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Episode 27: Beta Blocker and Intermittent Claudication


Author: Lisa Ling
Editor: Dr. Suneet Sood
Narrator(s): Lisa Ling


Today we are going to talk about the relation between beta blocker and intermittent claudication.

Let’s start with a case.

A 45-year-old chronic smoker had episodes of stable angina and was started on propranolol 80 mg daily. He developed bilateral calf claudication two weeks later. He had painful calf muscles after walking for a distance of 100 metres. The pain usually resolved after resting for 5 minutes. Within a week the claudication distance had shortened to 15 meters, and he came to his physician for review. On examination, the femoral pulses were palpable, but the popliteal, dorsalis pedis, and posterior tibial pulses were absent on both lower limbs. The limbs were warm, and the capillary refill was 3-4 seconds. Buerger’s test was negative, indicating that the limb ischemia was not critical. The ankle brachial index was 0.77, indicating moderate disease. His physician stopped the propranolol, and started nifedipine. His claudication distance rapidly improved to 200 meters. A few months later, he had another episode of angina. He visited a different physician, who restarted the propranolol. The claudication distance once again shortened to 15 meters. When propranolol was once again discontinued, the claudication distance improved to tolerable levels again.

Why do we use beta blockers in angina?

In angina we want to reduce both the preload, which is the left ventricular pressure, and the afterload, which is the peripheral resistance. Beta blockers block the effects of adrenaline at the beta adrenoceptors. They work on beta-1 and beta-2 receptors, depending on their selectivity. (1) Firstly, in the heart, beta blockers block beta-1 receptors, and result in a negative inotropic effect. Secondly, beta-1 blockers also suppress the release of renin in the renin-angiotensin-aldosterone system. Reduced renin leads to vasodilatation and reduced plasma volume, and this decreases the cardiac output. (2) Thus, the beta blockers help in angina by decreasing left ventricular pressure as well as the peripheral resistance.

How do beta blockers cause intermittent claudication?

Activation of beta-2 receptors relaxes smooth muscle. In the muscle, the effect is vasodilatation of the arteries to the muscles. Beta blockers oppose this dilatation. In addition, the sympathetic nervous system increases its activity in response to the lowered blood pressure. The unopposed alpha-receptor-mediated effects result in the narrowing of the peripheral vessels. (1) The obstruction of blood flow in the arteries may cause muscle ischaemia and pain in the calf, or rarely the thigh and the buttock, during exercise. (3) Cases have been reported of claudication symptoms worsening after starting propranolol, and improving after stopping propranolol. (4)

Note that beta blockers may be non-selective or selective. Early beta blockers, like propranolol and nadolol are non-selective, and block both beta-1 and beta-2 receptors.  Atenolol, metoprolol, and nebivolol are selective, and only block beta-1 receptors. Consequently, it is more rational to use selective beta blockers in angina and congestive heart failure.

Then, are non-selective beta blockers contraindicated in patients who have intermittent claudication?

A study showed that beta blockers lowered muscle blood flow by about 30%. (5) On the other hand, recent systematic reviews show no adverse effects. (6,7) Many studies in the systematic reviews were based on selective beta blockers, so one would expect fewer clinical effects. Overall, a reasonable approach would be to use selective beta blockers where indicated for angina or congestive heart disease, but to use them with caution in patients with severe peripheral vascular disease. (3,8)


  1. Katzung BG, Masters SB, Trevor AJ. Basic and clinical pharmacology. 12th New York: McGraw-Hill Medical; 2012. p. 151-68.
  2. Waller JR, Waller DG. Drugs for systemic hypertension and angina. Medicine [Internet]. 2018 Aug [cited 2020 Mar 19];46(9):566-72. Available from:
  3. Cassar K. Intermittent claudication. BMJ [Internet]. 2006 Nov [cited 2020 Mar 19];333(7576):1002-5. Available from:
  4. Fogoros RN. Exacerbation of Intermittent Claudication by Propranolol. N Engl J Med 1980; 302:1089
  5. Smith RS, Warren DJ. Effect of beta-blocking drugs on peripheral blood flow in intermittent claudication. Journal of cardiovascular pharmacology, 1982, Vol.4(1), pp.2-4
  6. Radack K, Deck C. ß-Adrenergic Blocker Therapy Does Not Worsen Intermittent Claudication in Subjects With Peripheral Arterial Disease. A Meta-analysis of Randomized Controlled Trials. Arch Intern Med. 1991;151(9):1769-1776
  7. Paravastu SCV, Mendonca DA, Da Silva A. Beta blockers for peripheral arterial disease. Cochrane Database Syst Rev. 2013 Sep 11;(9):CD005508
  8. Ministry of Health Malaysia. Clinical practice guidelines on management of hypertension. 5th Malaysia: Ministry of Health Malaysia; 2018 [cited 2020 Mar 10]. 160 p.


Episode 26: Spinal Anaesthesia


It was early in the morning. Dr. Anna, the surgeon was on her way to work when she
bumped into Dr. Lucy, the junior doctor who appeared to be in deep thoughts.
A: Good morning, Lucy.
B: Hey! Good morning, Dr. Anna.
A: What’s troubling you? I have called you several times, but you didn’t answer.
B: Oh! I am sorry, Dr. Anna. I was thinking about an unusual case which happened in the
ward recently.
A: What case is that? Tell me about it.B: There was a postmenopausal 60-year-old lady presented to the emergency department
after falling from the ladder while cleaning the windows for the Chinese New Year
celebration. She was brought in by wheelchair as she was unable to walk due to the severe
pain. She had no other significant medical history. Examination by Dr Raymond in the
emergency department showed that she was alert and conscious. The right hip was flexed,
adducted and internally rotated. Movement of the right lower limb could not be assessed
but the left side was normal. Neurological examination was unremarkable.
A: Any X-ray?
B: Yeah, the pelvic X-ray showed fractured right femoral neck. She was then admitted to the
orthopaedic ward and arranged for a surgical procedure to stabilise her pelvis. Spinal
anaesthesia was given prior to the operation. The procedure was successful, and she was
awake after that.
A: Sounds great! What happened after that?
B: She was disoriented and lethargic the next morning. Few hours later, she was found
unconscious with dilated pupils before the senior doctor who was busy in the clinic
managed to review. Full blood count, renal profile and ECG results were unremarkable. An
emergency CT scan was performed which showed the herniation of brain tissues into the
foramen magnum. There was a well-defined dural mass identified on the CT scan, suspected
to be a meningioma. She was referred immediately to the neurosurgical department.
Further history taken from her family revealed that she had headache which worsened for
the past 8 months.
A: That was interesting. The doctor should have taken a proper history preoperatively.
B: Exactly. The herniation was most probably caused by the pressure gradient created by
the cerebrospinal fluid leakage during the administration of spinal anaesthesia. But how
does a few drop of cerebrospinal fluid causing such a significant difference?

