MedPrepOnline

Spot Diagnosis Series 2

2012-12-17T23:09:00.001+05:00

Pinealoma

The patient usually presents with paralysis of conjugate upward gaze and is known as

Parinaud's syndrome. There can be bilateral papilledema. Accommodation is intact. Absence of pupillary light reflex. This is due to lesion in superior colliculi.

Mnemonic for remembering muscle bands and their components

2012-12-16T20:26:00.000+05:00

I found it very difficult during my usmle prep to remember the components of various bands in a muscle fiber. Even after multiple reads and memorization I still could not recall it. All that changed when I came up with a simple mnemonic .

I act at 5am hence my sleepiness

I = I band

act = actin

at = A band

5 am = actin + myosin

hence = H zone

my sleepiness = myosin

Autosomal dominant diseases mnemonic with a visual covering major diseases

2012-12-11T19:37:00.000+05:00

Click on image to enlarge.

Preparing for exams involving Biochemistry and Genetics can be tough as plethora of facts needs to be committed to memory. This is especially true when you are preparing for your USMLE Step 1 exam. Hopefully, the following visual mnemonic will help ease down your memorization process for remembering major Autosomal dominant diseases.

If you commit this statement listed below in your mind with the image to help you guide through, you will never have a hard time recalling the major Autosomal dominant diseases:

Osler Family is Hyper because Mary Huntington Von Turbo Sphereing MEN Across Hill.

Osler-Weber-Rendu syndrome (Osler)
Familial hypercholesterolemia (Family Hyper)
Marfan's syndrome (Mary)
Huntington's disease (Huntington)
Von Recklinghausen's Disease (Von)
von Hippel-Lindau disease (Von)
Tuberous sclerosis (Turbo)
Hereditary spherocytosis (Sphereing)
Multiple endocrine neoplasias (MEN)
Achondroplasia (Across)
Hypokalemic periodic paralysis (Hill)
Autosomal dominant polycystic kidney disease (ADPKD)

The picture shows a young Mary Huntington sphereing a globe full of MEN across a hill and she appears to be winning or probably have just won (Von), which makes the Osler Family very mad and hyper. Also note that the whole sphereing event is hosted by the ADPKD foundation.

By the way, sphereing or zorbing is a recreational activity/sport of rolling a transparent plastic spherical orb with passenger(s) down the hill.

I made this mnemonic myself to recall the autosomal diseases effectively and quickly. It works like a charm for me. Hope it helps you too.

Spot Diagnosis Series 1

2012-12-09T00:38:00.004+05:00

.
.
.
.

Achalasia

This barium swallow is characteristic of achalasia. The esophagus is dilated proximally and distally “bird beak” is seen which is the smoothly tapered distal portion.

Mnemonic for innervation of baroreceptors

2012-12-08T18:26:00.000+05:00

Many at times students come across questions in USMLE regarding baroreceptors, their location and their innervation. At times questions focus on the loss of innervation and its resultant effects on the body and its very critical to remember which baroreceptors are innervated by which nerves.

Arterial baroreceptors are located in the aortic arch and the carotid sinuses of the right and left carotid arteries. The baroreceptors found within the aortic arch monitor the pressure of blood delivered to the systemic circuit, and the baroreceptors within the carotid arteries monitor the pressure of the blood being delivered to the brain.

The glossopharyngeal nerves transmits impulses from carotid sinuses whilst the vagus nerves transmits impulses from the aortic arch. A simple mnemonic to remember this is:

GLOSSY CAROTID VISITS AORTA IN VEGAS

Following drug is useful in the treatment of angina pectoris...

2012-12-06T20:14:00.000+05:00

Question: Which of the following drugs is useful in the treatment of angina pectoris?
a. Digoxin
b. Quinidine
c. Quinine
d. Salbutamol
e. Propranolol

Correct answer: (e)

Propranolol is a non-selective beta-blocker. It blocks beta-1 and beta-2 receptors. By blocking beta-1 receptors, it decreases the heart rate and leads to decreased oxygen demand by the cardiac cells which prevents angina from occurring.

Digoxin (a) increases contractility; hence, increasing oxygen demand and precipitating angina.

