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Branding Your Livestock

February 10, 2013

Branding a Horse I was recently asked, by a reader, how to brand his horse without getting kicked. I told him this was a two part question and would take me more room than the comment box to answer him. He told me he was hunting this fall in Colorado, when his horse got away from him and he never saw him again. He did say that he had dog tags on the horse for identification, not to mention all his gear, but no one has contacted him yet about the horse.

Now he would like some information on how to brand his remaining horses for identification. This brings us to the two part answer. First, how to physically mark the horse without injury to yourself or the animal, and second, how brands are able to identify livestock for the return of an estray (the legal term for a misplaced animal).

There are two ways to brand an animal, fire and ice. The most common way to do it is with a fire heated steel branding iron, or an electrically heated steel iron. I will save the description of the actual brand for the identification section. The safest way to do this will be with the help of your local large animal veterinarian. He or she should have a good set of steel pens and a chute for cattle. Assuming there are no low overhead bars across the top of the chute that could injure a horse (horses are extremely claustrophobic compared to cattle), you should utilize the main working chute for the horse, NOT the squeeze chute. Think about how bucking chutes at a rodeo arena look. This is the kind of containment you are going for.

Here is a video of how wrong branding a horse can go. It is not my video and can be found on any YouTube search. Notice the chute. It does not have nearly enough bars on the sides of it. Horses can also kick between pipes that are too far apart. You only need enough room between the pipes to get the branding iron through.

Your vet will have drugs that will allow him to tranquilize the horse so that he does not overreact to the pain of the heated iron. The worst case scenario, you can always completely knock the horse out with drugs and lay him down out in the open, like would be done for a castration procedure. Care should also be taken to anchor the horse’s hind legs to his neck with thick, heavy, soft cotton rope in this down position, because he could still involuntarily kick and injure you. If you do lay him down like this, you should be careful to make note of the exact angle of his hip if you intend to apply the brand there because when you untie his hind legs and they return to their normal position, your brand will be in a different position from when you applied it. You will have to visualize how it would be in the vertical position when the horse is standing up.

All this being said, not all vets have experience with branding animals. Some of them may not even have a propane heater to heat the iron with. You will probably be looking for a cattle vet in this case more than a straight equine vet, but either way, call around and ask lots of questions. If you cannot find a vet you are comfortable with, sometimes farriers will do this sort of thing. They often have the drugs needed from dealing with young or unruly horses in their day to day work. There are also people out there who specialize in branding horses specifically, both fire and freeze branding. These guys will often have a set of number and letter brands as well, if that fits your brand. If you have a certain character brand, you will need to have it built and provide it. I will discuss this more in the second part of this discussion.

Now that we have determined how to properly restrain the horse, lets talk about the actual application of the brand, just so you know what to look for, even though you should really try to find an experienced individual to do this for you. First of all, if you’ve ever branded cattle, horses have MUCH thinner skin than cattle do. Even thinner than calves. A fire brand applied to a moderately hairy calf needs a good 5-6 seconds to leave an appropriate mark. On a horse, it will not be more than 2-3 seconds or else you can actually burn through the hide, which will take a long time to heal and result in a blotched brand that is unrecognizable. If your horse has a winter coat, I would recommend clipping the hair on the area to be branded. This will assure that the iron goes straight to the skin and doesn’t have to burn through the hair first. It should only take about 2 seconds this way.

The next thing to know is, no matter what you’ve seen in the movies or advertisements, your branding iron should NEVER be glowing red. This applies to cattle and horses. If it is red or has been red while in the heater, it is TOO HOT and will slip and smear across your horse’s body wherever you touch him with it. This will leave an ugly scar that he will have to wear the rest of his life instead of your well thought out brand. The iron should only be a plain old gray iron color, even while in the branding fire. You can test it on a piece of wood to see if it is hot enough. It should burn into the wood. Also, don’t push the iron into his skin like you were trying to stamp him with it. Let the heat do the work. You should only apply moderate pressure against his skin with the iron in order to stabilize it so it doesn’t move or slip.

Here are some other quick tips. Never apply a hot brand to a wet animal, like when its raining. It will scorch and make a big blotch. Never apply pour-onwormer to the area a hot brand will be placed, it will catch on fire and burn the animal badly. When designing your brand, don’t go crazy. Keep it simple and try to minimize the number of angles in it. Try not to have any acute angles (those that are less than 90 degrees) and try not to have any closed circles. All of these things concentrate too much heat in one spot and will blotch and then be harder to recognize, not to mention look bad. Things like a cross “+” have 4 90 degree angles touching one another. This symbol will likely blotch in the middle at the intersection of the angles. Even something simple like a 5 point star is likely to blotch at every one of the 5 points because each one is made of acute angles. The letter “N” can also be bad because of the two acute angles. Two ways to remedy it would be to round the angles when building the brand or vent the intersections with a grinder by making a small cut at each angle in the iron when it is being built. The vent or small cut will offer some relief and let a little heat escape from the hide before it blotches, and you will likely never see it in the actual brand.

The other style of branding is freeze branding. It takes dry ice and alcohol or liquid nitrogen and special copper branding irons. Steel can be used, but over time it will ruin the iron because it will become brittle. Freeze branding is much less painful to the horse, but is more difficult to apply. You will definitely have to employ a specialist to help you. Also, freeze branding does not actually leave a mark on the skin of the animal, but rather kills the pigment in the hair follicles, resulting in white hairs growing where the brand was applied. So as you can imagine, it does no good on white or grey animals. The area to be branded has to be clipped short and the time the brand is applied to the skin is VERY specific. It is best to have a professional do it if you should choose this route.

Here is a website with instructions on freeze branding if you want to check it out:

So now for the second and most complicated part of our discussion, identification of the animal. Let me start by saying, “It all depends!”. Most of it depends on which state you live in and what the specific branding laws for that state are. You need to familiarize yourself with the laws of the state where you live. Your state cattle association will be a good place to start. They should have information for you, or at least they can tell you which state agency to contact for the information you need.

Let me just go ahead and give you the bad news now. For the gentleman who asked me this question to begin with, the likelihood is your brand will not bring your horse home, especially when you cross state lines. What it does do is serve to determine ownership in the case of a legal dispute, like if you had happened to see your horse standing in someone else’s corrals as you were driving out of the mountains headed home. Unfortunately, the dog tags he had on his horse would be of more use in helping the horse get “returned” than a brand would because every state either issues or records brands within their borders only, and in Texas where I live, it is recorded county by county. There is no national registry, and in Texas there is no state registry. In other words, I could be using the same legally registered and recorded brand as a guy just twenty miles down the road in the next county. Its not a good idea, but completely possible. Also, in order to stand up in court, it has to have been properly registered ahead of time with the appropriate authorities according to the laws of your state. Otherwise, it is just so much scarring on the horse’s body. In Texas you register your brand with your County Clerk. You would be surprised at the number of people who come up with some horrible looking medieval torture device the size of a giant turkey platter, stick it in a fire until its glowing red to the point of melting and then jam it against the hide of their animals with the same pride as a three year old admiring his first Crayon mural on his mother’s freshly painted living room wall, and never bother to go to the courthouse and register said horrible looking medieval torture device legally in his name. That brand, as proud as they are of it, will never hold up in a legal dispute if its not registered. And more importantly, in Texas, it is illegal to brand an animal with an unregistered brand, and classified as a misdemeanor.

Another point that is important in brand registration is location. Animals can be branded on their hips, buttocks, ribs, shoulder and even on their jaw and the bridge of their nose. Also, right or left side of the animal must be recorded and any combination of locations recorded.

Finally, the most difficult part of the discussion is dealing with your individual state. Texas is one of the only states where a person can make up their own brand, as complicated or as simple as you want, and if no one else has that exact symbol or number combination or letter combination in the same location on the animal in the county that you want to register it in (ideally where the animals will be located), then you can simply go to the courthouse and register your new brand. It costs about $12-$25 per brand, to be determined by the county you register with. In Brazos county where I live, it costs $16. And you will have to renew it every 10 years. Now you’re in business.

For states like New Mexico or Colorado, it is not that simple. First of all, you are required by law to brand your livestock. Not so in Texas. Secondly, they no longer issue single character brands in those states. In New Mexico it will cost you $100 dollars to apply for a brand and it must be renewed every three years. In Colorado, all new brands registered must be three or more characters, and you are competing with the entire state for originality. It costs $50 just to apply for the brand, and then if it is accepted by the state it will cost you a $220 assessment fee to record the brand for the next five years, for a total of $270. Double and single character brands can still be obtained, but you have to inherit them or buy them from an individual who may be willing to sell his. You can do a google search for “brands for sale in New Mexico”. You are going to be surprised. These existing brands will bring anywhere from $500-$50,000. The smaller (number of characters) more unique the brand, the more expensive it will generally be.