A: Lucy, do you mean that how could the CSF support the brain tissue which weighs about
1200 g? (1) Hmmm… Do you remember about Pascal’s principle?
B: Yes. It is the principle stating that the input pressure will equal to the output pressure in
an enclosed fluid. (2)
A: Correct. One of the best examples of enclosed fluid in the body is the CSF. The pressure
of a liquid could also be defined as the force per unit area. Therefore, since the pressures
are equal, and F1/A1 = F2/A2, the force exerted will increase with the increase of the area.
Now let’s look at the size of human skull and vertebral canal. Clearly, the vertebral canal is
smaller with an anterior-posterior diameter ranging from 15 to 27 mm. (3) The average
anterior-posterior diameter of a woman’s skull is 171 mm. (4) Can you now calculate how
much force do the CSF need to support the brain?
B: Of course. Wow! We only need 105 g of CSF to support the brain that weighs 1200 g! It is
only about 9% of the brain’s weight!
A: Very good. This is why we should always take a complete history from the patient before
any procedure. But in this case, we could still miss it as it may be a benign tumour which is
slow growing and does not cause any noticeable symptom.
B: I think it will be important for us to watch out for this particular risk of spinal anaesthesia
although it is a rare one.
A: Totally agree!

1. Hartmann P, Ramseier A, Gudat F, Mihatsch MJ, Polasek W. Normal Weight of the
brain in adults in relation to age, sex, body height and weight. Pathologe [Internet].
1994 Jun [cited 2020 Mar 12];15(3)165-70. Available from:
relation-to-age-sex-body-height-and-weight/ doi: 10.1007/s002920050040
2. Fairman JG. Pascal’s principle and hydraulics [Internet]. U.S.A: National Aeronautics
and Space Administration; 1996 [cited 2020 Mar 12]. Available from:
3. Nadalo LA. Spinal stenosis imaging [Internet]. Medscape; 2017 Sep 21 [cited 2020
Mar 12]. Available from:
4. Occupational Health & Safety. Study: women’s skulls thicker, men’s wider; might
affect protection design [Internet]. Occupational Health & Safety; 2008 Jan 22 [cited
2020 Mar 12]. Available from:

Episode 25: When Collagen Fails…


Author: Adam Md Kamal
Editor: Dr. Suneet Sood
Narrator(s): Adam Md Kamal


Imagine this: you are halfway through your pediatric rotation and you are about to complete your first year of houseman-ship. You have already seen your fair share of extraordinary cases: patients with Down’s Syndrome, Alagile Syndrome and Marfan syndrome. But today, in the busy pediatric clinic, a 5 year old boy has come in with his mother. Today, your knowledge is about to be tested.

The 6-year old boy, Alfred is a rather thin and feeble looking boy. His mother, Julia has brought him in with a set of complaints. He easily bruises even after minor falls, explains Julia. She shows to you several bruises all over the body including his legs and arms, all at various stages of healing. “Something’s not right,” you think to yourself. You continue listening to Julia who reveals that he has dislocated his shoulders two times. When asked further, you are surprised to find out that this has happened twice, on each side.

You’re curiosity has peaked; how could a 6-year old have dislocated his shoulder 4 times in total and bruises all over the body? Could this be a case of Non-Accidental Injury (NAI). In other words: abuse? Your mind is racing, thinking of a list of possible abusers. You even begin to suspect Julia. You begin to distrust her more and more as she begins talking about Alfred’s social history. Your distrust gets the better of you; just as you reach the phone to call your supervisor to inform him of an NAI, the door opens. And there he is your supervisor, Dr Alex, a senior pediatrician. “Go on…tell us more” Dr Alex says. He had been listening to the history intently outside the room and you notice he is just as interested as you, if not more.

After further discussion, you notice that the only thing that stands out in Alfred’s history is the frequent shoulder dislocation and multiple bruises. The birth, immunization and drug history are all normal. The social history also seems normal, but you know better: in a case of NAI, you are to remain vigilant and not take the information at face value as even Julia can be the source of abuse. But Julia also mentions that a relative once told her that the child might have Marfan syndrome because Alfred appears quite lanky and his joints were strangely flexible so she is worried he might have Marfan syndrome. Dr Alex who had been listening intently then begins a physical examination and asks you to write down the findings which he says aloud during the examination.

“Crowded oropharynx….hyper-extensible joints……..flat feet. Yes, I can see why you’re worried about Marfan Syndrome” Dr Alex tells Julia. He continue saying aloud results of physical examination”….multiple bruises covering the legs and arms…have you got all that down?” Dr Alex’s asks you as he ends the physical examination. You nod reassuringly. “So what do you think this is?” he asks you. This time you shrug your shoulders, signalling your sheer cluelessness about reaching a medical diagnosis. “Take a guess” Dr Alex commands you. You look at the notes you wrote in Alfred’s file: Multiple bruises, multiple bilateral shoulder dislocations, flat feet, hyper-extensible joints. You think to yourself and blurt out an answer, which sounded more like a question “Marfan syndrome with possible abuse.”