Quinidine (b) is a derivative of quinine (c) which is an antimalarial and has no role in angina. Itself it is a class Ia anti-arrhythmic that blocks Na+ channels and prolongs the action potential duration. It has no role in angina.

Salbutamol (d) is a beta-2 agonist and has no role in angina. Beta-2 receptors are present on the bronchioles.

A case of 36 year old with seizures and motor deficits

2012-12-04T22:05:00.004+05:00

Image Copyright of Radiological Society of North America

Question: A 36 year old male presented with seizures and motor deficits. MRI scan of his brain revealed a homogeneously enhancing mass in the frontal lobe. Histological examination of the mass revealed it to be a B cell lymphoma. The most useful investigation in this patient would be to test for?

a. Epstein-Barr virus
b. Cytomegalovirus
c. Herpes simplex
d. HIV
e. Respiratory syncytial virus

Correct answer: (d) HIV

Immunocompromised patients are found to have a primary CNS lymphoma and 90% of such lymphomas are associated with EBV infection. In the above stated causes, HIV is a common cause of immunodeficiency. EBV (a) itself does not lead to a primary CNS lymphoma unless the patient is immunodeficient in the first place.

Cytomegalovirus (b) or CMV is associated with retinitis and/or interstitial pneumonia. It is not associated with lymphoma.

HSV (c) and RSV (e) are not associated with lymphomas.

URLologist medical humor

2012-12-02T03:57:00.000+05:00

Acute Mountain Sickness and Acetazolamide

2012-12-01T21:54:00.000+05:00

Physical pain and loneliness processed in the same area of brain

2012-11-30T04:05:00.000+05:00

Did you know?

Psychological pain, grief, and loneliness may be processed by the same neural pathways as physical pain in an area called anterior cingulate cortex.

"Brain Scan Shows Rejection Pain." BBC News. BBC, 10 Oct. 2003. Web. 29 Nov. 2012. http://news.bbc.co.uk/2/hi/health/3178242.stm.

Internal Jugular Vein Tributaries with Mnemonic

2012-11-29T04:06:00.001+05:00

Question: A woman with follicular thyroid carcinoma was being operated for total thyroidectomy and resection of the internal jugular vein as tumor was intraluminal involving right internal jugular vein tributaries. All of the followings are the tributaries of internal jugular vein, EXCEPT:
1. Middle thyroid vein
2. Superior thyroid vein
3. Inferior thyroid vein
4. Veins from pharyngeal plexus
5. Inferior petrosal sinus

Answer: (3) Inferior thyroid vein is not part of the internal jugular vein tributaries. The inferior thyroid vein arises in venous plexus on thyroid gland and drains into the brachiocephalic veins.

This question simply requires a recall of factual knowledge. A mnemonic to remember the tributaries of internal jugular vein is given below:

"Medical Schools Let Confident People In"

From inferior to superior:
Middle thyroid vein
Superior thyroid vein
Lingual vein
Common facial vein
Pharyngeal plexus
Inferior petrosal sinus

The Murmur Conundrum

2012-11-25T20:38:00.003+05:00

Systolic or diastolic, that is the question.

Many have panicked during the ward rounds and / or during examinations when asked about which murmurs are systolic or diastolic . Various mnemonics are memorized by students which work for some of them but why do that when there is a simple concept behind it.

The simple way to determine as to which murmur is systolic or diastolic is as follows:

1. Always think about the ventricles when asked about murmurs.

2. Think of the outflow or inflow tracks for the blood, for example in systole the blood can leave the left ventricle via the mitral valve or the aortic valve and in diastole the blood can enter the left ventricle via the the same valves.

So keeping that in mind, aortic stenosis murmur would be systolic because blood will leave the left ventricle via the stenosed aortic valve leading to turbulence and giving rise to a systolic murmur. It cannot be diastolic because blood does not leave the heart in diastole.
Blood can also leave the left ventricle via the mitral valve. Physiologically it does not but in pathologies like mitral valve prolapse and mitral regurgitation, it can, giving rise to a systolic murmur.

Aortic regurgitation murmur would be diastolic because the blood in aorta comes back towards the heart and is normally prevented from going back into the heart by the semi lunar valves.
Likewise, mitral stenosis murmur would be diastolic too since the atria will contract to force blood to move across the stenosed valve in the diastolic phase.

