Dr. Timothy Root’s ophthalmology book, videos and flashcards are entertaining, memorable, and super high-yield. In fact, according to the book’s subtitle, it is “The funniest, cartooniest, most high-yieldiest book about eye diseases ever written” – and I agree.

I consider these to be among the finest medical educational resources on the internet, and I recommend them very highly to anyone interested in ophthalmology. You can access everything for free here.

Mark Yoffe MD

Hat tip: Andy Neill, Emergency Medicine Ireland

[Please read important Disclaimer.]

The post Media Review: OphthoBook by Dr. Timothy Root appeared first in The Medical Media Review.

Multiple myeloma is associated with more laboratory abnormalities than any other disease.

Some notable ones are:

• Normocytic, normochromic anemia
• Hypercalcemia
• Renal failure: elevated BUN and creatinine, normal or high anion gap metabolic acidosis
• Hyponatremia
• Macrocytic anemia
• Rouleaux formation on peripheral blood smear
• High Erythrocyte Sedimentation Rate (ESR)
• High serum total protein and low albumin/globulin ratio
• Low anion gap
• Distal (Type 4) renal tubular acidosis: hyperkalemia, non-anion gap metabolic acidosis, increased urinary anion gap, low urine pH, low renin, low-normal aldosterone levels and blood pressure
• Proximal (Type 2) renal tubular acidosis: hypokalemia, low urine pH, non-anion gap metabolic acidosis
• Acquired Fanconi syndrome: hypophosphatemia, hypokalemia, Proximal (Type 2) renal tubular acidosis, phosphaturia, aminoaciduria, glucosuria on urinalysis with a normal blood glucose
• Nephrotic syndrome: hypoalbuminemia, hyperlipidemia, proteinuria (elevated protein on urine dipstick, elevated urine protein to creatinine ratio), peripheral edema
• High lactate dehydrogenase (LDH)
• Hyperuricemia
• Hyperammonemia
• Cryoglobulinemia
• Hyperviscosity (yes, there is a test for that!)
• Hypogammaglobulinemia
• Endocrinopathies

You confirm the diagnosis with:

• Serum and urine protein electrophoresis and immunofixation
• serum-free light chain assay
• Skeletal survey (plain radiographs, showing “punched out” lesions)
• Bone marrow aspiration and biopsy

Tumor burden is followed by

• Beta-2 microglobulin
• LDH

A Critical take home point

At minimum, you need to know that anemia, hypercalcemia, renal failure and back pain in a 50 year old or older is multiple myeloma until proven otherwise. You also need to know that such patients, when presenting with marked neurological deficits, need glucocorticoids emergently and an MRI urgently.

By Mark Yoffe MD

[Please read important Disclaimer.]

 References

• The Merck Manual for Health Care Professionals (accessed 5/9/2013)
• Sabatine, Marc S., MD, Pocket Medicine, 4e (2010)

The post Laboratory Findings in Multiple Myeloma appeared first in The Medical Media Review.

Laboratory medicine is one of the core competencies you must master if you want to become a superstar diagnostician within the span of one lifetime or less.

Here is my proposed “curriculum” for mastery of laboratory medicine:

• Urinalysis and Body Fluids, 5e, by Susan King Strasinger – a great book. Clear, fluid and memorable. I think every medical student should know what’s in this book. It’s core knowledge.
• Clinician’s Guide to Laboratory Medicine: Pocket by Samir P. Desai MD (2009, reviewed here); if you were to get only one book about laboratory medicine, this should be the one. It has the answers to the vast majority of important laboratory medicine questions.
• Acid Base Case Studies by Ira Kurtz MD (2004, reviewed here); this is, in my view, one of the best medical books of all time.
• Clinical Hematology Atlas, 4e by Bernadette F. Rodak MS MLS or Anderson’s Atlas of Hematology, 2e, by Shauna Anderson or Color Atlas of Clinical Hematology, 4e by Dr. A. Victor Hoffbrand. It’s very difficult for me to choose a “best” book among these three. They are all very good. The first is the clearest and most straightforward, while the last is extremely comprehensive and very well-correlated clinically. The middle one is, well, somewhere in the middle.
• An Atlas of the Clinical Microbiology of Infectious Diseases, Volumes 1 & 2 by Edward J. Bottone. These are amazing books about laboratory and clinical identification of infectious diseases. I will write fuller review when I’m done reading them.

Wanted: I’m still looking for a good or great laboratory medicine book about immunology and serology. Any suggestions?