Here is a website you can visit that will answer a lot of questions: It will touch on everything from Frequently Asked Questions to How to Design and How to Read a Brand.

I hope this helps. I am definitely not the final authority on the subject. Be sure and check with your state cattle association and learn the laws for your state. Also, one final note, most local police departments and even local sheriff’s departments are completely ignorant in the laws of branding. I am of course speaking in generalities and I am sure there are plenty of exceptions to this statement, but I have had personal experience with multiple departments in multiple counties in different regions of Texas and they were all clueless. In Texas, if you need help finding or identifying brands or locating ownership, you will need to contact the Texas and Southwestern Cattle Raisers’ Association Special Rangers division. These guys are good. They are also serious and not to be taken lightly. They are a special division of the Texas Rangers and they are packing.

Thanks for asking. If anyone else has any questions or things you’ve always wondered about dealing with cowboys, horses, dogs, or cattle, please feel free to ask me and I will do my best to give you an answer.

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Shin Splints

As you may recall from our intro post on kinesiology taping, we’re going to focus on each muscle group/joint and show you how to use kinesiology tape in three distinct ways:

  1. Immediately after injury  (for swelling and pain)
  2. During the healing process (correction techniques to restore normal position and allow for healing)
  3. Techniques to help improve strength + function

In this post, we’ re going to be talking about a taping application designed to decrease the amount of pull on the Anterior Tibialis. This is perfect for recovering muscles and tendons where you want to provide support and allow for rest so that the injured muscle/tendon can heal. The Anterior Tib is a commonly injured muscle with shin splints (aka tibial stress syndrome). This is a repetitive overuse injury that can be caused by tight calves and ankles, improper footwear, or abnormal mechanics (i.e. running/cycling form).

This type of application is called an inhibition technique. The key for using it is to use the anatomy! Remember, the tape is specifically made to pull on itself. That is what the weird spirals and shapes are when you look at the back of the tape. When trying to inhibit the muscle, you want the tape to move from the muscle insertion to origin so that when the tape pulls on itself, it results in an eccentric pull (eccentric = lengthening of the muscle). This is ideal for trying to diminish the contraction which will allow for rest and more importantly recovery.

The anterior tibialis is one of the easiest muscle to find in the lower leg. Start with your fingers on the shin bone and slide off the bone towards the outside of the leg. The first muscle you feel is the AT. It starts just below the knee on the tibia, runs down the front of the leg and then wraps across to the inside of the ankle. It is responsible for pulling the ankle up (dorsiflexion) and in (inversion). You can read more about the anatomy and surrounding muscles here.

What you will need:

1) Roll of kinesiology tape

2) Sharpest scissors in the house.

Prep work:

1) Clean skin. This means no oils or lotions of any kind. You want your skin to be clean and more importantly dry. Moisture of any kind = tape will fall off or fail to stick altogether.

2) Hair care. Ideally, the less hair the better. Guys, this means that for best results you will need to trim any long leg hair or shave the calf area.

3) If clean, dry, and hairless skin still = no sticking of tape. Time to get some adhesive spray like Tuf Skin.

4) The tape should last 3-5 days. You can get it wet and shower with it on. Just towel dry it after. No hair dryer! The tape is heat activated. ;)

Taping Techniques

1) Inhibition technique for the anterior tibialis with correction strip.

Key Points:

  • Prep the skin first. For this application you will want to put the foot and ankle on stretch (pull the toes down and in; this is similar to the position your foot would be in if you caught the outer edge of your foot and rolled your ankle).
  • There will be two strips for this application. The first will be anchored just below the pinky toe and then the two tails placed without without stretch (the first wraps under the arch, over the the top of the foot and then up the anterior tibialis muscle. The second tail follows this path but stays closer to the shin bone. Both tails are applied without stretch. Simply lay the tails down. The tape works by pulling on itself and you have already put the muscle on stretch to do the work for you.
  • A secondary correction strip can be applied to any specific sore spots. Cut the tape so that it is long enough to cover the painful area with 1-2″ of tape on either side (these are your anchors and must be applied without stretch). Round the edges, apply 50-75% stretch and place the tape. Then remove the paper backing and lay down the ends. Don’t sweat the 50-75%. Think medium stretch versus maximum “how far can I pull this tape” kind of stretch.
  • See the video above for full details.
  • For further instructions on how to incorporate kinesiology taping into your self treatment regimen click here.

1) Capobianco, Dr. Steven and van den Dries, Greg. (2009). Power Taping, 2nd Edition, Rock Tape Inc, Los Gatos, CA.

2) Hammer, Warren. (2007). Functional Soft-Tissue Examination and Treatment by Manual Methods, 3rd edition. Jones and Bartlett Publishers, Inc, Sudbury, MA.

3) Kase, Kenzo, Wallis, Jim, and Kase, Tsuyoshi. (2003). Clinical Therapeutic Applications of the Kinesio Taping Method.

4) Muscolino, Joseph. (2009). The Muscle and Bone Palpation Manual. Mosby, Inc, St. Louis, MO.

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Team Results Management

Brittany Waltz

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Team Results Management

Shelby Weatherman

- Cross Country Athlete Profile
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Davie County - HS
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Team Results Management

Pablo Perales

- Cross Country Athlete Profile
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Imlay City - HS
2014 Season - 10th Grade
5,000 Meters
8923:41.26Sep 6Corunna Invitational
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77 24:02Sep 16Lapeer County Press Cr...
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Team Results Management

Dylan Sadick

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20125' 7.00 V FJun 1CIAC Class M Champions...
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1068.21a Jv PDec 189th New Haven Invitati...
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9124' 6.00 Sm FApr 242010 O'Grady Relays
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Team Results Management

Luis Vargas

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CAO Gold Label Robusto

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With its beautiful Connecticut-Connecticut wrapper, the C.A.O. Gold Label has earned a much-deserved reputation for flawless construction, consistent quality, and a medium-bodied flavor that is the perfect “step up” for the smoker looking for something a bit more flavorful than the traditional mild cigars. Sure to become a mainstay in your humidor, the C.A.O. Gold Label is a smooth Nicaraguan cigar that offers flavors of mild spice with creamy vanilla and nutmeg accents.

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text:
Heaven Sent
(A Farriss) Your eyes are like deep wells of desire Once in your arms I'm on fire You were sent girl so perfectly true Changing my life Now I'm a survivor Heaven sent That's what I call you Late at night when the evening fire has died There's a look in your eye Seductive images fly One day you'll see what angels can see Dressed in black if she comes back I think I'll lose my mind Tuesday she works In the library uptown Some useful knowledge Can always be found Don't burn the library Til you've read all the books Sometimes in life You get a second look


text: @Article{acp-12-6629-2012, AUTHOR = {Gayet, J.-F. and Shcherbakov, V. and Voigt, C. and Schumann, U. and Sch\"auble, D. and Jessberger, P. and Petzold, A. and Minikin, A. and Schlager, H. and Dubovik, O. and Lapyonok, T.}, TITLE = {The evolution of microphysical and optical properties of an A380 contrail in the vortex phase}, JOURNAL = {Atmospheric Chemistry and Physics}, VOLUME = {12}, YEAR = {2012}, NUMBER = {14}, PAGES = {6629--6643}, URL = {http://www.atmos-chem-phys.net/12/6629/2012/}, DOI = {10.5194/acp-12-6629-2012} }


text:
[ banner - AUA NEWS ]

FOR IMMEDIATE RELEASE: February 03, 2011

Wendy Isett, AUA
410-689-3932, communications@AUAnet.org

LINTHICUM, MD, February 3, 2011—The American Urological Association (AUA) released today a new clinical Guideline on the Treatment of Benign Prostatic Hyperplasia (BPH), which updates current guidance on diagnosing and treating this common condition in men, which can lead to lower urinary tract symptoms (LUTS) and impact the quality of life for patients. The AUA released its own original guidance on BPH first in 2003. A full Executive Summary of the Guideline is expected to be published in an upcoming issue of The Journal of Urology. A Webinar about the guideline will soon be available online at www.AUAnet.org.