The same concept applies to the right side of the heart. So pulmonary stenosis and tricuspid regurgitation would be systolic murmurs whilst pulmonary regurgitation and tricuspid stenosis would be diastolic murmurs.

Then I Said... Medical Finals

2012-11-23T23:24:00.000+05:00

Autoimmune Hemolytic Anemia

2012-11-22T00:29:00.000+05:00

Autoimmune Hemolytic Anemias occur due to antibodies against red blood cells, which results in RBCs' destruction.

There are of two types:

1. Warm Antibody Autoimmune Hemolytic Anemia

2. Cold Autoimmune Hemolytic Anemia

Cold agglutinin disease
Paroxysmal cold hemoglobinuria

Warm Antibody Autoimmune Hemolytic Anemia:

Most common antibody is IgG.
IgG attaches itself to RBC at 37 C (body temperature), and then the spleen recognizes the Fc portion and removes it.
Findings:

Severe anemia & hyperbilirubinemia due to hemolysis.
Increased MCV.
Bite cells: The macrophages in spleen bite off these IgG portion out.
Spherocytes: Loss of membrane due to spleen biting off RBCs leads to spherical shape of RBCs. These spherocytes in turn get destroyed when they pass through the spleen.
Splenomegaly: Spleen enlarges as more and more RBCs get trapped.

Causes:

Idiopathic.
Secondary to:

Systemic lupus erythematosus (SLE).
Rheumatoid arthritis (RA).
Chronic lymphocytic leukemia (CLL).
Drugs (methyldopa).

Can also occur in immunocompromised patient.

Diagnosis:

Positive direct Coombs test.

Treatment:

Corticosteroids.
Splenectomy.
If refractory, use Rituximab.

Cold Agglutinin Disease:

Antibodies IgM directed against RBCs, which at low temperature, binds to RBCs.
When IgM binds to RBC at cold temperature, classical pathway of complement system is activated resulting in formation of membrane attack complex (MAC) causing intravascular hemolysis. If MAC is not formed, opsonization by C3b leads to extravascular hemolysis by spleen.
Causes:

Idiopathic.
Secondary to:

Mycoplasma pneumonia.
Chronic lymphocytic leukemia (CLL).
Infectious mononucleosis.
HIV.

Treatment:

Avoid cold triggers.
Steroids are ineffective.
Treat underlying cause.
Rituximab.

Paroxysmal cold hemoglobinuria:

Characterized by hemoglobinuria after exposure to cold conditions.
Due to polyclonal IgG anti-P autoantibody (Donath-Landsteiner IgG) which binds to RBC during low temperature.
RBCs are destroyed by complement activation resulting in intravascular hemolysis.
Causes:

Measles, mumps, Epstein–Barr virus (EBV), Cytomegalovirus (CMV), Mycoplasma pneumonia, syphilis.

Treatment:

Self-limited.
Chronic PCH: treat underlying cause, such as syphilis.

Carpal Tunnel Syndrome

2012-11-10T20:30:00.001+05:00

Simple schematic of Carpal Tunnel.

Question: 30-year-old secretary presents to your clinic with complains of hand weakness. She says this weakness is exaggerated along with feeling of pain after she types for long hours. She also mentions that when she wakes up, there is tingling in the first 3 fingers of both hands.

On examination, there is weakness in extending her thumb bilaterally. There is also atrophied thenar eminence. Tinel and Phalen signs are positive bilaterally. Probable diagnosis?

Diagnosis: Carpal Tunnel Syndrome due to entrapment of the median nerve under flexor retinaculum.

Signs and symptoms presented in this case are classic. There is paresthesia and loss of motor function of thumb, index finger, middle finger. There is thenar atrophy. Abduction and opposition of thumb is also lost.

*Sensation on palm is intact due to intact palmar cutaneous branch of median nerve.

Etiology can be remembered by the mnemonic: MEDIAN TRAP

Myxedema

Edema premenstrually

Diabetes mellitus

Idiopathic

Acromegaly

Neoplasm

Trauma (mostly occupational)

Rheumatoid arthritis

Amyloidosis

Pregnancy

Treatment: NSAIDS, physical therapy/splint, surgical decompression.