By Mark Yoffe MD

[Please read important Disclaimer.]

The post Teach Yourself Laboratory Medicine! appeared first in The Medical Media Review.

• Na+: 143
• Cl-: 100
• Serum bicarbonate: 16

First, you calculate the anion gap:

You know (or should know!) that the normal anion gap is 11. Here, the anion gap is 27. This, of course, suggests a high anion gap metabolic acidosis.

Next, you see if the serum bicarbonate is dropping by the same number of points that the anion gap is rising. As we said, here the anion gap is 27. A normal anion gap is 11, so the anion gap is too high by 16 points (27-11 = 16). Therefore, you should expect the bicarbonate to be similarly 16 points below the normal of 24. That is, you’d expect the bicarbonate to be 8 (24-16 =8).

Here, however, the bicarbonate is 16, which is 8 points higher than the expected 8. A higher than expected bicarbonate in a patient with no past medical history suggests a metabolic alkalosis. So this patient also has a metabolic alkalosis on top of his high anion gap metabolic acidosis.

Next, you look at the arterial blood gas:

• pH: 7.50
• pCO2: 20
• HCO3-: 15

Notice that the pCO2 dropped by 20 points (normal is 40). Had the respiratory compensation been appropriate, the pCO2 should have dropped by the same number of points as the bicarbonate. Why? That’s just how it is. (If you’re not convinced, just plug the numbers into the Winter’s formula and you’ll get the exact same result.) In any event, recall that this patient’s serum bicarbonate dropped by only 8 points, so his pCO2 should have dropped by only 8 points as well, leaving a pCO2 level of 32 (40 – 8 = 32). As we said, this patient’s pCO2 dropped by 20 points (40 – 20 = 20), which is way more than expected. A too-low pCO2 means that there is a respiratory alkalosis. So now we know that this patient also has a respiratory alkalosis on top of his high anion gap metabolic acidosis and his metabolic alkalosis.

Now that the arithmetic is done, it’s time to look back at the patient history and physical examination to see if your acid-base diagnosis fits the clinical picture. Recall that this was an afebrile, atraumatic 26-year-old male with no past medical history who presented with altered mental status. This history alone suggests a likely toxic ingestion and therefore a possibly high anion gap metabolic acidosis. He vomited. That fits with metabolic alkalosis. He was tachypneic. That fits with respiratory alkalosis.

And finally, he was vertiginous. That fits with a final diagnosis of salicylate poisoning with a characteristic triple acid-base disorder of high anion gap metabolic acidosis, metabolic alkalosis, and respiratory alkalosis.

By Mark Yoffe MD

The post How to Solve Complex Triple Acid-Base Problems Quickly in Your Head appeared first in The Medical Media Review.

You can get away with skimming or even skipping the discussions of efflux pumps, porins and aminoglycoside modifying enzymes, but no amount of cramming, Web-surfing or fooling around with silly mnemonics can substitute for the genuine understanding of antibiotics selection which this book provides.

By Mark Yoffe MD

[Please read important Disclaimer.]

The post About Antibiotic Basics for Clinicians, 2e appeared first in The Medical Media Review.

• To diagnose an exudative pleural effusion (the test is positive for exudate if the pleural fluid to serum LDH ratio is greater than 0.6 or if the pleural fluid LDH is more than two-thirds of the upper limit of normal)
• To rule out hemolysis
• To rule in ischemic hepatitis (in a patient with marked hypertransaminasemia, a very high LDH supports the diagnosis of ischemic hepatitis, or “shock liver,”  if LDH/ALT>1)
• To rule out Pneumocystis jiroveci pneumonia in immunosuppressed patients
• To diagnose renal infarction (LDH which is four times the upper limit of normal is supportive of this diagnosis)
• To diagnose germ cell tumors
• To diagnose acute coronary syndrome (a long time ago!)

• Brain: clinically negative for stroke
• Heart: no chest pain or shortness of breath, and/or negative troponins and electrocardiogram
• Blood: negative hemolysis workup (CBC, peripheral blood smear, reticulocyte count, bilirubin, haptoglobin)
• Liver: negative liver chemistry studies
• Skeletal muscle: negative creatine kinase

The post How to Use LDH in Clinical Decision-Making appeared first in The Medical Media Review.

