Pediatric Liver function test : smarter way

Wednesday, May 27, 2015

This post is basically to get rid of my own confusions on liver function test for smarter interpretation in sick children and Should anybody, comes across this and find it useful then all the better!

Part One: Tests that detect injury to hepatocytes (serum enzyme tests)


Primarily marker of hepatocellular injury (most sensitive, more specific than AST),
Liver cell death —> leaks in blood.
No correlation with extent of damage.

A) High ALT (>15-20 times)

          Ischaemia (Much Higher) (Shock, hypotension, CCF, comes down rapidly)
          Viral hepatitis, Autoimmune
          Drug toxicity (PCM), Severe toxic hepatitis
          Acute budd chiary syndrome

B) Moderate ALT (5-15 times)

          Liver – Chronic Liver disease (eg Chronic hepatitis)
          Cholestasis (with ALP, GGT)
          Cardiac –Severe hepatic congestion in cardiac failure
          Other: Muscle injury, Kidney injury

C) Slight increase in ALT (<5 times)

          Liver: Neonatal hepatitis
                    Autoimmune hepatitis
                    NASH, EHBA
                    Alpha1-antitrypsin deficiency, Wilson’s disease
          Infection: Infectious mononucleosis
          Drugs: Almost any drug. (ATT, AED, Antibiotics, NASAIDS), PCM therapeutic doses,

D) False low ALT: Dialysis, Pyridoxine deficiency
Note: Drugs more likely to cause an asymptomatic abnormality in liver function.

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Capnography supersimplified:Basic Interpretaion

Thursday, March 12, 2015

“ It is always usefull to start by asking: Is there any EtCO2? Is it normal or abnormal? and what is the trend? ”
John H. Eichhorn. University of Mississippi school of medicine/Medical centre, Jackson, Mississippi.

Second short post on simplified capnography focusing on how to simply understand abnormal capnograph. This is more theoretical post, it will be followed by graphical post on how to make specific interpretation in cardiac arrest, mechanical ventilation, sedation and other scenarios.

Never forget:
Most frequent abnormal capnograms results from technical problems like improper calibration, loose connection, cracks in connector of circuits specially in side stream capnography. These need to be ruled out before hand in case of sudden changes in trend and no correlation clinically or in relation with blood gases.


Phase I – Deadspace Gas
   Rebreathing? (1)
   Deadspace seem right?
Phase II – Transitional Phase
   Transition from upper to lower airways Should be steep. (3)
   Represents changes in perfusion.
Phase III – Alveolar Gas Exchange
   Changes in gas distribution.
   Increased slope = mal-distribution of gas delivery. (5)
   End of Phase III is the PETCO2. (6)
   Area under the curve represents the volume of expired CO2 (VCO2). (7)
Total Exhaled volume (8)


capnography simpified 2
1. Decreased alveolar ventilation.
eg. V/Q missmatch, decreased respiratory effort due to disease or sedation, decrease in tidal volume because of inappropriate ventilator settings or reduced compliance, partially obstructed airway due to secretion or kinks.
2. Increased rebreathing of CO2.
eg. Abnormally functioning exhalation valve, Inadequate inspiratory flow. Insufficient expiratory time, Malfunction of a CO2 absorber system (exhausted sodalime), Partial rebreathing circuits
3. Increased CO2 production.
eg. Fever, sepsis, malignant hyperthermia.
4. Sodium bicarbonate infusion.
Bicarbonate given for acidosis dissociates into CO2, if adequate arrangement for CO2 washout is not made, it may adversely can cause acidosis.

1. Increased alveolar ventilation.
eg. Increase in RR or TV, Hyperventilation from any cause, DKA,
2. No gaseous exchange.
eg. Apnoea, complete obstruction of upper airway.
3. Mechanical causes
eg. leak in circuit, broken sampling tube, dislodgement of ET tube.
4. Decreased CO2 production.
eg. Hypothermia, decrease muscular activity like use of muscle relaxant.
5. Decreased pulmonary circulation. Less CO2 is brought to the lung for exchange so less is exhaled.
eg. Low cardiac output states, Cardiac arrest, Pulmonary embolism, Inadequate chest compression while CPR.

Exponential decrease in PETCO2 reflects a catastrophic event in the patient’s cardiopulmonary system.
capnography simplifiedSudden Hypotension/massive blood loss
Circulatory arrest with continued ventilation
Pulmonary embolism
                                               Cardiopulmonary Bypass

Gradual decrease in PETCO2 indicates a decreasing CO2 production, or decreasing systemic or pulmonary perfusion.
capnography simplified1     Hypothermia
                                                     Decreasing Cardiac Output.