Dawn Phenomenon and Somogyi Effect

2012-11-06T21:42:00.001+05:00

Dawn Phenomenon and Somogyi Effect

Dawn Phenomenon:
It is nocturnal glycemia caused by decreased effectiveness of insulin and overnight growth hormone release. Therefore, it causes early morning hyperglycemia.

Treat it by moving night-time insulin dose as close as possible to bedtime.

Nocturnal glycemia: It is normal but due to decreased insulin and increased GH release, early morning hyperglycemia occurs.

Somogyi Effect:

It is nocturnal hypoglycemia which leads to activation of counter-regulatory hormones such as cortisol, glucagon, epinephrine, norepinephrine and as such, results in early morning hyperglycemia.

Treat this by decreasing night-time insulin dose.

Nocturnal glycemia in Somogyi: It is low, which then leads to rebound hyperglycemia in early morning.

How to diagnose whether the early morning hyperglycemia in patient is due to Dawn Phenomenon or Somogyi Effect?

Both Dawn and Somogyi have early morning hyperglycemia. To distinguish between the two, decrease the insulin dosage at night. It is crucial not to increase insulin dose since this can result in coma if the patient has Somogyi effect.

Two possible outcomes:

1. If early morning hyperglycemia persists, it is Dawn phenomenon.

2. If early morning blood glucose is normal or decreased, it is Somogyi effect.

Debate regarding Somogyi credibility continues whether Somogyi effect to hypoglycemia is due to nocturnal hypoglycemia or not. In fact, hyperglycemia due to Somogyi effect can actually be due to an insulin-induced insulin resistance¹.

1. Shanik MH, Xu Y, Skrha J, et al. Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse?. Diabetes Care. Feb 2008;31 Suppl 2:S262-8.

Intussusception

2012-10-27T16:46:00.000+05:00

Intussusception: An intestine within an intestine.

Intussusception is an abdominal emergency in a child due to telescoping of one bowel segment into a distal segment leading to intermittent abdominal pain and bowel obstruction.

Most commonly occurs at ileo-cecal junction. Intussusception is the most common cause of bowel obstruction in the first 2 years of a child's life and more common in males.

Common findings:

Sausage-shaped RUQ abdominal mass
Red currant jelly stools
AXR showing small bowel obstruction
Ultrasound revealing the target sign or doughnut sign (intestine within an intestine)

Air-contrast enema is both diagnostic and curative.

Revamping; new features to come

2012-10-08T13:25:00.002+05:00

MedPrepOnline to be featuring new content soon!

This site will be rigorously revamped in the next few weeks to come, with new features and a whole different look.

USMLE Step 2 CK Study Schedule

2011-07-26T03:05:00.001+05:00

Similar to my post on the Step I, here are my sources to study for the Step 2 CK:

1) Master the Boards: Book: This book is fairly new and written by Dr. Conrad Fischer. I've heard that although it has a few deficiencies, it's overall a pretty well written book. As of this post I'm about 75% done with my first read of it and I like it so far.

2) UWORLD question bank: Gunna try to complete all 2300 questions at least once. Hopefully twice. From what I hear, this is the single most important resource to study from.

3) Kaplan series: I've read the IM, Paeds, and GObs books back in med school. Maybe I'll read them again if I get time.

4) USMLE step 2 secrets: Ordered mine a few days ago from Amazon. Heard it's a great book to supplement with the others to really reinforce concepts.

Unfortunately, I don't really have that much time to study... a mere 6 weeks. But inshaAllah that'll be enough. Lemme know what you guys think.

USMLE Step I: The Basics

2011-05-28T12:06:00.001+05:00

The USMLE Step I is a test of the preclinical sciences; Behavioral sciences, anatomy, physiology, biochemistry, pharmacology, immunology/microbiology, and pathology. 350 clinically oriented multiple choice questions divided into 50 question, 60 minute blocks. This gives you roughly 72 seconds to both read and answer every question. The Step I is a computer based exam. The USMLE does provide two white boards and markers for you to write on if needed. These boards are not graded and are discarded after the exam is over.