DIC is commonly seen in patients with severe physiologic stressors. It can effectively ruled in or out with the following straightforward workup:

• Proof of the existence of a compatible physiologic stressor (for example, sepsis, burns, shock, trauma, obstetric complications, or acute promyelocytic leukemia)
• Proof of coagulopathy: PT/INR (↑).  Add an aPTT (↑) in patient with malnutrition or liver disease, or in whom anticoagulation with warfarin is suspected.
• Proof of intravascular hemolysis: peripheral blood smear showing schistocytes. If you cannot get a reliable peripheral blood smear interpretation, you can use a hemolysis workup  as a surrogate (complete blood count showing anemia, (↑) reticulocyte count , (↑) LDH , (↑) unconjugated bilirubin, urinalysis showing pink urine). Haptoglobin levels (↓) are usually not useful because in most facilities it takes too long to get the results back.
• Proof of clot formation and degradation: d-dimer (↑). A fibrin/fibrinogen degradation products assay (↑) may be used instead.

That’s it.

You don’t need dozens of tests which, at best, add nothing and, at worst, only muddle the clinical picture.

Now here comes the bonus section:

• Liver chemistry studies can help you determine whether liver disease might be an alternative or concomitant explanation for coagulopathy, anemia or thrombocytopenia.
• A single normal or elevated fibrinogen level is useless in terms of ruling out DIC because fibrinogen is an acute phase reactant that is commonly elevated in the presence of physiologic stress, with or without DIC. Nonetheless, serial fibrinogen levels, when trending downward, support the diagnosis of DIC because this shows that fibrinogen, which is used in clot formation, is being depleted.

References

• Laposata, Michael, MD, PhD., Coagulation Disorders: Quality in Laboratory Diagnosis (2010)
• Desai, Samir P., MD, Clinician’s Guide to Laboratory Medicine: Pocket (2009, reviewed here)

by Mark Yoffe MD

[Please read important Disclaimer.]

The post The Intellectually Frugal DIC Workup appeared first in The Medical Media Review.

• Laboratory error (repeat serum sodium, chloride, bicarbonate if necessary)
• Hypoalbuminemia (expected anion gap is albumen concentration x 2.5)
• Increased unmeasured cations (e.g. calcium, magnesium, potassium, lithium)
• Monoclonal and polyclonal gammopathy (check serum and urine protein electrophoresis and immunofixation, and with serum free light chain assay)
• Salicylate poisoning (check levels if necessary)

So what to do?

After calculating the anion gap and finding it to be normal, take a look at the serum bicarbonate again. If it is low, then you must be dealing with a metabolic acidosis, acute respiratory alkalosis or chronic respiratory alkalosis. If the history and physical examination do not clearly point to the cause of hypobicarbonatemia (like diarrhea or early acute renal failure), then assume that you are dealing with a pathological organic acid load, until proven otherwise.

You can help prove otherwise by checking the labs mentioned in the list above, or by measuring the organic acid levels directly (e.g. lactic acid, ketones and anything else that may be in your favorite high anion gap mnemonic).

And finally,

“[O]nce laboratory error and hypoalbuminemia have been excluded [as a cause of low serum anion gap], a search for accumulation of IgG should be initiated. In patients with disturbed mentation or unexplained clinical findings, the possibility of lithium ingestion, bromism, or iodide intoxication should be considered. When the serum anion gap is negative in the absence of laboratory error … bromide intoxication, iodide intoxication, and myeloma should be excluded.”

Jeffrey A. Kraut, Serum Anion Gap: Its Uses and Limitations in Clinical Medicine. Clinical Journal of the American Society of Nephrology, January 2007,  vol. 2  no. 1  162-174 (free here)

Your thoughts?

• Jeffrey A. Kraut, Serum Anion Gap: Its Uses and Limitations in Clinical Medicine. Clinical Journal of the American Society of Nephrology, January 2007,  vol. 2  no. 1  162-174 (free here)
• Kurtz, Ira, MD, Acid-Base Case Studies (2004, reviewed here)
• Sabatine, Marc, MD. Pocket Medicine (2010)
• Desai, Samir P., MD., Clinician’s Guide to Laboratory Medicine: Pocket (2009, reviewed here)

by Mark Yoffe MD

[Please read important Disclaimer.]

The post How to Spot a Falsely Normal Anion Gap appeared first on The Medical Media Review.