The update to the guideline, finalized in late 2010, includes a detailed diagnostic algorithm to guide a physician in diagnosing and treating LUTS secondary to BPH, as well as in-depth information on its basic management and the management of complicated cases. Physicians treating men with suspected cases of LUTS should obtain a relevant medical history, assess symptoms using the AUA Symptom Index and conduct a full physical examination (including a digital rectal exam). Laboratory tests should include a prostate-specific antigen (PSA) test and a urinalysis to exclude infection or other causes for LUTS. Frequency and volume charts may also be useful in providing a diagnosis.

The 2003 update provided key information on the use of pharmacologic therapies to treat BPH (in addition to surgical therapies available); the 2010 edition contains added recommendations for the use of anti-cholinergic drugs and the use of laser therapies. Additionally, the index patient age has been lowered to 45 from 50, to better guide physicians in treating younger men who may be experiencing lower urinary symptoms.

The Guideline also includes cautionary statements about intraoperative floppy iris syndrome (IFIS) in cataract patients taking alpha-blockers to treat BPH. The AUA cautions physicians to question patients about any planned cataract surgery prior to their starting an alpha-blocker regimen (men planning cataract surgery should avoiding initiating alpha blockers until after their surgery has been completed). Those men already taking the drugs should inform their ophthalmologists of their alpha-blocker regimen prior to surgery.

The increasing life expectancy and growth of our elderly population will increase the number of men who suffer from LUTS. This will place increased demands for treatment services, and necessitate the incorporation of evidence-based medicine in that treatment,” said Kevin T. McVary, M.D., chair of the panel that developed the Guideline. “This document provides much-needed guidance to doctors who are already treating LUTS, as well as those who will be in the future.”

The prostate is a walnut-sized gland that surrounds the male urethra. An enlarged prostate can lead to lower urinary tract symptoms, or LUTS, that can grow progressively worse as the gland grows. LUTS can be caused by direct bladder outlet obstruction (BOO) or by increased smooth muscle tone and resistance within the prostate, and can directly and significantly affect a man’s quality of life. In fact, for many men, the severity and degree of bother of LUTS symptoms are the most important motivators for them to seek treatment.

For more information on this Guideline or to schedule an interview with Dr. McVary, please contact Wendy Isett at 410-689-3932 or communications@AUAnet.org.

About the American Urological Association: Founded in 1902 and headquartered near Baltimore, Maryland, the American Urological Association is the pre-eminent professional organization for urologists, with more than 16,000 members throughout the world. An educational nonprofit organization, the AUA pursues its mission of fostering the highest standards of urologic care by carrying out a wide variety of programs for members and their patients.


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 Dean Road Elementary School

Welcome to Dean Road Elementary School

Our Mission

The mission of Dean Road Elementary School, the fundamental foundation of early childhood education, is to ensure each student recognizes his or her inherent value and strengths in order to achieve their highest educational and personal potential, through a system distinguished by:

- motivated educators

- academic success

- authentic learning experiences

- high moral standards

- respect for diversity

- an engaged community

Our Vision

Dean Road Elementary School, in partnership with families and community, will create a safe, nurturing, learning environment where challenging curriculum, high academic standards, and respect for diversity will maximize each student’s intellectual, artistic, technological, and physical potential to become a productive member of our global society.

Shooting for the Stars!

School Shield

              Student handbook

       2014 - 2015 Bus Routes

    School Supplies

Free and Reduced Forms Link

Families needing summer food assistance. Please call the Hunger Hotline. 1-866-3HUNGRY

Health Accessment Record Forms

A Look Ahead...

Summer 2014

July 17 - Kindergarten Screenings - Please call our office to schedule an appointment for your upcoming kindergartener

August 6 - Students' First Day of School

©Copyright 2014 | All Rights Reserved | Dean Road Elementary School | 335 S Dean Road | Auburn, AL 36830 | FAX: 334-887-0599 | PHONE: 334-887-4900


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modelSPORT magazine on DVD - Issue DMS0601

Mfn. No: DMS0601

Availability: In Stock. Ships within 24 hours.

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00:01:30 workBENCH
Painting the B-17
00:15:00 aboutENGINES
00:29:30 workBENCH
Fun World 3D
00:53:00 flightLINE
01:04:00 Sean McMurtry
01:08:00 Christophe Paysant-Le Roux
01:14:30 BME 110
01:19:00 Roland Matt
01:25:00 innerVIEW
Chip Hyde
01:29:00 Chip Hyde
01:26:00 Quique Somenzini
01:42:00 Jason Shulman
01:45:00 Mike McConville
01:54:00 newPRODUCTS
Falcon's Aero-Star 40 ARF trainer and Sullivan S753 SkyWriter smoke pump system
DMS0601_56k.wmv - 321k, play a 71 second streaming-sample for dial-up connections.
DMS0601_512k.wmv - a 4435k sample, for broadband internet connections.

workBENCH: "The trick to making a B-17 model look real lies in making the aluminum paint simulate the aluminum panels of the real thing." said Larry, while sharing in his unique way the hard won tips and tricks garnered in a lifetime of modeling.
aboutENGINES: When the FAI took their hands off engine displacements by specifying airframes instead of engine sizes, they unleashed a horsepower race. With the introduction of the friendly and powerful YS's FZ140-S (Sport), the trickle down benfits of competition have arrived for sportsmen everywhere!

Sullivan's Double Screen Fuel Filter installed

workBENCH: So much fun it raises the question, "Is it legal?" The neat World Models Fun World 3D features plug-in wing panels to transform the nearly 6-foot span into quite a manageable package. This airplane is perfect for learning 3D maneuvers and is both aptly named and a blast to fly!

World Model's Fun World 3D ready for the field

flightLINE: What makes the 21 best R/C model pilots in the world converge on Las Vegas, NV? Why, money, of course . . . and lots of it too! The combined prize package totaled more than $180,000, while the winner walked off with a cool 50,000 bucks! That's more money than any other aviation event in the world, model or full scale! Appearing by invitation only, these pilots made awesome flights seem routine.
newPRODUCTS: Falcon Trading Aero-Star 40 ARF trainer & Sullivan's SkyWriter smoke system.


WARC-Truncated: length

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Home Radio Road

Which tuner to get and getting the most from it. Thank God, for the radio!

"New" NAD 4020a

I made a post the other day in the vinyl forum and somebody mentioned listening to the radio and it got me thinking about getting a tuner even though I hardly ever listen to the radio. I have a tube system and thought that if I got a tuner it would have to be a tube tuner.

Well, I hit the thrifts and didn't find any tube tuners (of course) but I saw a NAD 4020a tuner. I decided to plug it in and in the middle of the store with out an antenna attached to it it pulled in a stereo signal. I figured that was a good sign and decided to purchase it.

I took it home and plugged it in and tuned in the classical station. It sounded pretty good but I was getting quite a bit of background hiss. I found my Terk AF-1 antenna and attached it to the tuner and it sounds great.

Now I can listen to the radio while I continue my search for a tuner with tubes in it.

This post is made possible by the generous support of people like you and our sponsors:
  Dynaco Doctor

Topic - "New" NAD 4020a - ChadHahn 20:25:53 10/09/11 (9)

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Eclipse SIR-ECL1 SIRIUS Radio Receiver Satellite Radio Receivers

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Connect the SIRIUS SIR-ECL1 radio to your compatible Eclipse stereo, and start enjoying SIRIUS Satellite Radio in the car. This in-car radio comes with the roof-mount antenna you need for reception and the cable you need to connect the radio to your stereo. The radio''s low profile makes it easy to install it in a convenient spot in your vehicle. A pass-through connection allows you to use the satellite radio and an Eclipse CD changer simultaneously.