You are allocated 45 minutes of break time which you can arrange according to your own schedule, however, a break cannot be taken until you have completed an entire block. Of the 350 questions, you will not be graded for 50 of them. These are experimental questions for future exams and statistics. Unfortunately, you do not know which questions these are as they are unmarked and mixed in throughout the exam. Answer options can range anywhere from as little as 3, to as many as 11. Since there is no negative marking it is in your best interest to attempt every question of the exam, even if you have to guess.

The final scoring report provides both a three digit and a two digit score. The three digit score is the amount of answer you got correct. The two digit score is a bit more complex. Although it's not a percentage, its a way to compare your score to someone who took a comparative exam in the past. Passing is set at a two digit score of 75. As international medical graduates (IMG's), your goal is to obtain two digit scores in the 90's, essentially aiming for 99's. If you fail the exam, you are allowed to take it again after a period of 3 months. However, there are some programs that will no longer consider your application if you have failed (there are also some that will). If you pass the exam, your score is valid for a period of 7 years. Additionally, you cannot retake the exam in those 7 years if you passed, and your initial score is the one that will stick with you. Thus the motto is to prepare for the test to pass with the highest score possible, in your first attempt.

'Competitive' scores vary for each program, and each specialty. The general consensus is that pediatrics, family medicine, internal medicine, and to an extent, psychiatry, are all the easier fields to match into for IMG's. This is because the quantity of positions is high and the requirements are low. On the contrary, plastic surgery, radiology, dermatology, anesthesiology, opthamology, and emergency medicine are the harder fields to match into. In addition to extremely high board scores, these programs admire extensive research publications in well known journals and multiple LOR's from well known U.S. physicians. Keep in mind that these are some SOME of their requirements.

The Step I can be taken anywhere in the world, including Karachi, Pakistan. The fees are approximately $850 U.S. dollars, plus another $150 if you decide to take it outside of the U.S. Click here to register for the Step I and for further information.

I hope this served as a general overview. If you have anymore questions regarding the Step I, please post them below. Thanks.

"California Letter"

2011-05-28T12:03:00.000+05:00

The state of California requires International Medical Graduates (IMG's) wanting to apply to programs in the state of California be required to submit a "California Letter" AKA- the PTAL. This takes about 1 year to complete and as of the time of this publishing, costs an extra $500.

More information regarding the PTAL can be found below including forms:
http://medbd.ca.gov/
http://www.medbd.ca.gov/applicant/application_international.pdf

Types of Residency positions

2011-03-05T12:38:00.001+05:00

There are two different kinds of positions to apply for during residency.

Categorical (cat):
These form the bulk of positions throughout programs across the States. Once an individual is accepted for a categorical position, they are destined to stay with a single, specific program for the entire duration of their designated residency. For example; A 5 year residency in the department of general surgery at Massachusetts General Hospital.

Although much harder to attain (especially for International Medical Graduates- IMG's), this is the position that you should strive for. Cats are essentially a guaranteed ticket to a successful completion of residency.

Preliminary (prelim):
Prelims are basically 1 year long paid internships. You are not guaranteed a job after 1 year of work. For example, a 1 year job at Massacheusetts general hospital in general surgery. After that one year, you have to find another place to work. Although there is a chance that the same place that offered you a prelim position will offer you another prelim year, or even a categorical position, its not guaranteed. Most of the time they don't. So then you have to reapply to match somewhere else. If you get offered a position at another place, you dont have to start over again. You simply continue as a PGY2 (second year) at the new institution.

Unfortunately, preliminary positions are commonly offered to IMG's. This doesn't mean always. Some programs can offer you a cat position even if you are an IMG, but this all depends on which institutions you are applying you, and which fields you are applying for.

Finally, there is a transitional year for which one can apply to. However, I do not have sufficient knowledge about these types of positions. I ask that if anyone else does, please post it down below. Thanks.

USMLE Step I Study Plan

2011-02-22T10:18:00.003+05:00

I'll kick this one off. Here's the list of books/resources I plan on studying from:

1) Kaplan USMLE Step I series.

2) Dr. Edward Goljaan Pathology lectures (audio). Thankfully, I've heard the complete series about 3 times while driving my car so this shouldn't be too bad. These lectures are awesome and I recommend them to everybody. But fyi, they are definitely time consuming.