• Hyperglycemia
  • Fasting  - increase basal insulin
  • Pre-lunch  – increase breakfast rapid acting insulin or increase morning NPH (intermediate acting)
  • Pre-dinner  – increase lunchtime rapid acting insulin or increase morning NPH
• Hypoglycemia
  • Fasting or nocturnal – decrease basal insulin at bedtime
  • Pre-lunch – decrease rapid acting insulin at breakfast or decrease morning NPH
  • Pre-dinner – decrease rapid acting insulin at lunch or dinner

Reference
Board Basics 3. 2013. American College of Physicians.

by Mark Yoffe MD

[Please read important Disclaimer.]

The post How to Fix Common Glucose Problems in Diabetics appeared first on The Medical Media Review.

The post Book Review: Robbins and Cotran Atlas of Pathology, 2e appeared first on The Medical Media Review.

• Low renin, high aldosterone
  • this points to primary aldosteronism, or to exogenous aldosterone
  • The most common causes of primary aldosteronism are adrenal hyperplasia (most common) or Conn syndrome (adrenal adenoma)
  • The next step is to confirm the diagnosis of primary aldosteronism with a salt suppression test (aldosterone will not be suppressed with an oral salt load) and imaging of the adrenal glands
  • treatment of adrenal hyperplasia is with spironolactone, while treatment of adrenal adenoma is with surgery
• High renin, high aldosterone
  • This points to secondary aldosteronism, meaning that the aldosterone is elevated because of something else, namely elevated renin levels. Elevated renin levels, or reninism, can itself be of two varieties:
    • Primary reninism: from a reninoma (a renin secreting tumor)
    • Secondary reninism: renin is elevated because of a secondary cause, such as renovascular disease or intravascular volume depletion (CHF, cirrhosis, nephrotic syndrome, Hypovolemic, diuretic use)
• Low renin, and low aldosterone
  • This points to non-hyperaldosteronemic hypermineralocorticoidism; it not “aldosteronism” because it is not caused by an increase in aldosterone
  • Most common causes non-hyperaldosteronemic hypermineralocorticoidism are Cushing syndrome (cortisol excess), Cushing’s disease (ACTH-hypersecretion), congenital adrenal hyperplasia (some forms), licorice ingestion, Liddle’s syndrome
  • Workup may continue here with dexamethasone suppression test

As a final note, the “opposite” of hypermineralocorticoidism is type IV (distal) renal tubular acidosis, whose symptoms are the exact time “opposite” of hypermineralocorticoidism. These patients may have hypotension, hyperkalemia, and metabolic acidosis. Hypovolemic (orthostatic) hyponatremia is sometimes also seen.

The post Hypermineralocorticoidism Explained appeared first on The Medical Media Review.

Here is my list, in no particular order, of the best basic science books for medical students:

1. Robbins and Cotran Atlas of Pathology (2009). Edward C. Klatt MD
2. Robbins and Cotran Review of Pathology, 3e. 2009. Edward C. Klatt MD
3. Basic Clinical Neuroscience (2007) by Paul A. Young PhD.
4. Netter’s Essential Histology. 2007. William K. Ovalle PhD.
5. Molecular Biology Made Simple and Fun. 2010. David P. Clark PhD.
6. A Clinician’s Guide to Statistics and Epidemiology in Mental Health. 2009. S. Nassir Ghaemi MD
7. Statistical Evidence in Medical Trials. 2006. Stephen D. Simon PhD.
8. BRS Physiology. 2010. Linda S. Costanzo PhD.
9. Atlas of Tropical Medicine & Parasitology. 2005. Wallace Peters MD. (Reviewed here)
10. Clinical Microbiology and Infectious Diseases: An Illustrated Colour Text. 2007. Dr. W. John Spicer.
11. Biochemistry Explained. 2002. Dr. Thomas Millar

Do you remember any medical books that you were particularly fond of while in medical school? Please let me know if you’d consider adding anything else to this list.

by  Mark Yoffe MD

[Please read important Disclaimer.]

The post The Best Basic Science Books for Medical Students appeared first on The Medical Media Review.

To become a great diagnostician, you need to excel in five different areas: (1) history-taking, (2) physical examination, (3) laboratory medicine, (4) radiology, and (5) electrocardiography.

History-taking

The two most important components of history-taking are knowing what to ask and how to ask questions.

Prepare and perfect scripted questions for common diseases and presentations. For example, heart failure and volume overload are commonly probed with questions about leg swelling, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. There are, however, many more questions that could be asked to help tease out symptoms of heart failure. These might include questions about diuretic or dietary noncompliance, weight gain, increased abdominal girth, missed hemodialysis, cough, wheezing ,etc. Learn all the scripted questions that are relevant to diseases that you see a lot of. (I am not aware of many excellent books on clinical history taking. A reasonable place to start might be The Patient History: Evidence-Based Approach (2012) by Mark Henderson. Others might prefer Symptom to Diagnosis: An Evidence Based Guide, Second Edition, by Scott Stern.)