Dr Alex shakes his head with clear disagreement and begins to explain his diagnosis, both to you and Julia:

“Right, so I think what Alfred has is a disease called Ehlers-Dahnlos Syndrome. I can see why you are worried that it could be Marfan syndrome because both conditions are quite similar. In Marfan Syndrome there is a defect in fibrillin (1) which causes the joint anomalies, heart problems and tall stature” Dr Alex pats you on the back, clearly signalling that he understood why you thought it was Marfan Syndrome. Dr Alex continues, “Although in people with Ehlers Dahnlos would also have joint hyper-mobility, the problem isn’t with fibrillin; the problem is with collagen. There are many types of collagen, all found in various parts of the body. In EDS, type III collagen is defective (2). A defect here causes many problems with blood vessels that make them weak and they tend to rupture and bleed easily. That’s why young Alfred here has bruises everywhere in different stages of healing which on the surface, may appear to be abuse”. Dr Alex then gives you a reassuring look, signalling he understood your concerns of NAI. He continues “But the thing that stood out for me was how lax Alfreds joints were; he had dislocated his shoulder several times which you, Julia, have mentioned and I myself felt how lax his finger, toes, knee and arm joints were when I examined him. The joints also have collagen, specifically type II and type I collagen found in the tendons and cartilage (3) So that’s why again, I think its EDS.”


“EDS itself has multiple sub-types which can affect joints, skin, blood vessels and even the heart. However, I can only pickup that Alfred may only have the vascular and hyper-extensible type of EDS; I couldn’t find any problems with the skin”

Julia thanks Dr Alex for his informative explanation and asks how to manage Alfred’s problem. “That’s why I’d like to first do blood test on Alex to confirm this diagnosis. If the diagnosis is confirmed, we can manage him appropriately. But if it’s not, then I would have to suspect other things, even abuse unfortunately, which may involve the police. But that would be highly unlikely and unnecessary because I’m quite sure based on my previous clinical experience, I’m quite sure this is EDS” Dr Alex says confidently.

Julia thanks Dr Alex and you, then leaves to the test room for the blood tests. Dr Alex then turns around to look at you straight in the eyes and says “See that’s why, don’t be so quick to judge and conclude that a child with multiple bruises and past history of joint injury could be an abuse case. Always think of all the medical causes, in this case Ehlers-Dahnlos. So tell me, what have you learnt today?” he asks you

You explain that Ehlers Dahnlos is a disease affecting collagen. There are many types of collagen including type I found in skin and tendons, type II found in cartilage and type III found in blood vessels (3) and that the sub-types of Ehlers Dahnlos depends on which type of collagen is affected.” You then explain that Marfan Syndrome may be confused with EDS but Marfan syndrome affects fibrillin, not collagen.


“Very good” Dr Alex says. “Now go on, call in the next patient”



“Eheler Dahnlos Screening – Google Search.” Accessed February 10, 2020.…0.1..0.192.1249.13j2……0….1..gws-wiz…….0i71j0i7i30j0i13.pEuJJn32iHM&ved=0ahUKEwj-64Gj78XnAhXB7nMBHU5KAsUQ4dUDCAs&uact=5.

“Ehlers-Danlos Syndrome: Background, Pathophysiology, Etiology,” November 21, 2019.

Lodish, Harvey, Arnold Berk, S. Lawrence Zipursky, Paul Matsudaira, David Baltimore, and James Darnell. “Collagen: The Fibrous Proteins of the Matrix.” Molecular Cell Biology. 4th Edition, 2000.

“Marfan Syndrome (MFS): Practice Essentials, Pathophysiology and Etiology, Epidemiology,” January 27, 2020.



Episode 24: Wheezing, Coughing, and not Reproducing


Author: Adam Md Kamal
Editor: Dr. Suneet Sood
Narrator(s): Adam Md Kamal


Imagine this:  you are a houseman in your obstetrics and gynecology posting currently seeing a couple complaining of fertility problems. You ask them fairly standard questions about their family history and discover that the 32-y/o wife, Cynthia, has had 3 children from a previous marriage, and the husband, 38 y/o Jake, does not have any children from his first marriage.  After more extensive questioning, you find no obvious causes from the couple: neither of them smokes, drinks excessively nor has abnormal BMI. They don’t have any medical illnesses of note and are fairly active physically, except that Jake complains of chronic coughing and having a flu very often.

And being the outstanding houseman you know yourself to be, you proceed to physical examination of the wife. The results are fairly standard: she’s a healthy 32 y/o woman with a Pfannenstiel scar, further dissuading you from suspicions towards her fertility.

Then you examine the husband. As with Cynthia, you don’t expect any problems. All is fine until you start feeling for his apex beat: it isn’t there. Not that it’s displaced anywhere, you can’t palpate for an apex beat, nor any beats for that matter on his left chest.  So you try auscultating, the left chest is strangely quiet. As you proceed to auscultating the right chest, you hear it: the unmistakable, distinct thumping of a beating heart, Jake’s heart, but it’s on the right side? You palpate the right chest for his elusive apex beat and there it is, 5th intercostal space, midclavicular line, on the right. “This could only mean one thing.” you say to yourself, trembling as you remove the stethoscope. “What’s that, doctor?” Jake asks you as you realize you were thinking aloud. You reply, “Situs inversus”.

But let’s take a step back for just a minute and recap.

A couple comes in to discuss fertility issues and you rightly suspect that issues may lie with the husband since the wife has 3 kids but he doesn’t. Jake also complains of frequent infections and chronic coughing and on examination you find the not-so-common situs inversus. The question is: could they all be related to each other and to the fertility problems? You ponder for a minute and relay your question to your O&G consultant who’s looking quite relaxed in the pantry and who you know is fond of teaching.

After a lengthy talk with him, a look of confidence flashes on his face. “Aha!”, he exclaims, “you, my friend, may have found a man with Kartagener’s Syndrome”. “Kartagener’s Syndrome?, ehm…what’s that, doctor?” you ask, puzzled. “Well, here’s the thing young man”, he says,  with proud tone liken to that of a professor “Kartegener’s Syndrome, apart from being one of the more difficult conditions to pronounce correctly, is also one of the rarer conditions. Frankly, I quite like its other name which is a bit easier to pronounce`: primary ciliary dyskinesia” (1)., “So something is wrong with the cilia”. (1) you say.

“Correct! So can you connect the dots now?” he asks. You take your time thinking about it and reply, carefully choosing your words. “So he has problems with his cilia and that affects his respiratory system’s ability to clean itself. Hmmm….I can see how that causes the frequent URTIs and chronic coughing (1)…but what about the infertility and situs inversus?”.