3) Rapid review Patho by Goljaan

4) High yield 100 page notes by Goljaan

5) I might substitute the Kaplan anatomy for High Yield anatomy only because I heard its its better from several sources. I'll have to skim them both out for myself and then make a judgement call and stick with whats better.

6) Kaplan USMLE Step I video lectures- Im pretty sure I'm only going to do the physio and biochem ones. I watched some during our 4th year days back in the library in Kemari and although they are good, but they are freaking LONG! It's going to be extremely time consuming to try to watch all the videos so I think i'm going to stick with what I suck at (which is biochem and a little bit of pharma), and with what i need to base my concepts on (physio). My roommate who is an AKU grad has been watching all the videos at 2x speed and he says that its better that way. So thats something to experiment with if interested.

7) First Aid- Step I. Also known as FA. I've heard that this is THE BOOK. Apparently it doesn't get any more high yield than this. I'm gunna try to memorize this cover to cover.

8) Online USMLE world questions. Also known as Uworld.

And thats pretty much it. I'll refer to BRS if I don't understand something or maybe even back to the reference books if needed. I'm planning on studying for 5 months, 6 if needed.

Lemme know what you guys think and if you have any recommendations.

BILIRUBIN METABOLISM - PHYSIOLOGY AND ALTERATIONS

2010-08-24T07:26:00.003+05:00

SOURCES OF BILIRUBIN:
Hemoglobin metabolism - accounts for 80% of all bilirubin production, with each gm of Hb producing 35mg of bilirubin by the action of biliverdin reducatse.
Ineffective or shunt Hb
Lysis of precursor cells in bone marrow

FACTORS RESPONSIBLE FOR INCREASED BILIRUBIN PRODUCTION IN NEONATES:
Neonatal bilirubin production is upto thrice that of adults, with neonatal production being 6-10mg/kg/day compared to adult bilirubin being 3mg/kg/day. The contributing factors include:
Increased RBC mass
Shortened RBC lifespan (70-90days)

BILIRUBIN - DIRECT AND INDIRECT:

Bilirubin produced by Hb metabolism is UN-CONJUGATED, and reacts as an INDIRECT agent in Van Den Bergh test. It is lipid soluble, thus easily crosses the BBB, and causes damage to brain cells. For the same reason, it can not be readily excreted in urine. For travelling in the blood stream, it binds to albumin ( 1gm albumin - 8.5 gm bilirubin). Free fatty acids and sulfasoxazole can displace bilirubin from albumin.

Bilirubin is CONJUGATED on reaching teh hepatocyte, when it dissociates from albumin and binds to Y-ligandin, forming bilirubin diglucoronide. It acts as a DIRECT reagent in Van den Bergh test. This is water soluble and maybe readily excreted in urine and bile. UDP glucoronyl transferase and quantity of Ligandin Y are the detreminants of this reaction of conjugation. Most of this conjugated bilirubin is excreted into the small intestines in bile, some hydolyses back to unconjugated variiety and reabsorbed in the enterohepatic circulation, while the remaining is converted to urobilinogen and stercobilinogen by intestinal flora to be excreted in urine and feces, respectively.

UNCONJUGATED / INDIRECT HYPERBILIRUBINEMIA

ETIOLOGY:

1. PHYSIOLOGICAL CAUSES:

a. Physiologic Jaundice
b. Breast Milk Jaundice

2. PATHOLOGICAL CAUSES:

Hemolytic
a. Crigler Najjar Syndrome
b. Gilbert Disease
c. Blood group incompatibility
d. Infection
e. G6PD deficiency
f. Thalassemia
g. Spherocytosis

Non-Hemolytic
h. Polycythemia
i. Internal hemorrhage
j. Infant of Diabetic Mother
k. Pyloric stenosis
l. Hypothyroidism
m. Immune thrombocytopenia

1a. PHYSIOLOGIC JAUNDICE - commonest cause of hyperbilirubinemia, yet a diagnosis of exclusion. Occurs due to Increased bilirubin due to increased RBC mass, shortened RBC lifespan, and hepatic immaturity. Peak bilirubin in term infants occurs on day 3, and on day 5 in premature ones. Levels in breats fed infants may rise upto 15-17mg/dl, while in non-breastfed ones stay till 12mg/dl.