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sound level meters

We're looking to buy a sound level meter to monitor background noise during human auditory psychophysical experiments. Ideally we'd like to find something that lets us set the centre frequency and bandwidth around the freq that we are testing at (eg 1kHz), can get a real time display and also gives us the data (in dB) to load into our computer. Does anyone know of a suitable instrument?

thanks a million

Penny Hill

Research Student
Dave Moore's Group
Oxford University

01865 (2)72495


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Monday, January 21

9:30 AM - 2:00 PM -College Democrats Inauguration Day
A viewing of President Barack Obama's Inauguration Day events
Evald Great Hall

4:00 PM - All LSFY Faculty Meeting
Wilson Center

5:00 PM - Faculty Research Proposals DUE to Mary Koski

6:30 PM - Augustana College High School Honor Band Finale Concert
Centennial Hall

7:00 - 9:00 PM - Darwin Week: Nature Reads
Professors and students will share their favorite accounts of the beauty of nature i nthese literature readings
Olin 304

7:00 PM - Augustana Film Series: Rome: Season 1 Episode 8: Caesarion"
Olin Auditorium

Tuesday, January 22

11:30 - 11:50 AM - Tuesday Reflection - Darwin Week - "Faith and Science" Workshop
Ascension Chapel, Founders Hall, 2nd floor

3:00 - 4:00 PM - Blue and Gold Certification: Google Drive
RSVP to Wendy Ramsdale, x8092
Olin 110

4:15 - 4:45 PM - Sign Language Table
This table is open to all levels. The group primarily converses in signed English, but those with knowledge of American Sign Language are encouraged to come
Brew by the Slough, 4th floor, Tredway Library

6:30 PM - Voice Seminar
Larson Hall, Bergendoff

8:00 - 9:00 PM - The Salon
Robert Tallitsch (Biology) (topic TBA)
Andreen Hall, Red Room

8:00 PM - General Student Recital
Wallenberg Hall, Denkmann Building

Wednesday, January 23

9:00 AM - 3:45 PM - SYMPOSIUM DAY - Keynote address "Healing the Relationship Between Humanity and the Environment: We Each Have a Role" presented by Molly Steinwald, Director of Science Education and Research, Phipps Conservatory and Botanical Gardens in Pittsburgh, Pennsylvania

9:00-9:45 Advising Group Discussion
10:00-11:00 Keynote AddressI / Concurrent Session I
11:15 - 12:15 Concurrent Session II / Lunch on your own
12:30 - 1:30 Keynote Address II / Lunch on your own
1:45 - 2:45 Concurrent Session III
3:00 - 3:45 Advising Group Meetings

Symposium Day Moodle Site

3:00 - 4:00 PM - Blue & Gold Certification: Beginning Power Point
RSVP to Wendy Ramsdale, x8092
Olin 109

5:00 - 6:00 PM - After Hours Poetry & Prose
Sorensen Break Room

7:00 - 8:00 PM - Discussion/Lecture: Paul Olsen will speak on "In the Beginning..What? Darwin and the Romantic Poets"
Olin 304

7:00 - 9:30 PM - 18th Annual Hispanic Film Festival: "Los viajes del viento (The Wind Journeys)"
Not rated. Free of Charge
102 Hanson Hall of Science

Thursday, January 24

9:00 - 10:00 AM - Coffee and Conversation
Community Engagement Center

7:00 PM - 12th Annual Augustana French Film Festival - "Les femmes du 6ème étage (The Women on the Sixth Floor)"
Film is in French with English subtitles
Free admission
Olin Auditorium

7:00 - 9:00 PM - Darwin Week Documentary: "180 Degrees South"
102 Hanson Hall of Science

Friday, January 25

4:30 PM - Deadline to submit nominations for Hasselmo Prize for Academic Pursuit to Margaret Farrar

4:00 PM - Friday Conversation - "E-Portfolios" presented by Farah Marklevits
3:30 PM - Refreshments
Wilson Center

6:00 - 9:00 PM - Augustana Sights and Sounds
The Sixth Annual Augustana Sights and Sounds exhibition will feature photography from Augustana students and local high school students, in addition to video narratives by Augustana Video Bureau
Bucktown Center for the Arts, 225 E. 2nd Street, Davenport, Iowa

7:30 PM - The Bock Eye (theatre)
Augustana College will present the world premiere of The Bock Eye, a bold and bawdy postmodern adaptation inspired by the Greek tragedy The Bacchae by Euripides. Written by American playwright Tommy Smith, The Bock Eye is a blend of old and new - a retelling of an ancient story, but with a strong contemporary attitude. The production will be directed by guest director Saffron Henke, who also directed the 2011 production of the Metamorphoses at Augustana.
As is the case with the classic Greek play that inspired it, The Bock Eye deals with adult themes and contains language that is not appropriate for children.$11 for adults or $9 for students and seniors
Potter Theatre, Bergendoff Hall

8:00 PM - Faculty Recital - Janet Stodd, flute
Featuring an alumni flute quartet: Elise Croner, Robin Gravert, Amy meier, and Janet Stodd performing "Harmony in Blue and Gold" by Eric Ewazen, and "Divertissement" by Johann Bach, "Sonata No. 1" by Eric Ewazen and "Airheads" by Gary Schocker.
Wallenberg Hall, Denkmann Building

Saturday, January 26

5:00 - 8:00 PM - Parents' Night Out  CANCELLED
Carver Center

6:00 - 9:00 PM - Darwin Week: Chuckfest
Musical celebration of life on Earth and the work of Charles Darwin
Loft, College Center, 3rd floor

7:30 PM - The Bock Eye (theatre)
$11 for adults or $9 for students and seniors
Potter Theatre, Bergendoff Hall

8:00 PM - Upright Citizens Brigade
The UCB Tour Co. show lasts about 90 minutes and consists of "longform improv." The  cast is picked from the best improv comedians in New York City and Los Angeles. UCB has brought audiences Amy Poehler, Horatio Sanz, Rob Corddry (The Daily Show), Ed Helms (The Daily Show, The Office), Rob Riggle (SNL, Daily Show), Paul Scheer and Rob Huebel (Best Week Ever), and many many more.
$10, free for Augustana students
Centennial Hall

Sunday, January 27

1:30 PM - The Bock Eye (theatre)
$11 for adults or $9 for students and seniors.
Potter Theatre, Bergendoff Hall

Volume 10, Issue 19 - January 21, 2013

The Faculty Research Committee solicits proposals for the Faculty Research Fund

Nature of this research fund:

Guidelines and selection criteria for the research fund (see Faculty Handbook for details):

1)      Five page maximum proposal including itemized budget

2)      Proposal must include:

3)      Criteria used by the committee to evaluate proposals: eligibility, clarity of presentation, appropriate budget prediction, prospects for publication and public attention, applicant's qualifications, inclusion of student researchers (student researchers are not required, but are often favorably reviewed)

4)      Expectation for funded work:

Please send your proposal by email attachment if at all possible (otherwise, six hard copies) by 5 PM on Monday, January 21, 2013 to Mary Koski in the Dean's Office.  Awards will be announced by February 11, 2013.   Direct questions to any member of the committee: Arbesú, Dan Conway, Paul Croll, Nathan Frank, Margaret Morse, or Eric Stewart.


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Augustana College printing logo

September 3, 2011

2011 Season - Shutout over Grinnell opens season

Sophomore Adam Wilson scored the only goal Augustana would need in the Vikings' season opener on Saturday, September 3 at Grinnell. He tallied at 35:48 in the first half as Augustana defeated the Pioneers 2-0.

GRINNELL, Iowa - Coach Brenton Joseph’s men’s soccer team got its season off on the right foot, hitting the road Saturday, September 3 and coming away a 2-0 victor over Grinnell. The Vikings are off to a 1-0 start in 2011, while the Pioneers drop to 1-1.

Sophomore midfielder Adam Wilson (Plainfield North HS, Plainfield, Ill.) became the first Viking this season to dent the scoreboard when he found the net in the 36th minute on an assist from freshman Chandler Brooks (University HS, Bloomington, Ill.). Sean Fidlow (Carmel Catholic HS, Gurnee, Ill.), a second team All-CCIW selection a year ago, made it 2-0 on an unassisted goal in the 64th minute.

Meanwhile, the Viking defense, led by Cory DeGrave (Fremd HS, Palatine, Ill.), Jason Beckus (Neuqua Valley HS, Naperville, Ill.) and Michael Buric (Notre Dame Prep, Scottsdale, Ariz.) was not allowing the Pioneers much in the way of scoring opportunities. Grinnell managed just three shots in the game, only one of which was on goal. Augustana goalkeeper Tyler Cowherd (Bettendorf HS, Bettendorf, Iowa) made the save on that shot and went the full 90 minutes for the shutout.

Augustana held a 15-3 edge in shots for the game. Nine of the Vikings’ shots were on goal. They also had an 8-3 advantage in corner kicks.

Joseph’s squad is next in action on Sunday, September 4, when it will host another Iowa Intercollegiate Athletic Conference opponent—Cornell—at 3:30 p.m. The Rams will be the opponent in the first men’s game ever at Thorson-Lucken Field.


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Wild About The Necklace

Animal prints are always in style. This pendant has been one of our most popular.