How to phrase your questions can be extremely important, especially when dealing with sensitive topics. “Always the beautiful answer who asks a more beautiful question,” is a quote that is attributed to e.e. cummings. “Do you hear voices?” or “Do you want to kill yourself” are rather inelegant and low yield questions. Test drive and flesh out phrases that make patients feel less uncomfortable, such as “Does your mind ever play tricks on you?” or “Did you ever feel as though life is not worth living?” You can always follow up later with more specific and direct questions. (See, The Psychiatric Interview (2011) by Daniel Carlat for lots of ideas on how to ask questions.)

Physical examination

By far, the best way to learn how to do a physical examination is to do it many times under the tutelage of a seasoned teacher. Nothing even comes close to this method of learning, especially, and somewhat ironically, when it comes to the musculoskeletal examination. Certain maneuvers cause “clicks” and sensations of “give” that one cannot even partially experienced by reading books or watching videos. Rather, you need to examine lots of “normals” and lots of “abnormals,” under competent, and preferably excellent, supervision and guidance. So try to stick around and watch as your consultants as they examine your mutual patients. Ask them what they are doing and ask them if they might be willing to watch you try whatever provocative test they are doing.

Laboratory medicine

Most clinicians can read and interpret a white blood cell count with differential or a basic chemistry panel without any difficulty. So focus instead on other common, high yield, and often extremely nuanced laboratory studies, such as liver chemistries, urinalysis, peripheral blood smears and acid-base pathophysiology.

Radiology

If you excel at reading chest radiographs and head CTs, can identify the most critical, deadly and dangerous radiology findings, and you otherwise choose the correct imaging studies, you can probably consider yourself excellent, or at least close to excellent, in this area.

If you can’t read a foot MRI, you can almost always wait for a competent radiologist to help you out. There is, however, no substitute for being able to interpret chest radiographs and head CTs on your own and in a timely manner. “Perhaps the most important clinical advice to the front line doctor with regards to emergency brain CT scans for trauma or any other reason is for you to look at the scan [and interpret it!] as soon as it is done.” Brain CT Scans in Clinical Practice by Usiakimi Igbaseimokumo MD (2009, p. 33)

So strive to be as best as you can be in these areas. Again, there are tons of good radiology books out there. So get started!

Electrocardiography

“If you think there’s another specialist who has all the answers, someone else who’s going to bail you out of trouble every time you have a question about ECGs, you are mistaken. That person may just as likely be wrong, so YOU must strive to become THE expert.”

Amal Mattu MD, ECG Interpretation of STEMI: Who’s the Expert?, Medscape. Mar 21, 2012.

I’ll add to that the rather obvious point that your patients will invariably live or die because of your EKG interpretations, try to excel in this area.

There are many good to excellent electrocardiography books and blogs out there, so get started and don’t every stop learning.

Final thoughts

Your time is finite, so focus more on diagnoses that are more common and that matter most in terms of patient outcome. Knowing how to distinguish pericarditis from STEMI, for example, matters a great deal. There is no substitute for you knowing how to make that distinction accurately and in a timely matter.

Also, focus as much as you can on toxicology and especially on iatrogenic conditions. Often the best way to clarify what’s going on with the patient is to stop some or all of the multitudinous medications that the patient is taking – and see what happens.

Please let me know if you have any other ideas on how to become a great diagnostician.

by  Mark Yoffe MD

[Please read important Disclaimer.]

The post How to Become a Superstar Diagnostician in One Lifetime or Less appeared first on The Medical Media Review.