1b. BREAST MILK JANDICE - no evidence of hemolysis is seen, occurs in 1st to 2nd week of life, indirect bilirubin may go upto 20mg/dl.Interruptiopn of breast feeding for a day or 2 significantly reduces teh levels, which don't rise again on resumption of breast feeding.

PATHOLOGICAL JAUNDICE:

if presents on 1st day of life

if bilirubin increases by > 0.5mg/dl/hour

if bilirubin is >13mg/dl in term infants

if direct bilirubin is >1.5mg/dl

if hepatosplenomegaly is present

if anemia is present

2a. CRIGLER NAJJAR SYNDROME - permanent deficiency of UDP glucoronyl transferase. Autosomal dominant variety responds to enzyme induction by phenobarbital, while autosomal recessive doesn't, resulting in kernicterus.

2b. GILBERT DISEASE - mutation of promoter region of UDP glucoronyl transferase, produces mild indirect hyperbilirubinemia.

2c. BLOOD GROUP INCOMATIBILITY - Due to abo, Rh, Kell and Duffy antibodies, hemolysis occurs resulting in hyperbilirubinemia.

2d. INFECTIONs

2e. INTERNAL HEMORRHAGE - cephalhematoma, splenic or hepatic hematoma

EXAMINATION:

Physical signs are visible on bilirubin levels of 5-10mg/dl, compared to adult ones on 2mg/dl.

INVESTIGATIONS:

a. INDIRECT AND DIRECT BILIRUBIN LEVELS
b. BLOOD TYPING
c. Coombs test
d. Complete blood count
e. blood smear
f. RETICULOCYTE COUNT

TREATMENT:

a. Phototherapy: effective and safe method. BLue and white lights both are good, but white is preferred as blue may conceal cyanotic changes, if any. Phototherapy converts the water-insoluble 4Z, 15Z bilirubin IX into water soluble, 4Z, 15E bilirubin IX which maybe excreted in bile. It also results in formation of LUMIRUBIN,which is water soluble and excreted in urine too.
Complications of phototherapy include increased insensible water loss, diarrhea, dehydration, maculopapular red rash, lethargy, masking of cyanosis, nasal obstruction by eye pads and possibility of retinal hemorrhage.

b. Exchange Transfusion: reserved for infants at risk of kernicterus, at a level of 20mg/dl for term infants weighing over 2kg (at bilirubin levels in mg/dl 10% of body weight in g). Assymptomatic infants with physiologgical jaundices may not require it until bilirubin is 25mg/dl or more. Amount of blood exchanged is equal to twice the infant's blood volume, determined by : weught in kg x 85ml/kg x 2. This amount removes 85% of infants RBCs, maternal antibodies, and exchangeable indtect bilirubin. Performed through umblical venous catheter placed in inferior vena cava. Complications include transfusion reaction, metabolic instability, infection, vessel perforation or hemorrhage, hypotension, necrotizing enterocolitis, thrombocytopenia and GVHD.

c. Heme Oxygenase Inhibitors: tin mesoporphyrin may reduce indirect hyperbilirubinemia and need for phototherapy.

CONJUGATED / DIRECT HYPERBILIRUBINEMIA

ETIOLOGY:

a. hyperalimentation cholestasis
b. CMV infection
c. TORCH infection
d. inspissated bile from prolonged hemolysis
e. neonatal hepatitis
f. sepsis
g. cystic fibrosis
h. biliary atresia

INVESTIGATIONS:

a. Liver enzymes
b. Bacterial and viral cultures
c. Metabolic screening tests
d. Hepatic ultrasound
e. Sweat ch;loride test

TREATMENT:

specific treatment for underlying cause
no exchange transfusion required / helpful.

note : bilirubin produced in fetus is transferred to maternal blood through placenta and is metabolized by maternal liver. The fetal bilirubin only mildly elevates in presence of severe hemolysis, inspissated bile stasis and conjugated hyperbilirubinemia.