Read basics of gradient between arterial and PEtCO2 in previous post on capnography here. Decrease in cardiac output and pulmonary blood flow causes decrease in PETCO2 but the arterial PaCO2 remains same therefore the difference between them increases causing high a-EtCO2 gradient. Thus if ventilation kept same, this gradient can be used for monitoring pulmonary blood flow or indirectly the cardiac output (Details in following post on capnography for cardiac arrest)

Increased alveolar dead space
     1. Low cardiac output
     2. Pulmonary embolism
     3. Other causes, Obstructive lung disease, Excessive lung inflation
This study in respiratory care in 2005 concluded presence of moderate to strong positive linear correlation between PETCO2 and PaCO2 difference for all ratios of dead space to tidal volume (VD/VT) ranges, although the strength of the correlation decreased slightly as VD/VT increased. As expected physiologically, the absolute difference between PETCO2 and PaCO2 consistently increased with increasing VD/VT.

ETCO2 and Metabolc acidosis
EtCO2 tracks serum HCO3 & degree of acidosis ( Decreasing EtcO2 = Increasing metabolic acidosis)
Thus helps to distinguish DKA from NKHHC and dehydration

ETCO2 and Synypnea
ETCO2 can help in distinguishing those patient with actual hyperventilation with same respiratory rate. ETCO2 is much more accurate than the RR. The RR is just a measure of how many times someone is breathing. The ETCO2 is how they are ventilating. 

There is lot more to make use of ETCO2

1. During Apnea Testing in Brain-dead patients.
(Eur J Anaesthesia Oct 2007, 24(10):868-75)
2. Evaluating DKA in children. No patients with a PETCO2 >30 had DKA.
(J Paeditr Child Health Oct 2007, 43(10):677-680)
3. Vd/Vt ratio and ARDS Mortality.  Elevated Vd/Vt early in the course of ARDS was correlated with increased mortality.
(Chest Sep 2007, 132(3): 836-842)
4. PCA Administration “Continuous respiratory monitoring is optimal for the safe administration of PCA, because any RD event can progress to respiratory arrest if undetected.”
(Anesth Analg Aug 2007, 105(2):412-8)

capnography supersimplified 4Trends are very important and gives a idea of changes in airway status, ventilation, and perfusion of lung as well as mechanical issues in critically ill children over a period of time.

It also can be utilized to audit the case in retrospect.
A time capnogram may be recorded at two speeds. A high speed capnogram (about 7mm/sec) gives detailed information about each breath whereas the overall CO2 changes (trend) can be followed at a slow (about 0.7 mm/sec) speed.

capnography supersimplified 5This image depicts the trend of capnography showing events that caused an decrease in end tidal CO2 as discussed above and possible causes including acute onset hypotension, circulatory collapse and pulmonary embolism can be suspected.

2. S David McSwain MD et al,  End-Tidal and Arterial Carbon Dioxide Measurements Correlate Across All Levels of Physiologic Dead Space. Respiratory care, march 2010 VOL 55 NO 3.
3. Madati PJ1, Bachur R.Development of an emergency department triage tool to predict acidosis among children with gastroenteritis. Pediatr Emerg Care. 2008 Dec;24(12):822-30.
4. Fearon DM, Steele DW. End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med. 2002 Dec;9(12):1373-8. PubMed PMID: 12460840.
5. D’MELLO, BUTANI. Indian J. Anaesth. 2002; 46 (4) : 269-278.
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Critical physiology: Dynamics of flow

Friday, February 13, 2015

Flow dynamics and application in critical care
flow physics
Image source:Wikipedia
1. Fluid dynamics is a subdiscipline of fluid mechanics that study fluid flow.
2. Dynamics is a science of fluids (liquids and gases) in motion.
3. Rheology is the study of the flow of matter, primarily in the liquid state.
4. several subdisciplines, including aerodynamics (the study of air and other gases in motion) and hydrodynamics (the study of liquids in motion).
5. Fluid dynamics has a wide range of applications in critical care.

Terminologies: 4 basic terms
1. Velocity
2. Pressure
3. Density
4. Temperature

Types of flow: Lamellar vs Turbulence
An object moving through a gas or liquid experiences a force in direction opposite to its motion.
flow image
Image source: Google images
Laminar flow occurs when a fluid flows in parallel layers, with no disruption between the layers. At low velocities the fluid tends to flow without lateral mixing, and adjacent layers slide past one another like playing cards. There are no cross currents perpendicular to the direction of flow.