• High anion gap metabolic acidosis with increased osmolal gap (increased osmolal gap is suggestive of toxic ingestion or administration)
  • Ethanol (check levels)
  • Methanol (check vision and serum methanol levels)
  • Ethylene glycol (check serum ethylene glycol levels, serum calcium levels, urine for fluorescence, and sediment for calcium oxalate crystals)
  • Propylene glycol (discontinue IV lorazepam, IV diazepam!!)
• High anion gap metabolic acidosis with normal osmolal gap
  • Lactic acidosis (most common cause of high anion gap in hospitalized patients)
  • Renal failure (late)
  • Ketoacidosis (diabetic, alcoholic, starvation; confirm by checking serum for ketones, unless diagnosis is clear; also check serum glucose to distinguish diabetic ketoacidosis from starvation, and alcoholic ketoacidosis)
  • Salicylate poisoning: check serum salicylate level and look for concomitant respiratory alkalosis (drop in pco2 > 10 x drop in bicarbonate), which is, in the setting of toxic ingestions, tinnitus and altered mental status, fairly specific for salicylate poisoning
• Normal anion gap metabolic acidosis with increased osmolal gap
  • Isopropyl alcohol (most common, check breath for “fruitiness”)
  • Ethanol
  • Mannitol
• Normal anion gap metabolic acidosis with normal osmolal gap
  • Negative urine anion gap (suspect extrarenal causes)
    • Diarrhea (most common cause of normal anion gap metabolic acidosis)
    • intestinal or pancreatic fistulas or drainage
    • dilutional
    • post-hypocapnia
    • acetazolamide
  • Positive urine anion gap (suspect renal causes such as early renal failure or renal tubular acidoses)
    • Hypokalemia
      • Urine pH > 5.5: distal Renal Tubular Acidosis (Type I)
      • Urine pH < 5.5: proximal Renal Tubular Acidosis (Type II; consider Fanconi syndrome if you see glucosuria, aminoaciduria, etc.)
    • Normokalemia (early chronic renal failure, Type I & II Renal Tubular Acidosis)
    • Hyperkalemia and urine pH < 5.5 (Renal Tubular Acidosis Type IV, hypoaldosteronism)
• Metabolic alkalosis
  • Chloride responsive (urine chloride < 20)
    • Vomiting (hypokalemic, hypochloremic metabolic alkalosis is fairly specific for gastric outlet obstruction, e.g., pyloric stenosis)
    • Diuretic use (remote)
  • Chloride resistant
    • Hypertensive
      • hyperaldosteronism (includes Cushing’s)
    • Hypo- or normotensive
      • Diuretic use (current)
      • Hyperaldosteronism (look for low serum potassium)
      • Milk-alkali syndrome (hypercalcemia, metabolic alkalosis, and renal insufficiency in the setting of ingestion of large amounts of calcium and bicarbonate)

References

• Pocket Medicine (2010) by Marc S. Sabatine MD, MPH
• Acid Base Case Studies (2004) by Ira Kurtz MD (reviewed here)
• Clinician’s Guide to Laboratory Medicine: Pocket (2009) by Samir P. Desai MD (reviewed here)

by  Mark Yoffe MD

[Please read important Disclaimer.]

The post Acid-Base Abnormalities and Their Causes appeared first on The Medical Media Review.

You can judge this book by its title.

Illegal Drugs: A Complete Guide to Their History, Chemistry, Use, and Abuse (2003) by Paul M. Gahlinger MD is, in fact, an extremely comprehensive treatment of both illegal and legal psychoactive substances, including their history, law, chemistry, processing and distribution, metabolism, neuroscience, medical management, linguistics, folklore, and popular culture. Hundreds of drugs are covered, from the more common ones such as marijuana, cocaine, heroin and methamphetamine to drugs which I kind-of-almost-never-heard-of such as ibogaine, cathinone, peyote and bufotenine. The book is truly a tour de force on the subject of substance abuse.

Most of the information in this book has stood the test of time. For example, according to the author, “tobacco is the most injurious drug in the world today.” This was true when  Illegal Drugs went to print in 2003, and it is equally true today. I nonetheless believe that readers would benefit from an updated edition of this book because there are now newer, incredibly dangerous drugs on the street. These include drugs that cause terrible soft tissue necrosis and old drugs with new and horrifying side effects. Further, drug laws have changed, sometimes dramatically.

Despite the above-mentioned minor limitations (and the fact that ethanol abuse isn’t mentioned at all), the book makes for a terrifically interesting, informative and enjoyable read. I recommend very highly to both physicians and laypersons who are interested in psychiatry, psychology or toxicology.

by  Mark Yoffe MD

[Please read important Disclaimer.]

The post Book Review: Illegal Drugs, A Complete Guide to Their History, Chemistry, Use, and Abuse by Paul Gahlinger MD appeared first on The Medical Media Review.

Clinician’s Guide to Laboratory Medicine: Pocket (2009) by Samir P. Desai MD is an excellent handbook about the use laboratory studies in clinical medicine.