Susie Henderson, Auntie's Beads Owner

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William Hill CrownBet

The Big Story On The Back Page

The Big Story On The Back Page

With a name of Back Page Lead, it was always meant to attract attention. Strangely however, this daughter of Brett Lee has done the contrary and raced very successfully for the best part of 18 months without any real fanfare.

Owned by Geoff Slattery and bred by AFL champion Tony Lockett, Back Page Lead is part of a tremendous family. The Brett Lee x Wave To Tammy litter has produced 6 individual city winners including Au Revoir, Exclusivity and Unequivocally. Wave to Tammy herself was a super bitch based in NSW, and was out of Rumble Spirit; the famous mother of Collide and Collision amongst others, while boom sprinter Renegade Chief sits closely in the family tree via another Rumble Spirit bitch, Teeze.

Without delay, Back Page Lead began its career in glory as it was successful at attempt number one in July 2011 with a maiden win at Sandown. The modest time of 30.42 didn’t suggest the makings of a champion, but would be the start of a long career for this true bred-and-butter dog.

Never straying from the metropolitan surroundings of Melbourne in its early part of its career, it only took the greyhound seven starts to find its second victory over the 600m in 35.74. Her form started to wain as connections tried the 700m journeys before a return to the sprint trip saw a 30.56 win at The Meadows – one that looks good in hindsight considering the feats of the second dog, Katie Merry.

Greener pastures beckoned however, and Back Page Lead was sent to Tassie and the kennels of Mick Stringer in December 2011. Not for the first time, the greyhound took one attempt to make an impression; a 29.92 win around Launceston was a good way to debut in its new home.

Over the next year, Back Page Lead would become one of the Apple Isle’s most versatile dogs, amassing multiple wins across all three tracks. While never improving that 29.92 set on debut around Mowbray’s sprint trip, she did win over the 600m in 35.33m, as well as three wins over both the 461-metre (26.29 PB) and 599-metres (34.38 PB) at Hobart and both of Devonport’s 452 and 580 metre courses (25.72 & 33.32 best).

Fast forward to late 2012, and a return to the mainland was arranged. The new found confidence found in our southernmost state would be put to the test, when new trainer Steven White would send it around the challenging NSW circuits, where most readers would become familiar with the 27kg chaser.

True to form, the travel didn’t faze the black flyer one bit, winning second up at Bulli over 515m in a Best-of-night 29.40. Increasing his already impressive record and ability to win over a massive variety of tracks and distances, Back Page Lead would now win at Richmond’s 535m in 30.88 and in the big smoke of Wentworth Park, running 30.23 over 520m.

Going from strength to strength, a chance at Group glory beckoned recently when it contested the Group 2 Summer Cup at Wenty, ironically running second in the heats to one of its main rivals from the Tasmanian days, Bell Haven. Qualifying for the final, she would eventually go down behind Irma Bale, placing third in one of his career best performances.

As recent as last Saturday, Back Page lead would take out the 720m event at Wentworth Park as even-money favourite, taking its total record to 19 wins and 17 placings from 57 starts. Those 19 wins have been strewed across three different states, eight different tracks and 14 different distances, making it one of Australia’s most honest, versatile, and hence underrated chasers. A continuing career of such merit has flown under the radar for so long; an unusual occurrence, for a chaser whose name is destined for the spotlight.

Peter Oliver

About Peter Oliver (All Articles)

Peter Oliver writes exclusively for Australian Racing Greyhound, combining his love of the longtails with a Bachelor of Arts (Communication and Media Management) Degree completed at the University of South Australia. His knowledgable contributions to the site are far reaching, with opinions and coverage of the South Australian, Western Australian, Victorian and Tasmanian greyhound scenes.


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Severe Complicated Malaria

Category: Education

Presentation Description

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Presentation Transcript

Slide 1:

Severe & Complicated Malaria Severe & Complicated Malaria 1 Prepared by: Dr. Rajsi D. Buch Dr. Ankur V. Tiwari

Slide 2:

“Now World is in hands of DOCTORS” O OBJECTIVES 1. Introduction 03 2 . Review 04 3 . Case : Description & discussion Case 1 31 34 Case 2 36 38 Case 3 39 42 Case 4 44 46 Case 5 48 51 Case 6 52 54 4 . Summary 56 5 . Acknowledgement 57 6 . Bibliograohy 58 ”’’ 2

Slide 3:

Slide 4:

Definition of SEVERE MALARIA by the working group of World Health Organisation (WHO) One or more of the following major criteria + the presence of asexual parasitaemia defines severe malaria. Major criteria: 1. Cerebral malaria (unrousable coma not attributable to any other causes). 2. Severe anaemia (haematocirt < 15% or haemoglobin < 5 g/dl). 3. Acute renal failure (urine output < 400 ml/ 24 hours in adults, or <12 ml/Kg/24 hours in children, failing to improve after rehydration; & s.creatinine >265μmol/l i.e. >3 mg/dl). 4

Slide 5:

4. Pulmonary oedema or Adult Respiratory Distress Syndrome (ARDS) 5. Hypoglycaemia (whole blood glucose < 2.2 mmol i.e., <40 mg/dl). 6. Circulatory collapse, shock, hypotension (systolic blood pressure < 50 mm Hg in children aged 1-5 years or < 70mm Hg in adults), with cold, clammy extremities. 7. Spontaneous Bleeding/Disseminated Intravascular Coagulation(DIC). 8. Repeated generalised convulsions (more than two episodes in 24 hours). 9. Acidaemia (arterial pH < 7.25) or Acidosis (plasma bicarbonate < 15 mmol/1). 10. Macroscopic haemoglobinuria. 5

Slide 6:

Minor criteria [newly added in 2000] 1. Impaired Conciousness. 2. Hyperparasitaemia (> 5% of RBCs are parasitised). 3. Hyperpyrexia (rectal temperature > 400°C). 4. Jaundice (Serum bilirubin > 50 mol/1 or > 3 mg/dl.). 5. Severe prostration. 6

Slide 7:

Others: 1. Fluid and electrolyte imbalance. 2. Vomiting of oral drugs. 3. Complicating or associated infections. 4. Other indicators of poor prognosis:- → leucocytosis → high CSF lactate and low CSF glucose → raised aminotransferases → low antithrombin III levels → peripheral schizontaemia → papilloedema / retinal oedema 7

Slide 8:

Summary of differences in the clinical features of severe malaria in adults and children Frequency of occurrence 8

Slide 9:

1. Cerebral malaria - clinical The most well-known severe manifestation of malaria Defined as: -unarousable coma persisting for more than one hour -with asexual forms of P. falciparum in the peripheral blood -other common causes of encephalopathy excluded* * None of the clinical features are pathognomonic, malaria parasitaemia is common in people living in endemic areas and coma may complicate many illnesses. Therefore, a clinical diagnosis of cerebral malaria is made only after other common causes of coma (e.g. meningitis) have been excluded. 9

Slide 10:

• Occurs most commonly in young children although non- immune adults are also at risk • Cerebral malaria can rapidly progress to death, even with appropriate treatment. Case fatality is between 20-30%. • In survivors, resolution of coma usually occurs within 1-2 days in children and within 2-4 days in adults but may be complicated by neurological sequelae in ~5% adults and >10% of children. The illness may start with drowsiness and confusion and then progress to coma. The loss of consciousness is often preceded by repeated convulsions. Retinal haemorrhages may be seen on fundoscopy. 10

Slide 11:

Cerebral malaria - pathophysiology The exact pathogenesis of cerebral malaria is not well understood. It is believed to result from sequestration of parasitised red cells in the small blood vessels in the brain. The consequences of this include: reduced cerebral blood flow cerebral hypoxia release of cytokines which in turn induce the release of nitrous oxide, a known depressor of consciousness. A young girl with cerebral malaria. Note the abnormal, decerebrate posturing Sequestration of parasitised red cells in different tissues probably underlies most severe manifestations of malaria A 3 year old boy with impaired consciousness, grimacing and marked extensor posturing of the arms 11

Slide 12:

2. Severe anaemia Defined as: - A haematocrit of <15% or -Haemoglobin concentration <5 g/dl. Occurs commonly in young children and pregnant women. Pathology Marked pallor in an African child with severe anaemia due to P. falciparum infection Bone marrow: Dyserythropoietic changes are prominent. Macrophages contain pigment and erythrophagocytosis may be seen. Iron is usually in plenty. Platelets & WBCs are usually normal. 12

Slide 13:

Spleen : Often dark from malarial pigment, enlarged, soft and friable. There is reticular hyperplasia. Recurrent malaria is associated with hard, fibrous splenic enlargement. Pathogenesis 1. Obligatory destruction of RBCs containing parasites at merogony. 2. Accelerated destruction of non-parasitised RBCs, parallels disease severity. 3. Bone marrow dysfunctions – reticulocyte count is low in acute phase. 4. Lowered threshold for splenic clearance of abnormal erythrocytes. Red blood cell survival is decreased. 5. Decreased concentrations of IL-10 and increased concentration of TNF alpha. 13

Slide 14:

Haptoglobin is a marker of haemolysis. Haptoglobinaemia may be considered as a useful indicator of falciparum malaria. Many patients require urgent transfusion. The condition may be rapidly fatal when blood transfusion is delayed. Blood Transfusion 14

Slide 15:

3. Acute Renal Failure The kidneys are often slightly swollen. Tubular abnormalities consistent with acute tubular necrosis (ATN) are seen. Sequestration in glomerular capillaries, mesangial endothelial cell proliferation, and immunoglobulin deposits may be seen. Cortical necrosis never occurs. When there is fulminant presentation of ARF with oliguria, there is high incidence of hepatic dysfunction (jaundice and bleeding tendency), metabolic acidosis, and pulmonary edema. 15

Slide 16:

Blood pressure is usually normal. Mild proteinuria may be there but urinary sediments are unremarkable. In subacute presentation with oligura/polyuria, serum creatinine rises over a period of days producing uraemic complications requiring dialysis or there is a gradual resolution. In survivors, urine flow resumes in 4 days. Creatinine returns to normal in 7 days. In certain studies, 30% of ARF was due to malaria. Renal failure may be associated with haemoglobinuria (Black water fever). Nephrotic syndrome can occur with P. falciparum. 16

Slide 17:

4. Acute pulmonary oedema This is a grave and usually fatal manifestation of severe falciparum malaria and occurs mainly in adults. Hyperparasitaemia, renal failure and pregnancy are recognised predisposing factors and the condition is commonly associated with hypoglycaemia and metabolic acidosis. Pulmonary edema results from increase in pulmonary vascular permeability which is not reflected in other vascular beds Cause of increased permeability is not known. Acute pulmonary oedema, developing shortly after delivery in a woman with severe P. falciparum malaria 17

Slide 18:

Pulmonary oedema/ARDS can develop at any time in falciparum malaria, even after several days of antimalarial treatment, and even in otherwise uncomplicated vivax malaria. It is particularly common in pregnant women, but rare in children. It may be difficult to distinguish from aspiration pneumonia. Heart sounds, pulmonary capillary wedge pressure (PCWP), and central venous pressure (CVP) are usually normal. The chest X-ray shows increased interstitial shadowing. 18

Slide 19:

5. Hypoglycaemia Blood sugar <2.5 mmol/L Increases the risk of mortality (40%) and sequelae in children with cerebral malaria; may present with convulsions or a deterioration in level of consciousness. Results from a combination of factors: 1. Increased peripheral requirement of glucose consequent upon anaerobic glycolysis. 2. Increased metabolic demands of febrile illness. 3. Obligatory demand of parasites. 19

Slide 20:

4. Failure of hepatic gluconeogenesis and glycogenolysis (parasites consume upto 70 times as much glucose as uninfected cells ). 5. Quinine stimulated insulin secretion from pancreatic beta cells. Hyperinsulinaemia is balanced by decreased tissue sensitivity. Hypoglycaemia contributes to nervous system dysfunction. ‘Malaria induced hypoglycaemia’ is often present at admission and response to glucose is unimpressive, while ‘quinine induced hypoglycaemia’ usually develops 24 hours after treatment, and response to glucose administration is dramatic. 20

Slide 21:

6. Circulatory collapse, shock, “algid malaria” Systolic BP < 50 mmHg in children and < 80 mmHg in adults defines hypotension/shock. Patient with severe malaria can develop sudden hypotension & become shocked. This is “Algid Malaria” The patient can have cold, clammy, cyanotic skin, peripheral vasoconstriction, and rapid feeble pulse with core/skin temperature difference of ≥ 10° C. 21

Slide 22:

In some cases there is septicaemia. In the majority, blood cultures are negative. Hypotension usually responds to saline infusions and ionotropes, but these therapeutic measures could provoke pulmonary oedema. The overall mortality is high. Circulatory collapse can also be seen in patients with pulmonary oedema, metabolic acidosis, GI haemorrhage, and ruptured spleen. Dehydration and hypovolaemia could also contribute to hypotension/ shock. 22

Slide 23:

7. Spontaneous Bleeding Coagulopathy & thrombocytopenia Severe haemorrhage is seen in 5% of severe malaria. There is accelerated coagulation cascade activity with accelerated fibrinogen turnover, consumption of antithrombin III, and increased concentration of fibrinogen degradation products (FDP). RBCs containing parasites and released cytokines are procoagulant. Prothrombin time (PT) and Activated partial prothrombin time(ApTT) are prolonged. Thrombocytopenia is caused by increased splenic clearance. Platelet turnover is increased. Role of platelet bound antibody is controversial. 23

Slide 24:

The patient may develop bleeding gums, epistaxis, petechiae, subconjunctival haemorrhages. Significant bleeding, malena, and haemetemesis occurs in < 10% cases. This is more common in non-immune individuals in the temperate zone Epistaxis 24

Slide 25:

8. Repeated Generalised Convulsions 25 ≥ 2 convulsions in 24 hours

Slide 26:

ECG & EEG recordings of patient having Repeated Generalised Convulsions 26

Slide 27:

9. Metabolic Acidosis This may result form renal failure, but more commonly there is a primary lactic acidosis (Type B). Arterial, venous, capillary, and CSF concentration of lactate increases in proportion to the severity. Lactic acidosis results from : 1. Anaerobic glycolysis due to microvascular obstruction. 2. Failure of hepatic and renal lactate clearance. 3. Production of lactate by the parasite. Lactate levels rise after generalised convulsions. Hyperventilation (Kussmaul breathing) with a clear chest on auscultation suggests metabolic acidosis 27

Slide 28:

Venous lactate concentration at 4 hours after admission to hospital is the BEST PROGNOSTIC INDICATOR in severe malaria. pH compared with pH chart pH strips & urine sample Blood sample in vacutaineers 28

Slide 29:

10. Haemoglobinuria or “Blackwater Fever” This results from massive intravascular haemolysis. The condition presents with severe pallor, jaundice and passage of dark urine due to haemoglobinuria. It may be associated with acute renal failure. A 3 year old boy with severe anaemia Typical dark urine of (Hb 3.3 g/dl) and dark urine Haemoglobinuria on (shown in the container) Day 0 & cleared by Day3 29

Slide 30:

Malaria in pregnancy More than 45 million women become pregnant in malaria endemic areas each year. Common adverse effects of malaria in pregnancy : Maternal anaemia Stillbirths Premature delivery and Intra-Uterine Growth Retardation (IUGR) result in the delivery of Low Birth weight (LBW) infants The WHO now recommends Intermittent Preventive Treatment (IPT): the administration of anti-malarial drugs (e.g.sulphadoxine-pyrimethamine) during antenatal care whether or not women show symptoms. IPT has been shown to substantially reduce the risk of maternal anaemia in the mother and low birth weight in the newborn. Previously, chemoprophylaxis (e.g. With chloroquine) was recommended for all women living in malaria endemic areas. 30

Slide 31:

Case 1 Description: A 30 year old male was admitted to Dhiraj General Hospital with chief complaint of -Abdominal pain in para-umbilical region since 4 days -High grade fever with chills since 3 days -loss of appetite since 2 days -Constipation since 2 days On elaborating history of present illness, he told that pain was dull aching & aggravated by movements. Also fever showed step-ladder pattern with peak at afternoon. Fever was accompanied with chills & no rigors. He gave past history of heavy alcohol intake since many years. 31

Slide 32:

Examination (at the time of addmission) revealed: significant pallor, high-grade fever, temp 102°F, mild icterus. Tenderness present over umbilical & right hypochondriac region with Liver enlarged about 2 fingers & guarding present. No h/o nausea & vomitting. Investigation: P/S- P.faciparum + P.vivax Haematology- Microcytic Hypochromic Anemia Hb- 7.2gm/dl Thrombocytopenia Raised Prothombin Time(PT), 17 sec Urine- pale yellow Liver Function Tests(LFT)- altered S.bilirubin-elevated, Alkaline Phosphatase(ALP)-244 32