In laminar flow the motion of the particles of fluid is very orderly with all particles moving in straight lines parallel to the pipe walls(Parabolic velocity profile). In fluid dynamics, laminar flow is a flow regime characterized by high momentum of diffusion and low momentum convection.
Image source:unknown
This flow profile of a fluid in a pipe shows that the fluid acts in layers and slides over one another.
Arrow shows adhesive forces between fluid and surface and relatively stationary flow at surface. Flow velocity increases towards the center gradually.
How to decide which type of flow ?: NR
Laminar and Turbulent flows is characterized and quantified by using Reynolds Number established by Osborne Reynolds and is given as

Where v = mean velocity, D = vessel diameter, ρ = blood density, and η = blood viscosity
Thus Reynolds number is directly proportional to velocity & inversely proportional to viscosity !
If    NR < 2000 – laminar flow
       NR > 4000 – Turbulent flow
Reynolds number for Blood flow in brain ~ 100 and Blood flow in aorta ~ 1000.

Application: Airway
From estimates of the Reynolds number and the dimensions of the airways obtained from anatomic casts, flow in the large airways is turbulent. Laminar flow becomes established between the 4th and the 15th generation of airways, depending on the flow rate of the gas.

If the gas in a long, straight tube is moved in a laminar fashion by a sinusoidal pressure generator, the flow profile has to reverse with each cycle. The gas in the center of the tube will reverse velocity greater than that close to the wall. This type of flow regime is most applicable during high-frequency oscillatory ventilation and is responsible for gas mixing.

It is also relevant in small endotracheal tubes for newborns during conventional ventilation of >60 breaths/min, when the inertia of the gas can cause an underestimation of airway pressure of several cm H2O.

Heliox: Flow in the large airways is turbulent, and the resistance in this flow regime is density dependent. In cases of extreme large-airway obstruction, the resistance can be reduced by reducing the density of the gas with the use of a mixture of helium and O2 (Heliox). This reduction may help to relieve obstruction such that intubation of the patient is avoided. The primary limitation is the O2 requirement of the patient that dilutes the helium in the mixture.

Airway resistance is affected by the aerodynamics of flow through tubes. Flow through the airways is driven by a pressure drop between the alveoli and the atmosphere or the endotracheal tube (Bernoulli's principle). In laminar flow, the gas has a precisely ordered velocity profile, with the flow in the center being the greatest, decreasing to zero at the walls. Laminar flow has the least possible pressure drop or energy dissipation for a given flow and tube diameter therefore unnecessary kinks in vent tubes as well as inappropriate tube diameter should be avoided.

Application: blood flow
No turbulence occurs until the velocity of flow becomes high enough to break flow lamina. Therefore, as blood flow velocity increases in a blood vessel or across a heart valve. There is not a gradual increase in turbulence, Instead, turbulence occurs suddenly when a specific Reynolds number (Re) is reached.
fluid 3
In large arteries at branch points, in diseased and narrow arteries and across stenotic heart valves laminar flow can be disrupted and become turbulent. When this occurs, blood does not flow linearly and smoothly in adjacent layers, but instead in chaotic fation, this can also occur in ascending aorta cause of high flow velocity.

Laminar flow can be disturbed at the branches of arteries, and the turbulence created may cause atherosclerosis over a period. Constriction of an artery also increases the velocity of blood flow through the constriction, producing turbulence and sound. Examples are bruits over constricted  arteries and the Korotkoff sounds. Turbulence occurs more frequently in anemia because of lower viscosity. This may be the explanation of the systolic murmurs that are common in anemia.
Elevated cardiac outputs, even across anatomically normal aortic valves, can cause physiological murmurs because of turbulence.

Perfusion pressure and terbulent flow
flow physics in critical pediatrics

Turbulence increases the energy required to drive blood flow because turbulence increases the loss of energy in the form of friction, which generates heat.

When plotting a pressure-flow relationship (see figure to right), turbulence increases the perfusion pressure required to drive a given flow. Alternatively, at a given perfusion pressure, turbulence leads to a decrease in flow.

Newtonian and non Newtonian fluid
Newtonian fluid obeys the law which states that viscosity  of fluid remains constant regardless of any external stress that is placed upon it, at constant temperature and pressure.
For, Non-newtonian fluids, flow is affected by their viscosity and affected differently for different fluid due to different coefficient of viscosity (n).