Almost every lab abnormality contains an extensive differential diagnosis, along with an intelligent and efficient approach to further workup and diagnosis. It contains dozens of useful charts, algorithms and tables. The hematology and nephrology sections are especially well-developed. This makes sense as these subspecialties are very heavily reliant upon laboratory investigations. (In contrast, the neurology, endocrinology and pulmonary sections are much smaller, whereas, unfortunately, an infectious diseases section is absent altogether.)

I particularly like the author’s approach to anemia. While most authors approach anemia by dividing it into microcytic, normocytic, and macrocytic, Dr. Desai begins his approach with determining the reticulocyte production index. This makes a lot sense for several reasons:

• reticulocytosis is an extremely important and rather specific hematological finding.
• reticulocyte count is not included in the complete blood count and so is easy to forget; and finally,
• an increased reticulocyte count can artificially “change” a microcytic anemia to a normocytic anemia, etc.

As such, it is extremely important to think about the reticulocyte count early in the evaluation of anemia. So why not think about it first?!

The book is small and can fit into one’s shirt pocket or lab coat pocket. Unfortunately, the font is tiny so you’ll need good eyes or good glasses to be able to make use of the book.

I recommend this book very highly to anyone who is interested in clinical medicine, from medical students to fully-trained clinicians.

Special thanks to the Philip A. Hoover MD Library at York Hospital for stocking this excellent book. It is one of the best medical books of all time.

by Mark Yoffe MD

[Please read important Disclaimer.]

The post Book Review: Clinician’s Guide to Laboratory Medicine: Pocket by Samir P. Desai MD appeared first on The Medical Media Review.

Primary Care Otolaryngology is a free downloadable publication by the American Academy of Otolaryngology-Head and Neck Surgery. You can get it here. The original version of the book was written by J. Gregory Staffel, MD more than fifteen years ago and was most recently updated in 2011. It was written primarily for medical students, but it would serve as an excellent refresher for residents and attendings as well.

The book is sharp, short, and to the point. It is only 139 pages long and can be read in only a couple of hours. Topics include ENT emergencies, dizziness, hearing loss, nasal obstruction, thyroid cancer and sinus radiology, among others. Epistaxis, for example, is covered in only about a page and a half. The text addresses the various causes of epistaxis which, of course, include “digital trauma” (i.e., nose-picking), cocaine abuse and coagulopathies. The treatment options are presented in a clear and straightforward manner as well. These include external pressure, alpha agonists, nasal packing and balloon tamponade.

Similarly, instructions for performing an emergency surgical airway are extremely straightforward:

A good rule of thumb about a tracheotomy is: If you think about performing one, you probably should. It is easier to revise a scar on the neck than to bring the dead back to life…. Please remember the airway is best found in the neck by palpation, not inspection. Take a moment and palpate your own cricothyroid membrane, immediately below your thyroid cartilage. To do an emergency cricothyrotomy you need only a knife. Feel the space, cut down and stick your finger in the hole, feel, and cut again, and again until you are in the airway. Do not worry about bleeding. Place an endotracheal tube in the hole (again, by feel). Be sure not to push it past the carina. By this time, you will be shaking like a leaf—it is okay to let someone else squeeze the bag. Pressure with a dressing will address most bleeding. Occasionally, you might need to use some sutures to stop the bleeding.

(Page 21)

This, to me, is a nearly perfect tutorial because it prepares the reader from both a technical and an emotional standpoint: this is going to be a bloody mess and you are going to be terrified. So just expect that and don’t waste any time: grab a number whatever blade and make a hole so air can get from Point A to Point B as quickly as possible.

It’s a great little book.

by Mark Yoffe MD

The post Book Review: Primary Care Otolaryngology by the American Academy of Otolaryngology-Head and Neck Surgery appeared first on The Medical Media Review.

Acing the Hepatology Questions on the GI Board Exam, the Ultimate Crunch-Time Resource by Brennan M.R. Spiegel (2012)  is an excellent choice for anyone who is looking for a solid understanding of hepatic pathology, diagnostics and therapeutics.

The book is vignette-driven and features most of the important and high-yield hepatic conditions including acetaminophen overdose, viral hepatitides, and dozens of other infectious and metabolic liver disease. There are also excellent radiographic images and H&E stains.