“Well, fairly good try but not accurate enough, young man” he says. “All this man’s problems are related to a single enzyme, an enzyme called dynein (1). So dynein is found in within all the cilia in a person’s body and is a type of ATPase*(1). Hopefully, you will remember that an ATPase breaks down ATP for energy. In normal people, dynein generates this energy to allow for proper ciliary movement, specifically bending. However, in Kartagener’s this enzyme is defective. So the person’s cilia can’t convert this energy to proper bending movements of the cilia. So, yes, you correctly mention why his respiratory to tract fails to perform mucociliary clearance well, it could even lead to bronchiectasis in severe cases (1).

But cilia in other places are also affected. In the reproductive system, cilia in the sperm and cilia in the fallopian tubes causes infertility for both men and women respectively (2).”

“And even before birth, during embryogenesis, there are crucial roles played by the cilia. In a normal person, the cilia in the primitive knot at the anterior end of the primitive streak in the embryo can beat regularly. This sweeps the organs into their normal orientation (3)(4). However, in people with Kartagener’s the cilia cannot beat and can only rotate clockwise. So the organs aren’t able to move into their correct position because of the defective cilia, leading to a mirror image of normal organ orientation, in other words, situs inversus” (2).

And with that brilliant answer, everything suddenly makes sense to you now. “So all this patient’s problems are caused by a defect in a single enzyme in the cilia! That’s amazing!” you exclaim with much enthusiasm. “Well, yes it is quite amazing for a young houseman like you. Kartagener’s is a rare occurrence so you’re quite lucky to have the opportunity to come across and manage one. But your patient would probably not consider himself quite so lucky, you see” the consultant replies.

Your enthusiasm now becomes concern, and empathetically you ask, “So how can we help this man?”. “Well first thing’s first” he replies, “we must confirm the diagnosis. We can do a screening test measuring nasal nitric oxide levels.(5) We could further do light microscopy to look at the ciliary beat patterns but that might be a bit expensive. Either way, we have to manage him symptomatically. We can refer the husband and wife for assisted reproductive therapies (ARTs) to help them with fertility (6). Artificial insemination might be useful for them (6). Also, you need to tell them that since the condition is autosomal recessive there’s a good chance their children may be carriers as well, and that the man may have inherited it from his parents who were also carriers” (1).

“Can you remember all that?” your consultants barks, breaking you out of your stuporous posture. “Ehmm yes…..kind of. So Kartegener’s Syndrome aka primary ciliary dyskinesia, is an autosomal recessive medical condition that arises from defective dynein, an ATPase found in cilia. Because of this the cilia are defective, leading to classical symptoms of chronic respiratory tract infections, lung problems like bronchiectasis, situs inversus and infertility.

“Very good!”, the consultant replies, with an empathetic expression. He stares into space for a moment. Then suddenly his expression changes “Well, that’s enough lecturing for me today, off you go! I’ve got a Caesar to do in an hour.”


  • “Primary Ciliary Dyskinesia: Background, Pathophysiology, Epidemiology,” November 8, 2019.
  • Stern, Brittany M., and Girish Sharma. “Ciliary Dysfunction (Kartagener Syndrome, Primary Ciliary Dyskinesia).” In StatPearls. Treasure Island (FL): StatPearls Publishing, 2020.
  • Cartwright, Julyan H. E., Oreste Piro, and Idan Tuval. “Fluid-Dynamical Basis of the Embryonic Development of Left-Right Asymmetry in Vertebrates.” Proceedings of the National Academy of Sciences of the United States of America 101, no. 19 (May 11, 2004): 7234–39.
  • Nonaka, Shigenori, Satoko Yoshiba, Daisuke Watanabe, Shingo Ikeuchi, Tomonobu Goto, Wallace F Marshall, and Hiroshi Hamada. “De Novo Formation of Left–Right Asymmetry by Posterior Tilt of Nodal Cilia.” PLoS Biology 3, no. 8 (August 2005).
  • “Nitric Oxide in Primary Ciliary Dyskinesia | European Respiratory Society.” Accessed January 30, 2020.
  • Sha, Yan-Wei, Lu Ding, and Ping Li. “Management of Primary Ciliary Dyskinesia/Kartagener’s Syndrome in Infertile Male Patients and Current Progress in Defining the Underlying Genetic Mechanism.” Asian Journal of Andrology 16, no. 1 (2014): 101–6.

Episode 23: Unintentional Overdose


Author: Adam Md Kamal
Editor: Dr. Suneet Sood
Narrators: Adam Md Kamal


On a dark, damp night, 21-year-old Jenny is brought into the emergency department on a stretcher wearing vomit-stained clothes. Appearing dazed, confused and sweating profusely, the situation for her appears dire. She doesn’t appear to be conscious at the moment, so taking a history from her would be far from easy. Thankfully, her mother is available; she was the one that brought her daughter to the hospital. She’s distressed, but she seems cooperative and willing to talk. In fact, she even looks keen to talk to someone, anyone really.

At the centre of this is you, a junior houseman, just starting your rotation in A&E. Being the thoughtful and valiant doctor you know yourself to be, you approach the distressed mother in hopes of alleviating her very appreciable anxiety. She introduces herself as Judith.

“What’s the matter?” you ask Judith. Anxiously, Judith replies “My daughter, Jenny, I’m very worried about her….I think she tried to kill herself when she took those pills”. “What pills?” you ask, “Why would she try to end her life?”.

“Lately, she’s been having trouble with her studies, she failed her psychology unit and has to repeat a year. The news hit her very hard”. As Judith tries to maintain composure as best as she can, she goes on, “A couple of days ago after hearing the news, I saw her taking a lot of paracetamol pills. I’m sure she took 20 tablets because we ran out of our entire household supply within a day! Of course, I asked her why. She said she wasn’t feeling very well and was quite dizzy. Anyway, after that she started feeling very nauseous and sweaty, so I thought she was telling the truth about feeling sick. The next day she appeared well, and I thought it was over. But today, 4 days after I noticed she took those tablets, I noticed she started looking sick again, much worse than before (1) and started vomiting all over the place. Then she got really drowsy and slept on the couch for a while. I tried waking her up in the evening and when I couldn’t wake her up, I brought her here.” Judith now appears visibly sad, but much less anxious after talking to you. Perhaps your genuine concern has eased her. She hands you a pack of the paracetamol her daughter took.