What generates Viscosity ?
“When fluids flow they have a certain amount of internal friction called viscosity”.  It exists in both liquids and gases.

Whats is coefficient of viscosity?
Fluid in contact with surface is held to that surface by adhesive forces between the molecules of the fluid and surface. Therefore, the molecules at the surface of the stationary wall are at rest and the molecules at the surface of the moving plate will be moving with velocity v. The stationary layer of fluid in contact with the stationary wall will retard the flow of the layer just near to it. This layer will retard the layer near and so on. The max flow velocity will be present in centre. With different adhesive forces for different fluid, the velocity will vary. This is coefficient of viscosity (n).

Different fluid have different coefficient of viscosity. It is one of the several determinants of flow rate of gases and blood in body.

Earlier, blood was treated as a Newtonian fluid. However Thurston reported that viscoelasticity is known to be a basic rheological property of blood. The viscoelastic properties which make human blood non- Newtonian depend on the elastic behavior of red blood cells.

“Blood is not a Newtonian fluid. (Viscosity differs constantly). The viscosity depends strongly on the fraction of volume occupied by red cells (Hematocrit).”

Viscosity of blood increases with1.Increased hematocrit
2.Constrictions in vessels                                                                                                    3.Decrease flow rate of blood through vessel (RBCs adhere to each other, and the vessel walls.)
Viscosity of blood decreases with1.Increased flow velocity
2.vessel diameter below 300 μm (reduced η when RBCs get aligned in small vessels. This is called as Fahraeus-Lindqvist  effect.
3.In very small vessels (< 20 μm), η increases as RBCs fill the capillaries, “tractor tread” motion.

Dynamic of Blood flow (Rheology)
1.The macroscopic rheologic properties of blood are determined by its constituents.
2.In large arteries, the shear stress exerted on blood elements is linear with the rate of shear, and blood behaves as a newtonian fluid. In the smaller arteries, the shear stress acting on blood elements is not linear with shear.
3.The aorta and arteries have a low resistance to blood flow compared with the arterioles and capillaries.
4.When the ventricle contracts, a volume of blood is rapidly ejected into the arterial vessels. Since the outflow to the arteriole is relatively slow because of their high resistance to flow, the arteries are inflated to accommodate the extra blood volume. During diastole, the elastic recoil of the arteries forces the blood out into the arterioles.

Thus, the elastic properties of the arteries help to convert the pulsatile flow of blood from the heart into a more continuous flow through the rest of the circulation.

The Moens-Kortweg wave speed
The Moens-Kortweg wave speed
(Steeping of pressure pulse with increasing distance away frm heart)
Equation was obtained by Thomas Young in 1808, and is known as the Moens-Kortweg wave speed. Steepening of the pressure front as it travels from the heart toward the peripheral circulation . Wave speed also varies with age because of the decrease in the elasticity of arteries and increasing intramural pressure. (Axial length and trans-mural pressure both affect)

The arteries are not infinitely long, and it is possible for the wave to reflect from the distal end and can travel back up the artery to add to the pressure.

blood flow in curved tubeThe arteries and veins are generally not straight but have some curvature, especially the aorta, which has a complex three-dimensional curved geometry.

Effect of curvature on blood flow, can be understood by a steady laminar flow in a plane curved tube . When a steady fluid flow enters a curved pipe in the horizontal plane, all of its elements are subjected to a centripetal acceleration relative to their original directions and directed toward the bend center.
Branching is clearly an important contributor to the measured pressures in the major arteries.

Flow in microcirculation
“Concept of a closed circuit for the circulation was established by Harvey (1578–1657). The experiments of Hagen (1839) and Poiseuille (1840) were performed in an attempt to elucidate the flow resistance of the human microcirculation…“
                                                                    (Berman and Fuhro, 1969; Berman et al., 1982)
The term “microcirculation” is for vessels with internal diameter that is multiple of major diameter of the RBC. This definition includes primarily the arterioles, the capillaries, and the postcapillary venules.

The capillaries are of particular interest because they are generally from 6 to 10 μm in diameter, which is about the same size as the RBC. In the larger vessels, RBC may tumble and interact with one another and start moving streamlined as they travel down the vessel. In contrast, in the microcirculation the RBC must travel in single file through true capillaries.

The viscosity of blood has a primary influence on flow in the larger arteries, while the elasticity, which resides in the elastic deformability of red blood cells, has primary influence in the arterioles and the capillaries.

