17T02:06:00.000-07:00

Thursday June 17, 2010
Therapeutic ranges anti-Xa level for adequate anticoagulation

This is important to note that therapeutic ranges anti-Xa level are different with different anticoagulation.

Heparin: 0.3-0.7 units/mL

LMWH:

0.4-1.1 units/mL for SQ q 12 hr dosing.
For once daily LMWH dosing, the therapeutic range is approximately 1-2 units/mL.

Prophylaxis of DVT: There is no defined target range for prophylaxis of DVT. When anti-Xa levels are measured, the values are lower 0.45.

2010-06-16T02:18:00.000-07:00

Wednesday June 16, 2010
Pulmonary Artery Occlusion Pressure and PEEP

There are 3 ways to correct/manage pulmonary artery occlusion pressure or pulmonary capillary wedge pressure (PCWP) in patients with PEEP (positive end-expiratory pressure) over 10.

1. Follow the trend of PCWP co-relating with other clinical data and interventions.

2. Corrected PCWP = Measured PCWP - .5 x (PEEP/1.36)

e.g. If measured PCWP is 20 and applied PEEP is 16:

Corrected PCWP = 20 - .5 (16/1.36) = 14.12

3. Corrected PCWP = measured PCWP - esophageal pressure.Temporary discontinuation of PEEP to measure PCWP is not safe and should be avoided.

References: click to get abstract/article

1. Influence of positive end-expiratory pressure on left ventricular performance - NEJM, Feb. 1981, Volume 304:387-392

2. Monitoring Pulmonary Artery Pressure - Crit Care Nurse 2004 Jun;24(3):67-70

3. Swan-Ganz Catheterization - online emedicine.com

2010-06-15T00:13:00.000-07:00

Tuesday June 15, 2010
Pulmonary Embolism - needs faster anticoagulation

Background: Acute pulmonary embolism (PE) may be rapidly fatal if not diagnosed and treated. IV heparin reduces mortality and recurrence of PE, but the relationship between survival and timing of anticoagulation has not been extensively studied.

Methods: We studied 400 consecutive patients in the ED diagnosed with acute PE by CT scan angiography and treated in the hospital with IV unfractionated heparin from 2002 to 2005. Patients received heparin either in the ED or after admission. Time from ED arrival to therapeutic activated partial thromboplastin time (aPTT) was calculated. Outcomes included in-hospital and 30-day mortality, hospital and ICU lengths of stay, hemorrhagic events on heparin, and recurrent venous thromboembolism within 90 days.

Results:

In-hospital and 30-day mortality rates were 3.0% and 7.7%, respectively.
Patients who received heparin in the ED had lower in-hospital (1.4% vs 6.7%; P = .009) and 30-day (4.4% vs 15.3%; P less than .001) mortality rates as compared with patients given heparin after admission.
Patients who achieved a therapeutic aPTT within 24 h had lower in-hospital (1.5% vs 5.6%; P = .093) and 30-day (5.6% vs 14.8%; P = .037) mortality rates as compared with patients who achieved a therapeutic aPTT after 24 h.
In multiple logistic regression models, receiving heparin in the ED remained predictive of reduced mortality, and ICU admission remained predictive of increased mortality.
Conclusions: We report an association between early anticoagulation and reduced mortality for patients with acute PE. We advocate further study with regard to comorbidities to assess the usefulness of modifications to hospital protocols.

Early Anticoagulation Is Associated With Reduced Mortality for Acute Pulmonary Embolism - CHEST June 2010 vol. 137 no. 6 1382-1390

2010-06-14T03:56:00.000-07:00

Monday June 14, 2010
Holiday Heart Syndome

Holiday Heart Syndome was originally defined as "arrhythmias of the heart, sometimes apparent after a vacation or weekend away from work, following excessive alcohol consumption; usually transient". Same has been reported with recreational use of marijuana. The most common rhythm disorder is atrial fibrillation, which usually converts to normal sinus rhythm within 24 hours. It occurs in patients without structural heart disease and its clinical course is usually benign. Even modest alcohol intake may trigger paroxysmal atrial fibrillation.

Most patients with no evidence of structural heart disease can be discharged without further treatment once arrhythmia has stabilized with advise against the excessive use of alcohol. Patients with sustained tachyarrhythmia require treatment if the ventricular rate is excessive. Patients with structural heart disease needs further workup.