But now your interest peaks; it is now you wanting to talk a bit more, to learn about Jenny’s predicament.  Specifically, because you remember from medical school that the toxic dose for acetaminophen in adults is 7.5-10 g (1). Reading the packet Judith gave you, it says 250 mg per tablet. Using a bit of mental acrobatics, you calculate that she took (20×250 mg) 5.0 g. You double check your math and yes, you are certain she took 5.0 g of acetaminophen. In short, something isn’t adding up. You know it, you feel it. Just as you are thinking to yourself, you notice a senior doctor order routine blood tests and a drug toxicity work-up for Jenny. You await the results with much trepidation yet here is her mother right in front of you, clearly open to conversation. So you probe further.

“Does Jenny have any other medical conditions? I’m sorry to ask this, but this isn’t adding up…I’m not so sure that it’s just the paracetamol tablets involved here.” At first Judith appears apprehensive, but seeing the genuine concern from you, she replies. “Actually doctor, she does. She has had seizures since she was a teenager, so her doctor has given her carbamezapine for this (2) and she’s quite diligent: she takes them as she is supposed to.”

Then it strikes you; could it be some sort of drug interaction? Possibly, but you don’t know exactly how. You’re absolutely sure the liver’s involved (1) but you’re not sure how. Just as you ponder to yourself, your pharmacologist friend Pharah passes by. “She’s quite the bookworm”, you think to yourself, “I’m sure she’ll know a thing or two about paracetamol pharmacology, or at least much more than I remember from medical schoolJ”. You seize this opportunity to ask her about the case.

As you explain Jenny’s case to her, Pharah appears to grow increasingly uninterested from the story and stops you. She does seem to get the main point though, and then says “Look, it’s so simple, there’s an enzyme in the liver called CYP2E1 (3), part of the cytochrome P450 system. This enzyme converts acetaminophen into a metabolite called NAPQI (1)(3), and this NAPQI is very toxic. Usually, this enzyme would produce a small amount of NAPQI, and the body is able to convert it by glutathione into another safer metabolite which can be excreted safely (1)and this enzyme is not overwhelmed unless you exceed the 7.5-10 g (1) toxic dose which you are aware of. You’re aware of this aren’t you?”. You nod, confidently. Pharah goes on, “So in your patient, the presence of carbamazepine in her system induces the enzyme CYP2E1, potentiating its effect (4). Therefore more NAPQI is produced, at a lower dose, so even though your patient only took 5 g, still well below the toxic dose, she is producing a disproportionately large amount of NAPQI. It accumulates and causes her symptoms of hepatotoxicity (4). You look clueless….” she pauses, observing you with your mouth hanging wide open with bewilderment “does this makes sense to you?”. “Yes, that was crystal clear, thank you, Pharah you’ve cleared my doubts. For a moment there, I was doubting my ability to calculate correctly. Thank you again” you reply with gratitude. “No problem.” Pharah replied with a forced but sincere smile as she leaves you hastily to attend to other matters.

Just as Pharah leaves, you notice Jenny’s blood results have been delivered to her bed. And sure enough the results are consistent with your initial thoughts, AST is markedly elevated at 12,500 U/L. Simultaneously, you overhear the senior doctors discussing why is the AST so elevated, “Does she have a liver problem?” one of them asks.

Just as they began to discuss, you modestly relay what you have just learnt, about how carbamazepine (which Jenny was taking) along with other anticonvulsants potentiate the effects of CYP2E1, causing a disproportionate increase in NAPQI, a toxic metabolite, which overwhelms the liver thus causing hepatoxicity. Just as you mention this, the consultant hears your explanation. Clearly impressed, he says jokingly “Genius! Ever thought of staying with us at A&E after housemanship? We could definitely use more doctors like you.”



Episode 22: Catch 22



Author: Adam Md Kamal
Editor: Dr. Suneet Sood
Narrators: Adam Md Kamal


Picture this: it’s a busy morning in the emergency department, as usual. You, a junior houseman, have just finished following your senior doctors for rounds. Just as you’re about to rest, your supervising medical officer approaches, looking visibly flustered. Dr. Lee is usually very friendly to you, but today he looks like he’s in a rush. “He must be very busy”, you think to yourself. Just as you try to smile to Dr. Lee, with a serious expression, he tells you “Hey, I have an urgent case that I need to attend to now. Like right now. There’s a child over there, just admitted, the mother looks distressed. Talk to them, get a history. OK?”

“Sure, doctor. Will do”, you reply. Not that you had a choice.

So you go to the mother and child and begin talking to the mother, who introduces herself as Maryam. You begin discussing about her 7-month old son, Ali.

“See Ali here, he’s always sick” she says, “always coughing, he keeps getting sick”. “How sick?” you ask. “It’s always like a flu-kind of thing; sneezing and coughing but not vomiting or pooping problems. He has 3 older siblings, and I know, I just know, that Ali seems to be a lot weaker than them.” “Hmm…that sounds distressing. So you think he falls sick easily, at least, compared to his siblings?” you ask. “Yes I’m sure of it” she replies. Now your past medical knowledge starts conjuring ideas in your mind. “Maybe some sort of immunosuppressed state? Perhaps leukocytopenia?” you think to yourself “Perhaps, pancytopenia?” You continue asking Maryam “what other problems do you feel Ali is experiencing?”

She continues, “Yes, today, I noticed he’s very stiff, like he is all tense up for some reason. I noticed this when I was trying to breastfeed him. The worst part is, I noticed he wasn’t suckling, like he’s too tense to suckle. THAT’s what worried me the most. That’s when I brought him here, to the hospital”.