Principles of Preoperative & Operative Surgery (Part I)

2010-04-22T22:29:00.008+05:00

Preoperative Evaluation-
Aim is not to screen broadly for undiagnosed disease but rather to identify and quantify any comorbidity that may have an impact on the operative outcome. Used to identify risk factors for postoperative morbidity and mortality. Communication between the surgeon and consultants is essential to define realistic goals and to expedite surgical management.

Cardiovascular:
ASA Classification for anesthetic risk has 5 strata:

I- Normal healthy patient
II- Patient with mild systemic disease
III- Patient with severe systemic disease that limits activity but is not incapacitating
IV- Patient who has incapacitating disease that is a constant threat to life
V- Moribund patient not expected to survive 24 hours with or without an operation

Cardiac Risk Indices-
Goldman Cardiac risk Index (1977), Detsky Modified Multifactorial Index (1986), Eagle’s Criteria for Cardiac Risk Assessment (1989), & Revised Cardiac Risk Index.

The current AHA/ACC recommendations are to start Beta-blockers therapy in the medium to high risk patients undergoing major to intermediate risk surgery as early as possible preoperatively and titrate to a heart rate of 60 beats/min.

An easy, inexpensive method to determine cardiopulmonary functional status for noncardiac surgery is the patient’s ability or inability to climb two flights of stairs. Two flights of stairs are needed because it requires greater than 4 metabolic equivalents (METs).

Pulmonary:

Preoperative evaluation of pulmonary function may be necessary for either thoracic or general surgical procedures.

Necessary tests include FEV1, FVC, and the diffusing capacity of carbon monoxide. Adults with an FEV1 of less than 0.8 L/sec, or 30% of predicted, have a high risk for complications and postoperative pulmonary insufficiency.

Preoperative interventions that decrease postoperative pulmonary complications include smoking cessation (>2 months before planned procedure), bronchodilator therapy, antibiotic therapy for preexisting infection, and pretreatment of asthmatic patients with steroids.
Perioperative strategies include the use of epidural anesthesia, vigorous pulmonary toilet and rehabilitation, and continued bronchodilator therapy.

Hepatobiliary:

Evidence of hepatic dysfunction may be seen on physical examination. Jaundice and sclera icterus may be evident with a serum bilirubin level greater than 3 mg/dL. Skin changes include spider angiomas, caput medusa, palmar erythema, and clubbing of the fingertips. Abdominal examination may reveal abdominal distention, evidence of fluid shift, and hepatomegaly. Encephalopathy or asterixis may be evident. Muscle wasting or cachexia can be prominent.

Here are ways to approach a patient with liver disease in selected cases:

Acute Hepatitis-
Postpone elective surgery at least until liver function tests have normalized.

Chronic Hepatitis-
Surgery is generally considered safe in these patients.

Obstructive Jaundice-
1) Perioperative fluid management to prevent renal dysfunction
2) No dopamine or mannitol
3) Lactulose may be helpful
4) Antibiotic prophylaxis
5) No routine preoperative biliary drainage
6) Check for abnormal coagulation parameters

Cirrhosis-
Child’s A and B- Treat ascites, coagulopathy and proceed to surgery
Child’s C- Postpone until the patient’s Child’s class could be improved or cancel surgery for conservative management

Coagulopathy- Target PT to be no more than 2 seconds above normal
1) Vitamin K- 10 mg subcutaneous
2) FFP if no improvement with Vit K
3) Give cryoprecipitate as needed

Ascites-
1) Fluid restriction
2) Diuretics- Furosemide and/or Spironolactone
3) Paracentesis- may be diagnostic or therapeutic with simultaneous administration of albumin

Encephalopathy-
1) Treat with lactulose
2) Prevent by treating precipitating conditions such as GI bleeding, alkalosis, uremia, avoidance of sedatives

Patients with cirrhosis may be assessed with the Child-Pugh classification, which stratifies operative risk according to a score based on several variables. Child’s class A, B, and C have mortality rates of 10%, 31%, and 76% respectfully during abdominal examinations.

Malnutrition is common in cirrhotic patients and is associated with reduction in hepatic glycogen stores and reduced hepatic protein synthesis.

References:
"Sabiston: Textbook of Surgery" Townsend, Elsevier. 2008

More to come soon...