1. Ganongs Review of medical physiology
3.Fluid flow, viscosity, poiseuille's law. visual physics. school of physics university of sydney australia.
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Capnography super-simplified : The basics

Friday, January 30, 2015

is synonymous with patient safety during anesthesia and sedation, and a boon during CPR. Since the first infrared CO2 measuring and recording apparatus by Luft in 1943, capnography has evolved into an essential component of standard anesthesia monitoring armamentarium. In 1978, Holland was the first country to adopt capnography as a standard of monitoring during anesthesia.
WHY CAPNO? IN PICU Beware the falsely reassuring statement " He must be breating, sats are ok " Use Etco2 to guage ventilation.

Picture1The patient admitted in ED and critical care are too sick unlike the OR where the patients are relatively stable and screened for fitness of procedure or surgery.
The risk of encountering major airway complication in ICU,s is about 66 times more often than OT/OR because of lack of continuous capnogarphy monitoring.
1. Capnography helps in the differential diagnosis of hypoxia to enable remedial measures to be taken before hypoxia results in an irreversible brain damage.
2. Provides information about co2 production, pulmonary perfusion, alveolar ventilation, respiratory patterns, and elimination of co2 from the anesthesia circuit and ventilator.
3. Effective in the early detection of adverse respiratory events.
4. Capnography and pulse oximetry together could have helped in the prevention of 93% of avoidable anesthesia mishaps according to asa closed claim study.
5. Better detection of potentially life-threatening problems than clinical judgment alone (cote et al).

What is Capnography  
= Measurement of co2 during expiration

Infrared absorption of CO2 as a principle of operation..Uses Beer-Lambert law. A known concentration of infrared light is traverses through the exhaled gases. Carbon dioxide, being a poly atomic gas, absorbs infrared light. The remaining beam of light is detected by detectors and exhaled CO2 values are computed.
Carbon dioxide selectively absorbs specific wavelength of infrared light 4.3 micrometer. The ammount of light is proportional to ammount og co2 molecule, the measured absorbence is compared with standard absorbence and the co2 at et end is calculated.

Main-stream capnographs
1. A sample cell or cuvette, airway adapter, is inserted directly in the airway.
2. A lightweight infrared sensor, emitted light is detected by a photo detector located on the opposite side of the airway.
3. Produces waveforms that reflect real-time CO measurements during a respiratory cycle without a delay.
Side-stream capnography
1. Sensor located in the main unit , away from the patient, and a pump aspirates gas samples from the patient’s airway into the main processing unit.
2. The capnographs will have a delay in displaying co2 concentration
3. A main problem encountered in the ICU setting is the blockage of the sampling tubes
Advantage of side-stream capnography is that expiratory gases can be obtained from the nasal cavity using nasal adaptors or with a simple modification of the standard nasal cannula. These devices are easy to connect, do not require sterilization as they are disposable, and can be used in awake patients.

Image source: Reference 2
Best thing about sidestream capnography is it can be used in spontaneuosly breathing patients, Specialised nasal cannula are available with device itself or simple modification of regular nasal cannula like this can be done to use sidestream capnography device.
(Image source: The ICU book, Paul Marino)


Real time main stream capnogarphy vs sidestream with delayed reflection of respiratory cycle.

Qualitative CO2 measurement
Quick and simple method of determining if an endotracheal tube has been placed properly. Devise contains filter paper that is impregnated with a PH-sensitive indicator that changes colour
Image source: Reference 2
with detection  of CO2. The outer perimeter of the device contains colour coded section indicating the concentration of exhaled CO2 associated with each colour change

1. Capnometry:
The measurement and display of CO2 on a digitial or analogue monitor. Maximum inspiratory and expiratory CO2concentrations during a respiratory cycle are displayed.
2. Capnography:A graphic display of instantaneous CO2 concentration during a respiratory cycle (CO2 waveform or capnogram)
3. Capnograms: Time and Volume
Can be of two types: ETCO2 can be plotted against expired volume or against time (time capnogram) during a respiratory cycle.
4. PETCO2:Partial pressure of CO2 at the end of expiration.
5. (a-ET)PCO2:Arterial to end-tidal CO2 tension/pressure difference or gradient.
Waveform phases 
Little bit of lung physiology will help understanding typical waveform, so during expiration the first air the sensor breaths is from deadspace which contains no to very low co2 this air is then mixed with the air from conducting zone and the co2 content increases rapidly, lastly followed by air in alveoli with highest concentration of co2.
Image Source: Reference 6
A time capnogram can be divided into inspiratory and expiratory segments. The inspiratory segment is further divided into three phases.

phase I (Anatomical and apparatus dead space gases)

phase II Rapid rise (Mixture of Anatomical dead space and Physiological dead space gases)

phase III alveolar Plateau (Co2 rich gas from alveoli and reflects alveolar evolution of CO and always has a mild positive upslope. This positive up slope is not well appreciated in a time capnogram. In Volume capnogram, the positive slope is prominent as CO concentration is plotted against evolving expiratory volume. 