Now, the history seems clearer: Frequent infections, poor feeding and some sort of generalized spasm. When you approached the mother and child, all your attention was towards the mother,  but now you direct it towards the child. You take a good look at baby Ali and notice several key features. First: the hands appear to be in a sort of shape. You’ve seen this before from your previous rotations. Then you remember it, yes, it’s called a carpopedal spasm (3), but you forgot what this indicates. And you also notice that Ali is generally tensed up, just as Maryam described. But in addition to these, you notice several other more striking features: Ali’s face appears dysmorphic, but it doesn’t quite look like Down’s syndrome facies (4). Yet, his head appears long, his jaw appears small and teeth are also unusually small (5). Most noticeably, he has a cleft palate (5). You ask Maryam and she confirms that indeed, he’s had a cleft palate since birth.

You proceed to conduct a thorough physical examination and find peripheral cyanosis (5) and URTI symptoms of sneezing in addition to the previous abnormal facies and cleft palate. Other systems are unremarkable. So you stand there pondering as Maryam nurses Ali, pondering for a diagnosis. Sounds a lot like a chromosomal abnormality like Down syndrome (4), but something doesn’t add up: the spasms. They are not very typical of Down Syndrome children. Then, you take peak at Ali’s lab results.

After a good look at those results, you summarize the findings to yourself. Blood results shows low white cell count, but other blood cell counts are normal. Leukocytopenia, which you anticipated earlier based on the frequent infections (5). But surprisingly amongst the normal results, you notice one striking result, low serum calcium. You now suspect the hypocalcemia to be the cause of Ali’s spasms. To confirm your suspicions,  you tap on the posterior end of Ali’s mandible. Sure enough, a positive Chvostek’s sign indicating hypocalcemia (3). At this point you notice Ali has been stabilized adequately by the staff, the nurses don’t seemed concerned with him and attend to other patients. “At least he’s stable”, you think.

Going back to the results, you summarize your findings as concisely as possible: hypocalcemia, leukocytopenia, cleft palate, abnormal facies. You think about this for a very long time. The longer you think, the more you find yourself giving up on reaching a diagnosis. Frustration sets in.

Just when you were about to capitulate and all hope seems lost, here comes Dr. Lee again. This time he looks a lot happier &  a lot like his usual self. With a large grin on his face, he asks you, “So, how’s things? Diagnosis?”. You relay all your findings from history to investigations to Dr. Lee who listens intently. Then, he scratches his chin, pauses and casually says, “DiGeorge Syndrome”.

“DiGeorge syndrome? What’s that?” you ask. ”Well, see here its quite simple actually, if you remember your embryology. You do remember your embryology, don’t you?” he asks cynically. You remain silent and smile.

So, he goes on. “Anyway, just recall that there are pharyngeal pouches which develop into other structures around the neck (6). Specifically, let’s talk about the pharyngeal pouches 3 & 4. These will eventually lead to the formation of the thymus, parathyroid gland, and part of the palate and heart by conotruncal development which separates the pulmonary artery from the aorta (6). So in DiGeorge syndrome, there’s a chromosomal defect in the location 22q11 (5), which carries genes for the development of the pharyngeal pouches 3 & 4 (7). Therefore, the results are as you expect: aplasia of the thymus leads to leukocytopenia, defective parathyroid gland leads to hypocalcemia, defective conotruncal development leads to congenital heart disease, (a lot of types but we aren’t sure which one yet in Ali’s case) and of course the cleft palate (7). Common sense isn’t it?”.

Listening to Dr. Lee’s explanation, you say, “Wow, that was a really good explanation Doctor. So basically, all the symptoms, hypocalcemia, leukocytopenia, cyanosis and cleft palate all relate to the defective embryological development of pharyngeal pouches 3 & 4? (5)(7)” you ask. “Yes, that is exactly right. In case you want to remember this disease well you can remember the mnemonic CATCH-22:

C for Cardiac abnormalities

A for Abnormal facies

T for Thymic aplasia

C for Cleft palate

H for Hypocalcemia

& 22 for chromosome 22q11 defect.

Memorize this mnemonic and you’ll be alright in case you see another DiGeorge syndrome patient.” Dr. Lee says.

You stand there, trying to digest everything Dr. Lee said for a moment. He interrupts the silence, “Anyway, that’s enough lecturing for one day, I’m not paid for it anyway J ……help me prop up the child one moment, I want to  examine the child.” You oblige, continuing your work despite the fatigue and information overload.



  1. UCSD’s Practical Guide to Clinical Medicine [Internet]. [cited 2020 Jan 30]. Available from:
  2. Phillips KA, Ospina NS. Physicians Interrupting Patients. JAMA. 2017 Jul 4;318(1):93–4.
  3. Hypocalcemia Clinical Presentation: History, Physical Examination [Internet]. [cited 2020 Jan 30]. Available from:
  4. Down Syndrome: Practice Essentials, Background, Pathophysiology [Internet]. [cited 2020 Jan 30]. Available from:
  5. DiGeorge Syndrome: Practice Essentials, Background, Pathophysiology. 2019 Nov 12 [cited 2020 Jan 30]; Available from:
  6. Duke Embryology – Craniofacial Development [Internet]. [cited 2020 Jan 30]. Available from:
  7. DiGeorge Syndrome: Practice Essentials, Background, Pathophysiology. 2019 Nov 12 [cited 2020 Jan 30]; Available from:


Episode 21: Bleeding time


Author: Dr. Suneet Sood
Editor: Thong Yi Kun
Narrators: Thong Yi Kun, Ceceilia Ling


C: I can see you have an interesting story today

Yi Kun: Yes. I was recalling the case of one of my cirrhotic patients. This man was in the ICU, and had a platelet count of only 30,000 per microliter.

C: Ah yes, because of the splenomegaly, right?

Yi Kun: Partly, yes, the splenomegaly can cause a pancytopenia, including thrombocytopenia. However, it seems that in cirrhosis there are other mechanisms that lower the platelets. Anyway, we were wondering about the risk of spontaneous haemorrhage in this case.

C: Can it occur at a platelet count of 30,000?

Yi Kun: Not likely. Spontaneous haemorrhage tends to occur only if the platelet count falls below 20,000. [ref ] Anyway, one of my housemen asked me if we could request a bleeding time test and I agreed. So a BT was done, and it was reported as 3 minutes. The normal range is 2-8 minutes, so the team was happy. But the same houseman asked me how it was that the BT was normal despite such a low platelet count.

C: Valid question.