2010-06-13T06:58:00.000-07:00

Sunday June 13, 2010
Effect of statin therapy on reperfusion arrhythmia - Interesting study

Background In animal models, pretreatment with statin can prevent reperfusion arrhythmia. In the observational study, we investigated whether pretreatment with statin may prevent reperfusion arrhythmia in patients who underwent primary coronary intervention for acute myocardial infarction (AMI).

Method and results A total of 226 consecutive patients who underwent successful primary angioplasty for a first AMI were studied. Reperfusion arrhythmias were defined as all arrhythmias that occurred within 2 h after successful primary angioplasty. The reperfusion arrhythmia was found in 130 of 226 patients. There were no significant differences in clinical characteristics between the patients with and without statin pretreatment.

The 41 patients receiving statin treatment before admission had lower incidence of the reperfusion arrhythmia than those without it (19.5% and 65.9%)
Multivariable logistic regression analysis revealed that absence of statin pre-treatment was a significant predictor of the reperfusion arrhythmia along with absence of pre-infarction angina and inferior AMI

Conclusion Pre-treatment with statin could reduce the reperfusion arrhythmias after acute myocardial infarction in human.

Effect of statin therapy on reperfusion arrhythmia in patients who underwent successful primary angioplasty - Clinical Research in Cardiology, Volume 97, Number 3 / March, 2008, 147-151

2010-06-12T00:53:00.000-07:00

Saturday June 12, 2010
Oxygen toxicity!

Oxygen is essential to life but can turn into a poison too. Most molecular oxygen used by mitochondria is metabolically reduced completely to water during normal cellular respiration, but a certain quantity of partially reduced, reactive oxygen metabolites is also generated. Chief among these toxic metabolites are superoxide anion, hydrogen peroxide and reactive hydroxyl radicals. Of these, the last are believed to be the most toxic.

According to literature available - On 100% oxygen breathing

After 6 hours - decreased tracheal mucus velocity is detectable
After 12 hours - signs of tracheobronchitis appear
Between 24 - 30 hours - abnormalities in gas exchange are detectable
At 72 - 96 hours - edema can be documented
After 96 hours - fibrosis may began

Jackson RM. Oxygen therapy and toxicity. In: Ayres SM, Grenvik A, Holbrook PR, Shoemaker WC, eds. Textbook of Critical Care. 3rd ed. 784-789

2010-06-11T08:23:00.000-07:00

Friday June 11, 2010
Dopamine or NE?

Background: Both dopamine and norepinephrine are recommended as first-line vasopressor agents in the treatment of shock. There is a continuing controversy about whether one agent is superior to the other.

Methods In this multicenter, randomized trial, we assigned patients with shock to receive either dopamine or norepinephrine as first-line vasopressor therapy to restore and maintain blood pressure. When blood pressure could not be maintained with a dose of 20 µg per kilogram of body weight per minute for dopamine or a dose of 0.19 µg per kilogram per minute for norepinephrine, open-label norepinephrine, epinephrine, or vasopressin could be added.

The primary outcome: rate of death at 28 days after randomization;
Secondary end points: number of days without need for organ support and the occurrence of adverse events.

Results The trial included 1679 patients, of whom 858 were assigned to dopamine and 821 to norepinephrine. The baseline characteristics of the groups were similar.
There was no significant between-group difference in the rate of death at 28 days (52.5% in the dopamine group and 48.5% in the norepinephrine group; P=0.10).
There were more arrhythmic events among the patients treated with dopamine than among those treated with norepinephrine (207 events [24.1%] vs. 102 events [12.4%], P less than 0.001).
A subgroup analysis showed that dopamine, as compared with norepinephrine, was associated with an increased rate of death at 28 days among the 280 patients with cardiogenic shock but not among the 1044 patients with septic shock or the 263 with hypovolemic shock
Conclusions Although there was no significant difference in the rate of death between patients with shock who were treated with dopamine as the first-line vasopressor agent and those who were treated with norepinephrine, the use of dopamine was associated with a greater number of adverse events.