Phase 0 (Fresh Co2 free gas is inhaled and CO2 conc falls rapidly to zero)

Alpha angle (Angle bewteen phase 2 and phase 3. Generally reflect V/Q status of lung )
Beta angle (Angle between phase three and descending limb. Generally its is 90 degree)
Volume capnography is much more beneficial in the PICU setting. The volume capnogram can be related to components of tidal volume; physiological dead space and alveolar ventilation .

A noninvasive estimate of physiological dead space can be obtained from volume capnography.
Magnified Capnogarph of a mechanical breath showing various phases mentioned above where ETCO2 is plotted against time.

Capnograph where ETCO2 is plotted against Tidal volume.

a-ETCO2 GRADIENT Index of alveolar dead space:
Normally , the PETCO2 < PaCO2 (average of all alveoli) by 2-5 mmhg as a result of temporal, spatial, and alveolar mixing defects.
“In children, the (a-et)pco2 gradient is Smaller (0.65-3 mm hg) than adults. This is due to a better V/Q matching, and hence a lower alveolar dead space in children”.

                                      ETCO2 CLOSELY RESEMBLES PACO2
Therefore, changes in alveolar dead space correlate well With changes in (a-et)pco2  “Hence (a-et)pco2 is an Indirect estimate of V/Q mismatching of the lung”

Increases in alpha angle (angle between phase II and phase III) and the slope of phase III are a good refection of V/Q perfusion status of the lung.  In chronic obstructive airway disease, the slope of phase III is increased together with  an increase in the alpha angle.  The morphology of capnogram can offer tremendous information about underlying V/Q abnormality.
Figure showing virtual spaces occupied  by   verious volumes when capnograph is plotted.
   X is  total exhaled volume.
   Y is alveolar dead space and reflects   quantitative V/Q missmatch.
    Z is anatomical dead space.

Gas exchange abnormality
Increased anatomical dead space
Open vent circuit
Shallow breathing
Increased alveolar dead space
Obstructive lung disease
Excessive lung inflation
Low cardiac output
Pulmonary embolism

While interpreting abnormal capnogarph these should be taken in consideration first
sampling error
calibration error
leaks or occulsion in sampling lines
difficulty in obtaining a true end-tidal CO2 

2.The ICU book by Paul Marino
3.Kodali, Bhavani Shankar Anesthesiology. 118(1):192-201, January 2013.
4.National audit project
5.Quick guide to capnography philips
6.Capnography in pediatric Intensive care medicine, Ajay Desai, Great Ormond Street Hospital, London
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Monitoring in septic shock and surviving sepsis

Tuesday, July 15, 2014

By Ramaning Loni, CMC Vellore
Sepsis is always a hot topic in 
pediatric critical care medicine.

The mortality rate of severe sepsis 
and septic shock in most
centers remains unacceptably high. 

This presentation focuses on the 
critical point of monitoring in pediatric septic shock, the
new surviving sepsis guidelines
2012 and the Early Goal-Directed therapy in the Treatment
of Severe Sepsis and  Septic
Shock by Dr Emanuel Rivers.
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Lorazepam vs Diazepam for Pediatric Status Epilepticus: Which is better?

Saturday, July 5, 2014

Recently a study of 259 patients was publisheed in JAMA by James M. Chamberlain, on efficacy of Lorazepam vs diazepam for pediatric status epilepticus, it was a randomized clinical trial.

Both Diazepam and lorazepam are benzodiazepines used in treatment of status epilepticus. They differ in potency and in the time-course of their action. As a sedative, diazepam 10 mg is equivalent to lorazepam 2–2.5 mg. Diazepam is better absorbed after oral than after i.m. administrations but this does not apply to lorazepam. The clinical effect and amnesia begin more rapidly with diazepam, but last longer following lorazepam. 

Diazepam but not lorazepam is approved by the US Food and Drug Administration for status epilepticus in children, although both drugs are widely used for this purpose.

Benzodiazepines are considered first-line therapy for pediatric status epilepticus. Some studies suggest that lorazepam may be more effective or safer than diazepam, but lorazepam is not Food and Drug Administration approved for this indication.

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