Yi Kun: Quite valid! So I asked my team if anybody knew the relationship between BT and platelet count, and my chief resident, a really bright chap, said he had read that there was an equation for this. This equation was valid at counts below 100,000 per microliter.

C: What equation?

Yi Kun: You divide platelet count by 3850. Subtract the result from 30.5, and you get the expected bleeding time in minutes.


Bleeding time (minutes) = 30.5 – (platelet count/3850)


C: So, for this patient…

Yi Kun: 30,000 divided by 3850 is 7.8. Subtract 7.8 from 30.5 and you get 22.7.

C: So this patient should have had a bleeding time of over 20 minutes?

Yi Kun: Yes, 22.7 minutes, and the lab reported 3 minutes, so there was a glaring discrepancy.

C: There sure was!

Yi Kun: …and nobody could explain it, so I asked the same girl how the test was done. She said the lab technician came and did the test by puncturing the finger-tip and seeing how long the bleeding continued.

C: I thought we were supposed to puncture the ear lobe?

Yi Kun: You are right, actually, but first let me tell you what happened. So I asked the houseman to do it herself using the Ivy method. She said she didn’t know what it was, and I asked her to Google it, so she did. In the Ivy method you apply a BP cuff above the elbow, and make a small puncture at the elbow. The exact dimensions of the puncture are written in the books. Anyway, she called me after 20 minutes and said that the bleeding is not stopping, what to do, and I said hold on. Finally, it turned out that the bleeding stopped after 24 minutes.

C: Wow!

Yi Kun: Then I asked her to look up the literature. The next day she reported that the first method was, as you rightly pointed out, by puncturing the ear lobe. This was the Duke method. Later the method was modified by Ivy, using a BP cuff, and this was much more sensitive.

C: Amazing! But why did the lab use the finger-tip to test the BT?

Yi Kun: My guess is that somewhere down the line people wondered why ear lobe, the finger should work as well, and modified the method without referring to the literature. You know how we all are, quick to take short cuts!

C: So the right method of doing bleeding time is the Ivy technique?

Yi Kun: Yes, it is. Of course, these in vivo tests are less often used now. Still, if one has to do the bleeding time, one should do it properly.

C: Can’t disagree with that!



Harker LA, Slichter SJ. The Bleeding Time as a Screening Test for Evaluation of Platelet Function. N Engl J Med 1972; 287:155-159

Mielke CH, Kaneshlro MM, Maher IA, Weiner JM, Rapaport SI. The standardized normal ivy bleeding time and its prolongation by aspirin. Blood 1969; 34 (2)204-215

Panzer S, Jilma P. Methods for testing platelet function for transfusion medicine. Vox Sanguinis (2011) 101, 1–9

Episode 20: Hereditary spherocytosis


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Author: Dr. Suneet Sood
Editor: Dr. Suneet Sood
Narrators: Alan Koay, Thong Yi Kun


Why so glum?

Ah, nothing

No, there’s something on your mind

It’s that Professor Rahman. He asks the strangest questions. And I have to come up with an answer by tomorrow.

What strange question?

Well, I was presenting a case of hemolytic anemia, and the patient had hereditary spherocytosis. Prof Rahman sked what are spherocytes, so I told him that normally our red cells are biconcave, but in HS they become spheres, so we call them spherocytes. I also told him that HS may be autosomal dominant or autosomal recessive.

That’s correct.

Then he asks, “What’s the benefit of biconcave red cells over spheres?” And I told him that the biconcave structure allows the cells to be deformable when they pass through the spleen.

That’s also correct, so what was Prof Rahman’s issue?

So then he asks if there are any other benefits of a biconcave shape, and I didn’t know.


Do you know?

Yes, I do.


I’ll tell you. But go on. What else did Prof Rahman say?

He asked, “What defect causes the RBC to become a spherocyte?”


And then he asks me this really weird question. What’s the relationship of the surface area of a sphere to its volume, and how is that relevant in HS?


And who knows the answer to such strange questions? Do you know?


So tell.

Okay. Well, first, the benefits of the biconcave shape are two. One, as you pointed out, the biconcave shape allows deformability. The RBCs can easily pass through the splenic cords of Billroth. The second advantage of a biconcave shape is that it provides a much larger surface area to the RBC. You remember your geometry, don’t you?

Not really.

During our maths classes in school, we learnt that a sphere has the smallest surface area for a given volume. Obviously the biconcave shape gives the cell a much larger surface area, which allows for better oxygen absorption.

Ah! Of course!

The second question is, why does the RBC become a spherocyte? Well, in HS, there is an inborn defect of cell membrane proteins, particularly proteins called spectrin and Ankyrin. The defect makes the cell membrane unstable and results in a loss of surface membrane area. So HS is primarily a deficiency of RBC surface membrane area.

Oh, and a loss of surface membrane area means that the cell has to occupy the smallest possible surface area for its volume, and become spherical!

True. Interesting, isn’t it, how the laws of geometry intrude into the pathology of hereditary spherocytosis?

Not at all interesting. I prefer geometry to stay back in school, where it belongs.



Diez-Silva M, Dao M, Han J, Lim C-T, Suresh S. Shape and Biomechanical Characteristics of Human Red Blood Cells in Health and Disease.MRS Bull. 2010 May; 35(5): 382–388.

Rajpoot HC. Why sphere minimizes surface area for a given volume? Stack Exchange, 2015,, accessed 14 Apr 2018

Episode 19: PPI’s and Hypomagnesemia


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Author: Dr. Suneet Sood
Editor: Dr. Suneet Sood
Narrators: Thong Yi Kun, Alan Koay



What are you going to tell us today?

Let me tell you about an old man I saw yesterday. Interesting case, and taught me something.


This gentleman lives in an old age home. His children are abroad, but he is well looked-after, and fairly happy in this home.

Uh huh…

Over the preceding few months, he had complained of increasing weakness and irritability, and was brought by the workers of the old age home to our general physician. This physician looked at him, and, in my opinion, took a somewhat cursory history. Anyway, examination showed nothing.

Maybe malnutrition?

Yes, actually malnutrition is common in inmates of old age homes. In any case, our physician ran a battery of tests, and came up with slight hypocalcemia and hypokalemia, but severe hypomagnesaemia. The ECG changes were consistent with this electrolyte pattern.