Comparison of Dopamine and Norepinephrine in the Treatment of Shock - Volume 362:779-789, Number 9, March 4 2010

2010-06-10T06:15:00.000-07:00

Thursday June 10, 2010
A note on Amiodarone vasodilatory property

One often less know property of Amiodarone, a class III antiarrhythmic agent, is its potent coronary as well as veno vasodilatory property. Amiodarone acts as a venodilator through the cyclooxygenase pathway, activation of nitric oxide synthase, blockade of -adrenergic mechanismsn and cyclooxygenase-dependent relaxing endothelial factors. Amiodarone hasalso shown in laboratory the calcium channel blocking effects. Due to its multiple effects amiodarone therapy has shown beneficial effect in heart failure.

On side note - Hypotension from IV amiodarone (particularly bolus) is also contributed due to its solubilized vehicle called polysorbate 80 which may have histamine releasing effect.

2010-06-09T00:10:00.000-07:00

Wednesday June 9, 2010
Collection of Lactic acid and Tourniquet - bedside tip

Monitoring of Lactic acid level is helpful in both identifying potentially serious ill patients as well as identifying in the ICU patients with high morbidity and mortality. Elevated lactate levels may be related to sampling error as a result of recent patient activity, tourniquet use, or delayed sample processing.

When a patient arrives to an ED or ICU and that patient is hypotensive (BP less than or equal to 90 systolic), the nursing staff often starts an IV and if possible draws the patient's initial blood tests off that first IV site. This initial work up by the nursing staff takes 15 -20 minutes before a physician may see the patient.

It is recommended to draw lactic acid without a tourniquet or immediately after applying the tourniquet. If the tourniquet is applied for an extended time, remove the tourniquet and let the blood circulate two minutes prior to retrying the draw. Collect specimen in gray top tube. Invert specimen container gently to mix. Transport on ice. Specimen must be delivered to Chemical Pathology Laboratory within 15 minutes of collection.

2010-06-08T05:48:00.000-07:00

Tuesday June 8, 2010
Pharmacy

Q: Tell few off-label (or experimental) uses of Metformin?

Answer:

Prediabetes
Polycystic ovary syndrome (PCOS)
Non-alcoholic fatty liver disease (NAFLD)
Premature puberty
Gestational diabetes (?)

Prophylactically against pancreatic cancer

2010-06-07T02:57:00.000-07:00

Monday June 7, 2010

Picture Diagnosis

Answer: Septic pulmonary embolism (SPE)

Note following features

Round or wedge-shaped multiple peripheral opacities
Usually measure approximately 1-3 cm in diameter,
Frequently cavitated
Well-defined or poorly defined margins
Findings on CXR tend to be nonspecific, CT may yield helpful clues that may suggest the diagnosis of SPE. Parenchymal lesions related to SPE are usually multiple and nodular with a peripheral distribution and a tendency for cavitation. “Feeding vessel” sign (a vessel leading to a peripheral lung lesion) is described as a characteristic feature of SPE, but is not always present.

2010-06-06T11:21:00.000-07:00

Sunday June 6, 2010
Arizona Immigration Law and Medical Practice -

Published at www.nejm.org June 2, 2010

To the Editor: The new Arizona state immigration bill (SB-1070) signed into law on April 23 will seriously obstruct, if not undermine, the practice of medicine in the state of Arizona...........

Read full letter here

2010-06-05T05:41:00.000-07:00

Saturday June 5, 2010

Q: Role of Ethanol, Fomepizole and Hemodialysis are well known in Methanol toxicity. Describe the role of bicarbonate in Methanol toxicity meanwhile above 3 treatments/antidote get arranged?

Answer: It is true that Ethanol, Fomepizole and Hemodialysis are mainstay of treatment in Methanol toxicity but often ignored is the role of bicarbonate in Methanol toxicity.

Actually Methanol itself has a relatively low toxicity. The adverse effects are from the accumulation of formic acid, a metabolite of methanol metabolism. Upon ingestion, methanol is quickly absorbed in the gastrointestinal tract and metabolized in the liver. In the first step of degradation, methanol is transformed to formaldehyde via the enzyme alcohol dehydrogenase (ADH). The next step is the transformation of formaldehyde to formic acid via the enzyme aldehyde dehydrogenase. Bicarbonate may help to decrease the amount of active formic acid. In addition, Bicarbonate potentially may reverse visual deficits.