This book has an interesting feature that I have never seen in any other Board review book. Each vignette is followed by a small “Why Might This Be Tested?” section. This is a very useful feature for test-takers. We all know that certain esoterica keep showing up over and over on Board examination. No one, until now, ever took the time to explain why. Dr. Spiegel explains these things very well. For example, according to the author, celiac disease is frequently tested on the Boards because:

sprue is a prevalent condition that is frequently missed. Board examiners will want to know that you can make this diagnosis on a timely basis…. Finally, Board examiners have a number of content “check boxes” they need to check off when putting an exam together. This topic works well because it covers several areas, including both luminal GI and liver disease. (p. 86)

This is a very useful book for anyone who wants to excel in hepatology. I recommend it most especially to advanced internal medicine residents and attendings, and to junior gastroenterology and hepatology fellows.

by Mark Yoffe MD

[Book Review: Acing the Hepatology Questions on the GI Board Exam by Brennan M.R. Spiegel (2012) was originally published in The Medical Media Review on February 11, 2013. Please read important Disclaimer.]

The post Book Review: Acing the Hepatology Questions on the GI Board Exam by Brennan M.R. Spiegel (2012) appeared first on The Medical Media Review.

My overall favorable impression of this unique publication is essentially unchanged since I reviewed the 2011 edition, about which I wrote:

For almost any infectious disease, the text advises you about which antibiotic to use, along with the appropriate dose, route, frequency and duration. In addition, the text provides you with various alternatives and contingency antibiotic choices for special situations such as  allergies, pregnancies, etc….

New improvements to this edition include a separate section for sepsis and an algorithm for Early Goal Directed Therapy.

There are a couple of things  that I would like to see in future editions. First, there are some conditions that point to other conditions so cross referencing and additional annotations might help. For example, thrush and vulvovaginal candidiasis, especially when severe, can be red flags for underlying immunosuppression. Early learners might benefit from having this type of information included in the “Pearls” section which follows the respective headings. Second, I’d like to see an entry for rhinocerebral mucormycosis. It is quite rare, but it is one of the deadliest infections in the developed world, so it might be worth mentioning in  an emergency-medicine-oriented infectious diseases publication such as this.

Again, as I wrote in my review of the previous edition:

[T]he guide is concise, “Board-worthy” and memorizable. It is a core title in Infectious Diseases: A Curriculum for Self-Guided Learners, and I recommend it very highly to doctors and to doctors in training.

by Mark Yoffe MD

[The post Book Review: 2013 EMRA Antibiotic Guide by Brian J. Levine MD was originally published in The Medical Media Review on January 31, 2013. Please read important Disclaimer.]

The post Book Review: 2013 EMRA Antibiotic Guide by Brian J. Levine MD appeared first on The Medical Media Review.

• CBC with differential, peripheral blood smear, iron, and iron-binding capacity, serum ferritin
• Liver chemistry studies
• Serum electrolytes
• Pregnancy testing

• Habif, Thomas P. Skin Diseases, Diagnosis and Treatment (2011)
• The Merck Manual for Health Care Professionals (accessed on 1/29/2012)

The post Systemic Causes of Pruritus (Itching) appeared first on The Medical Media Review.

I’ve been looking at Acid-Base Case Studies (2004) by Ira Kurtz MD for a long time now, at least since I’ve written several months ago, wrongly, that a solid book with a case-based approach to acid-base disorders does not exist. It does in fact exist, and this is it.

The book presents the reader with dozens of  clinical scenarios and dissects them from an acid-base standpoint. Cases covered include diabetic ketoacidosis, methanol intoxication, salicylate poisoning, diabetic ketoacidosis and many other common and rare clinical scenarios. The problems range from straightforward to highly complex.

The philosophy of the book can perhaps be summed up with this quote:

“If more than one acid-base disorder is present in a patient, there is frequently more than one pair of diagnoses that can account for the values of the acid-base parameters. A good clinical assessment is often helpful in distinguishing between the various possible acid-base diagnoses.”

(p. 86)

In other words, one doesn’t solve acid-base problems; rather, one interprets the values in a manner that fits the clinical situation. These is where many acid-base books get it wrong, and where Acid-Base Case Studies gets it exactly right.

Acid-base interpretation is relevant to every branch of medicine so few, if any, learners would not benefit from mastering this book inside out. And while many medical books contain lots of clinical “pearls,” this book is almost all pearls. It seems as though almost every case presented was, is, or should be, a Board question somewhere.

Get it. It’s one of the best medical books of all time.

by Mark Yoffe MD

[The post Book Review: Acid-Base Case Studies (2004) by Ira Kurtz MD was originally published in The Medical Media Review on January 22, 2013. Please read important Disclaimer.]