Slide 33:

Diagnosis: Severe Malaria Malaria with mild Jaundice, Severe Anemia, Thrombocytopenia Ring forms or trophozoites; many red cells infected – some with more than one parasite 33

Slide 34:

Discussion: It is clearly evident from the history, examination & investigations that pt. is suffering from malaria. It is diagnosed to be P.falciparum & P.vivax both. He is also suffering from mild Jaundice, severe malaria & Thrombocytopenia. Jaundice would have been precipitated due to hepatic dysfunction as a result of superinfection of malaria alongwith chronic Alcoholic Liver Disease (ALD). The condition is being worsened as a result of superseded Severe Anemia & Thrombocytopenia due to hemolysis of RBCs & platelets because of impaired liver functon and sequestration of parasitised blood cells. 34

Slide 35:

He has shown good response to the line of treatment. He’s been supplemented with Quinine & Primaquine therapy for radical treatment of malaria. Also antibacterial cover has been provided with Amoebicide. Besides these health management provided comprised of Blood Transfusion on 5th day, vit.B12, folic acid & iron supplementation. As a result of above management pt. recovered by 8th day & his symptoms subsided. 35

Slide 36:

Case 2 Description: a 34 year old primigravida at 22 weeks of gestation was transferred to hospital with fever (temp-39.8°c), right abdominal discomfort, nausea, vomiting and rapidly worsening hemolytic anaemia, severe thrombocytopenia and raised concentration of aspartate(AST) & alanine(ALT). 3 days earlier, she had been admited to a local hospital with similar symptoms. At that time Hb% was 8.8gm%, WBC - 6700cumm, platelets – 95 Thousand, AST- 64 IU/L, ALT- 44 IU/L. Abdominal USG was normal and no signs of foetal distress detected. 36

Slide 37:

On admision, the patient complained only of fatigue and physical examination revealed vague abdominal tenderness. BP was 120/62mmHg, Pulse-110 bpm, temp- 37.4°C. On day 3 after admision, CRP was high (210mg/l, normal <10mg/l), prothrombin time – 17s (prolonged). Blood cultures remained sterile. Trophozoites of P.falciparum in P/S 37

Slide 38:

Discussion: The combination of haemolysis, high concntrations of AST and ALT, and low platelet count suggested HELLP (haemolysis,elevated liver enzyme and low platelets) syndrome. Her blood smear was also taken. The smear was positive for P.falciparum and the initial parasite count was 20%(corresponding to 570000 parasites per µL of blood). Treatment with quinine was started immediately. After 24 hrs, exchange blood transfusion was started with rapid reduction of parasite density and eventually complete recovery of the patient. Treatment with 1 wk of clindamycin was given. In about 4 months the patient gave birth to a healthy daughter. 38

Slide 39:

Case 3 Description: A 12 year old child presented with high fever for 5days followed by a sudden development of severe jaundice and drowsiness. She was well before 5 days. Then she started with high fever for which the local doctor treated her. The details of her treatment were not available. Within two days of development of jaundice and drowsiness, she was hospitalised for the same. There was no history of anorexia, nausea or vomiting, nor was there a history of clay coloured stools or high coloured urine. On direct questioning there was oliguria, though the parents attributed it to poor intake over last 2 days due to drowsiness. No significant past or family history. 39

Slide 40:

Physical Examination Well built and properly nourished. Temp- 102 F Pulse- 160 / min RR – 35/min BP – 90/55 mmHg Markedly Pale. Deep Icterus. Mild edema feet. Raised JVP. No ecchymosis or purpura. Liver 7cm +, firm, tender, hepatojuguler reflux present. Liver span 10cm. No ascites. Spleen 4cm+, firm. No engorged abdominal veins. CVS- Soft systolic functional murmur. CNS- Drowsy No localising signs. 40

Slide 41:

Investigations Hb- 4gm% WBC- 10000/cumm P 60 L 32 E 5 M 3 Platelets- 75000/cumm Peripheral smear shows trophozoites of P.falciparum. Parasitic index 5% Serum Bilirubin – 38mg% Direct 28mg% ALT- 180u/dL Serum ammonia normal. Blood sugar normal. Prothrombin time(PT) normal. Serum proteins normal. Blood urea – 120mg% Serum creatinin- 3.5mg% Serum electrolytes normal. Trophozoites of P.falciparum 41

Slide 42:

Discussion: It is evident in the history that, Jaundice in this child has appeared after 5 days of high fever. Hence it is likely that primary illness which has caused high fever, led to a secondary hepatic involvement coming on after a few days or it is a complication of drugs taken for primary illness. Febrile illnesses with subsequent liver involvement include typhoid fever, malaria & leptospirosis. On examination, though a deeply jaundiced child with hepatic failure can bleed & therefore present with significant pallor, such bleeding is obvious and has not been reported in this child. Therefore sudden developement of severe pallor, severe enough to push the child into cardiac failure, along with jaundice, suggests acute hemolysis. However, even in acute hemolysis, jaundice is rarely severe; the severity of the illness favours the possibility of falciparum malaria. 42

Slide 43:

Investigations suggest that the child has a multisystem involvement affecting the liver primarily, but also the brain and the kidney besides causing severe hemolysis. Drowsiness is not due to hepatic encephalopathy in view of the normal serum ammonia, blood glucose & prothrombin time, but may have resulted from cerebrovascular sludging due to malaria. Renal failure could also be a result of a similar pathology in the renal vasculature. Even though there is a hemolysis, the predominant bilirubin in falciparum malaria is direct bilirubin due to involvement of liver cells. The patient was treated with IV quinine & supportive therapy including packed cell transfusion. The serum bilirubin came down to 12mg% within the next 2 days, drowsiness improved and so also the urine output. The child made a complete recovery within next 5 days. Ref: Dr. Umesh Buch, Paediatrician 43

Slide 44:

Case 4 Description: One year old, 8.5 kg male child was hospitalized in a critically ill state with history of fever, breathlessness and excessive crying for two days. Child was in gasping state, had severe anaemia, congestive cardiac failure and moderate hepatosplenomegaly. Anterior fontanelle and neurological examination were within normal limits. Investigation revealed: Hb% - 4gm%, TLC - 6000/cumm, Peripheral blood film(PBF) – dimorphic blood picture with severe hypochromia, microcytosis, hypersegmented neutrophils and ring forms of plasmodium vivax. Platelet count was – 48000/ Liver and Renal function tests were normal. 44

Slide 45:

On the third day of hospitalization, child developed upper GI bleed, deterioration of sensorium and seizures followed by generalized hypertonia. Repeated PBF showed numerous gametocytes of P.vivax with severe thrombocytopenia(Platelet count going down to less than 20000). CSF findings were suggestive of Intracranial bleed. Optimal malaria antigen test was positive for P.vivax and negative for P.falciparum. CT scan head showed massive intracerebral bleed in right fronto-parietal region with communicating hydrocephalus 45

Slide 46:

Discussion: This case provides sufficient evidence that plasmodium vivax infection was complicated with cerebral manifestations in association with profound thrombocytopenia and massive intracranial bleed which latter on led to hydrocephalus. The child was treated with chloroquine,blood transfusions, diuretics, digitalis & antibiotics for aspiration pneumonia. 46

Slide 47:

Child was given platelet transfusions, steroids and anti- convulsants for recurrent seizures. In view of persistent parasitemia child was treated with iv quinine dihydrochloride for 10 days followed by primaquine for 5 days. Patient became afebrile but developed symptomatic hydrocephalus which required shunt surgery latter on. 47

Slide 48:

Case 5 Description: Four year old male child presented with history of fever, blood stained stools, vomiting for four days and altered sensorium with recurrent seizures for one day. Child was in shock and coma, was initially provisionally diagnosed and managed on the lines of shigellosis with encephalopathy. Investigations revealed: Hb-7.2gm%, TLC-10000/ Peripheral blood film revealed normocytic blood picture with moderate hypochromia, platelets were adequate and no hemoparasite detected. Urine examination, CSF and blood biochemistry was within normal limits. 48

Slide 49:

Child was treated with iv fluids, antibiotics, anticonvulsants and blood transfusions. He remained Febrile and persisted in encephalopathy after 2 weeks of antibiotics. OptiMAL malaria antigen test (delayed because of financial reasons) was positive for Plasmodium vivax and negative for Plasmodium falciparum. Fundus examination was normal. CTscan head revealed mild hydrocephalus. IV Quinine dihydrochloride was given then for 10 days followed by a single dose of Fansidar (sulfamethazone+ pyrimethamine) after which fever settled and sensorium improved. However, behavioural changes and headache persisted which necessitated acetazolamide. 49

Slide 50:

The features and course of illness suggested cerebral complications of Plasmodium vivax malaria. At follow up after 4 weeks child had improved in behaviour and headache had resolved. P.vivax in brain sample of person with cerebral manifestations 50

Slide 51:

Discussion: The second case had presented with gastrointestinal manifestations in the form of desentry, encephalopathy and hydrocephalus which improved on follow up without surgical intervention. Though the peripheral blood film did not show any haemoparasite, the OptiMal malaria antigen test was positive. This test detects the presence of plasmodium lactate dehydrogenase (pLDH); an enzyme produced both by the sexual and asexual forms of parasite. The presence of pLDH is revealed using monoclonal antibodies directed against isoforms of enzyme. 51

Slide 52:

Case 6 Description: A 40 yr old man, presented with high-grade fever, chills, malaise and headache of 3 day duration. The patient’s peripheral blood revealed a total leucocyte count of, with 52.2% neutrophils, 31.2% lymphocytes, 15.2% monocytes and 1.52% basophils. The platelets count was 3.54 lacs. The peripheral blood smear was exained after 2 hrs, which revealed a heavy parasitemia consisting of the ring forms, gamatocytes and ameboid trophozoites of P.vivax. In addition several filamentous microgametes were seen outside the erythrocytes. 52

Slide 53:

The finding was correlated with literature and confirmed to be Exflagellated microgametes of P.vivax. The patient showed good response to Chloroquine and primaquine therapy. Exflagellated microgametes of P.vivax 53

Slide 54:

Discussion: The patient received chloroquine and primaquine therapy. Three days later, a post-therapy follow up peripheral blood examination revealed a complete response to treatment with the absence of parasite. This is one of the rare cases of the presence of Exflagellated microgametes in human peripheral blood. Literature in standard medical textbooks mention that trophozoites, schizonts ad gametocytes of the malarial parasite are typically found in human blood and are useful for diagnosing and typing malarial infection. 54

Slide 55:

The remaining forms, like exflagellated microgametes, ookinetes and oocysts are found in the mosquitoes and are not expected to appear in the human blood. This is the first case to be reported of its kind from India, a country with many endemic areas for malarial infection ! 55

Slide 56:

56 Summary Malaria though one of the simplest diseases is one of the most life threating disease. This is due to malaria getting complicated with several ailments. Most of the complicated malaria is due to P.falciparum infection but some of them might also be due to P.vivax or both. We saw that how severe malaria can precipitate the complications of health. Presence of these complications is more severe in previously diseased & even more disastrous in Pregnancy. As seen in these cases Cerebral Malaria & Severe anemia, Thrombocytopenia & Jaundice are the most prevalent & life endangering complications. Quick, timely & adequate management can completely cure the patient

Slide 57:

57 Acknowledgement Our work, “Severe & Complicated Malaria” is dedicated to our families, who have been always encouraging us to take initiatives & do newer things; providing a strong support to us & enabling us to Aspire, Organise & Execute them. We salute u all, Mr. Vipin Tiwari Mr. Durgesh Buch Mrs. Vibha Tiwari Mrs. Dipti Buch Ms. Ruchi Tiwari Ms. Mansi Buch, Also we are thankful to our friends who have been always there for us & helped us to get going even when it was tough, Dr. Mansi, Dr. Shail, Dr. Hardik & Dr. Ridhima. Last but not least we want to thank our guides, Dr. Umesh Buch, Paediatrician Dr. JD Lakhani, Physician & HOD Medicine dept.

Slide 58:

58 BIBLIOGRAPHY 1. Association of Physicians of India (API) 2. Harrison’s Textbook of Medicine 3. Journal, Indian Academy of Medicine 4. Journal, Infectious Diseases 5. 6.

Slide 59:

A doctor whose breath smells has no right to medical opinion. ~ Martin H. Fischer A doctor must work eighteen hours a day and seven days a week. If you cannot console yourself to this, get out of the profession. ~ Martin H. Fischer Every disease is a physician. ~ Irish Proverb When you are called to a sick man, be sure you know what the matter is - if you do not know, nature can do a great deal better than you can guess. ~ Nicholas de Belleville Drugs are not always necessary. Belief in recovery always is. ~ Norman Cousins “Quotes” Thank You !

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Volkswagen Transporter van video review

22 Aug, 2013 11:15am

The Volkswagen Transporter is thoroughly tested in this video review, offering a great drive and cheap running costs.

The Volkswagen Transporter is now in its fifth generation, and this latest version is even better to drive and cheaper to run than ever, as we find out in this video review.

It comes in two body lengths and three roof heights, and all Transporters come with a handy side door that opens wide enough to fit a euro pallet through.

Optional extras include rails to secure loads to, a rubberised floor mat which provides grip, and you can either stick with the standard van doors or you can have an optional lift up tailgate.

The Transporter has a load bay volume of 5.8 cubic meters to 9.3 cubic matters, and payloads range from 740 to 1340 kilograms. All Transporters come with a 2.0-litre diesel engine, and you can now get a wide variety of power output ranging from 84bhp to 180bhp in the bi-turbo model. The Blue Motion version, Volkswagen claims, can return 44.8mpg and emits just 116g/km of CO2.

Overall, we think the Volkswagen Transporter is an extremely well-built van;  many go on to cover huge mileages and resale values are high, too. It's easy to drive, cheap to run, and there's an option of four-wheel drive. But, it's expensive to buy, you can't get secondary wide-angle mirrors and the lack of a full-length bulkhead really is an issue. Watch the video review to find out more.

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Next-Gen BMW 1 Series May Not be US Bound

Next-Gen BMW 1 Series May Not be US Bound

Available at dealerships across America, the BMW 1 Series may soon disappear from our shores.

Rather than a new version of the 1 Series you’re thinking of (the coupe and convertible currently on sale), the next-generation 1 Series will be a front-wheel-drive compact that was previewed in the BMW Concept Active Tourer.

It’s not the lack of sales for the current 1 Series that is deterring the German automaker from confirming that it’ll be US bound; but rather that it’s built in Europe and exporting it to America makes it expensive, along with the threat that it’ll cannibalize MINI sales.

The decision of importing the next-generation 1 Series from Europe will actually depend on how successful Mercedes-Benz and Audi are with their compact luxury models such as the CLA and A3.

SEE ALSO: BMW Concept Active Tourer Aims for Style, Efficiency

“Where we have the 1 Series close to the 3 Series in terms of the price ladder, what Mercedes and Audi are doing is giving more focus in the below-$30,000 price range,” said Paul Ferrailo, BMW’s head of product planning and strategy for North America. “We’re going to watch that and in the future—well, the battleground has now moved to this $30,000 price point. We’re working hard to take advantage of that market.”

Replacing the current 1 Series in the US will be the new 2 Series model, which will essentially be a next-generation version of the current car.

GALLERY: BMW Concept Active Tourer

[Source: Car and Driver]

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NHTSA Ends Investigation into Jeep Gas Tank Fires

NHTSA Ends Investigation into Jeep Gas Tank Fires

The National Highway Traffic Safety Administration (NHTSA) has ended its investigation into 2.7 million Jeep SUVs for gas tank fires without demanding a new recall.

“The agency has been in close communication with Chrysler and has no reservations at this time with their announced actions to move forward,” NHTSA said in a statement.

The American automaker had agreed to recall 1.56 million SUVs in June 2013 but stated that the fix wouldn’t address all the concerns raised by NHTSA. The investigation, which began in 2010, looked into the potential fire hazard with Jeep gas tanks. Chrysler has been adamant that its vehicles are safe and are at no higher risk than any other SUV on the road.

SEE ALSO: Chrysler Refuses to Recall 2.7 Million Jeep SUVs

“Consumers should have their vehicles serviced promptly once they receive final notification from Chrysler. NHTSA will continue to monitor consumer outreach as the recall process continues.”

The June 2013 recall has Chrysler installing trailer hitches that would protect the gas tank to 1992-1998 Grand Cherokees and 2002-2007 Jeep Liberty vehicles. NHTSA has cited reports of 51 deaths in rear-end accidents in which older Jeep gas tanks leaked and caught fire.

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