2010-06-04T05:01:00.000-07:00

Friday June 4, 2010
Use of noninvasive positive pressure ventilation during pregnancy

Noninvasive positive pressure ventilation (NIPPV) is increasingly used to treat acute respiratory failure in nonpregnant patients, but literature of its use during pregnancy is almost none. Acute respiratory failure (ARF) remains a leading cause of ICU admission in obstetric patients. We found a report of case series of successful use of NIPPV in pregnancy.

Report is the outcome of treatment with NIPPV of four sickle cell disease pregnant patients with ARF caused by acute chest syndrome. Median APACHE II score for the four cases was 27.

Results:

Intubation was avoided in all cases.
None had aspiration.
Mean duration of NIPPV was 40 h
ICU discharge after a mean of 4 days

Conclusion: In closely monitored pregnant patients with Acute Respiratory Failure, NIPPV seems to have the potential to shorten ICU and hospital stay. A well-conducted randomized controlled clinical trial is required to confirm this finding

Use of noninvasive positive pressure ventilation during pregnancy: Case series - Ann Thorac Med. 2007 Jan–Mar; 2(1): 23–25

2010-06-03T06:11:00.000-07:00

Thursday June 3, 2010

Q: How Desmopressin (DDAVP) helps in coagulation?

Answer: Desmopressin (DDAVP) helps in coagulation via 2 mechanism

1. Desmopressin stimulates release of factor VIII and von Willebrand factor (vWF) from endothelial cells due to stimulation of the V1a receptor.

2. Desmopressin is shown to be efficacious even in bleeding disorders not involving a deficiency or dysfunction of factor VIII or vWF, including congenital and acquired defects of platelet function as those associated with chronic kidney and liver diseases.

Reference: Click to get abstract
How do you treat bleeding disorders with desmopressin? - Postgrad Med J 2007;83:159-163

2010-06-02T07:10:00.000-07:00

Wednesday June 2, 2010

Scenario: 52 year old male after emergent exploratory laparotomy is admitted to ICU. Patient has Lactated Ringer's solution going at 125 cc/hr. 2 units of pRBC were ordered. Why it is a bad idea to mix Lactated Ringer's solution and pRBC through same IV line?

Answer: Lactated Ringer's solution contains calcium which may bind to the citrate (use as anticoagulant) in blood products. This may promotes clot formation.

2010-06-01T12:45:00.000-07:00

Tuesday June 1, 2010
Stenting versus Endarterectomy for Treatment of Carotid-Artery Stenosis

Background: Carotid-artery stenting and carotid endarterectomy are both options for treating carotid-artery stenosis, an important cause of stroke.

Methods : We randomly assigned patients with symptomatic or asymptomatic carotid stenosis to undergo carotid-artery stenting or carotid endarterectomy.
The primary composite end point was stroke, myocardial infarction, or death from any cause during the periprocedural period or any ipsilateral stroke within 4 years after randomization.

Results: For 2502 patients over a median follow-up period of 2.5 years,

There was no significant difference in the estimated 4-year rates of the primary end point between the stenting group and the endarterectomy group
There was no differential treatment effect with regard to the primary end point according to symptomatic status
The 4-year rate of stroke or death was 6.4% with stenting and 4.7% with endarterectomy. The rates among symptomatic patients were 8.0% and 6.4%, and the rates among asymptomatic patients were 4.5% and 2.7% , respectively.

Periprocedural rates of individual components of the end points differed between the stenting group and the endarterectomy group: for death (0.7% vs. 0.3%, P=0.18), for stroke (4.1% vs. 2.3%, P=0.01), and for myocardial infarction (1.1% vs. 2.3%, P=0.03). After this period, the incidences of ipsilateral stroke with stenting and with endarterectomy were similarly low (2.0% and 2.4%, respectively; P=0.85).

Conclusions: Among patients with symptomatic or asymptomatic carotid stenosis, the risk of the composite primary outcome of stroke, myocardial infarction, or death did not differ significantly in the group undergoing carotid-artery stenting and the group undergoing carotid endarterectomy. During the periprocedural period, there was a higher risk of stroke with stenting and a higher risk of myocardial infarction with endarterectomy.

Stenting versus Endarterectomy for Treatment of Carotid-Artery Stenosis - Published at www.nejm.org May 26, 2010