How severe was the hypomagnesaemia?

Fairly severe. Zero-point-five millimoles per liter. Normal values are above zero-point-eight.

Well, we know that old age inmates can develop hypomagnesemia.

That’s true. And that’s what the physician thought: this is a very common setting for hypomagnesemia. In fact, oral treatment with magnesium lactate improved the patient, who felt much better after a few days of treatment.

The staff in these old age homes often does not care. Anyway, how did you get involved? You are a gastroenterologist.

That’s the point. The physician send sent the patient to me so that I could look at this patient for his chronic gastroesophageal reflux problem, perhaps scope him. When I took the history, I was a little surprised. The old age home which the patient attends is part of a chain with an excellent reputation. In fact, one of my relatives lives in one of these. I’ve visited him, and I thought the staff was actually very good.


 So I asked around, and, sure enough, the patient was actually well cared for in this home. The inmates here do not get malnourished.

Well, this patient surely did. Otherwise how do you explain his severe hypomagnesemia?

That’s what I’m coming to. I realized that this patient has been on omeprazole for a long time. Proton pump inhibitors are among the important causes of hypomagnesemia.


Yes. The other important cause of hypomagnesemia is diuretic therapy. In addition, several other drugs have been implicated.

How do PPIs cause hypomagnesemia?

It seems that they interfere with absorption of magnesium.

Is this hypomagnesemia dose-related?

Maybe, but there’s some recent evidence that it’s not, so I think that it causes low Mg levels in susceptible persons only.

So you stopped the omeprazole?

Well, I can’t. He needs the PPI for his reflux. My options are to try to control the Mg levels with supplements. If this does not work, I’ll have to send him to a surgeon for anti-reflux therapy.

Thank you.




Cheungpasitporn W, Thongprayoon C, Kittanamongkolchai W, Srivali N, Edmonds PJ, Ungprasert P, O’Corragain OA, Korpaisarn S, Erickson SB. Proton pump inhibitors linked to hypomagnesemia: a systematic review and meta-analysis of observational studies. Ren Fail. 2015 Aug;37(7):1237-41. doi: 10.3109/0886022X.2015.1057800.

Chowdhry M, Shah K, Kemper S, Zekan D, Carter W, McJunkin B. Proton pump inhibitors are not associated with hypomagnesemia, regardless of dose or concomitant diuretic use. J Gastroenterol Hepatol. 2018 Mar 7. doi: 10.1111/jgh.14141.

Fulop T. Hypomagnesemia. Medscape, available at, updated 16 June 2016, accessed 24 Mar 2018

Hoorn EJ, van der Hoek J, de Man RA, Kuipers EJ, Bolwerk C, Zietse R. A case series of proton pump inhibitor-induced hypomagnesemia. Am J Kidney Dis. 2010 Jul. 56(1):112-6.

Kieboom BC, Kiefte-de Jong JC, Eijgelsheim M, Franco OH, Kuipers EJ, Hofman A, et al. Proton Pump Inhibitors and Hypomagnesemia in the General Population: A Population-Based Cohort Study. Am J Kidney Dis. 2015 Nov. 66 (5):775-82.

Episode 18: Varicoceles


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Author: Dr. Suneet Sood
Editor: Dr. Suneet Sood
Narrators: Thong Yi Kun, Alan Koay, Siah Tse Nin


Dr Jagdip was speaking. Lecturing, really, I thought, trying to fight boredom.

There were six of us in the urology ward, discussing a patient with a varicocele. I stole a glance at Perminder, standing to my left. Perminder was all attention, as usual. And now he had started to wring his hand, a sure sign that he was upset because something Dr Jagdip was saying didn’t make sense to Perminder. Perminder, the class genius, always got upset when things didn’t make sense.

“…so we ligate the testicular veins in order to treat a varicocele,” Dr Jagdip was saying. “This is called Palomo’s operation. Something on your mind, Perminder?”  She, too, noticed Perminder’s agitation.

“Er, well, you just told us that a retroperitoneal tumor or a left renal tumor can cause varicocele by blocking off the testicular vein…”

“Yes, I did. On the left side, the testicular vein enters the renal. A renal tumor can grow and block off the testicular vein, resulting in a varicocele. In fact, a recent left-sided varicocele in a 40+ male should make you think of renal tumor.”

“But, if obstruction of the testicular vein causes varicocele, why should surgical ligation of the testicular vein result in curing a varicocele?”

“Well, Well, that’s the way medicine is. It works. Everything doesn’t always make sense.” Dr Jagdip faltered. Clearly she hadn’t thought of this.

We were all amused, as were some of the other students, but we didn’t smirk for too long. Dr Jagdip was quite a nice person, actually, even though she was a little dull. As she finished teaching, she asked a last question.

“Why is a varicocele more common on the left side?”

I answered. I had read it in the surgery book last night.

“It’s because the left testicular vein enters the left renal at a right angle, while the right testicular vein enters the vena cava at an obtuse angle. These hemodynamics favor higher left-sided pressures, which predispose patients to left-sided varicoceles.”

I had impressed Dr Jagdip. In fact, I had impressed myself: I had been able to quote the book verbatim.

But Perminder was wringing his hands again. Only this time he remained silent.

As soon as the class finished, I asked him, “What?”

“What what” asked Perminder.

“You didn’t agree with that answer about why left-sided varicoceles are more prevalent.”

“No, I didn’t. Your answer was wrong.”

“But that’s what the book says.”

“I know” said Perminder. “But the book is wrong.”

I knew better than to scoff. Perminder was Perminder. “So tell me.”

“The angle makes no difference. The pressures are transmitted in accordance with the laws of physics, and are transmitted very well across angles. The real reason for the increased frequency of left-sided varicoceles is that the pressure in the left renal vein is much higher than that in the vena cava. The left testicular vein drains into a high-pressure system. The right drains into a low-pressure system.”

“But why is the pressure in the renal vein so high? It drains blood only from the kidney! And the IVC carries much more blood.”

“That’s true, but the IVC is wider than the renal vein. Therefore the pressure in the renal vein is higher than the IVC. Remember Poiseuille’s law? Pressure is inversely proportional to the fourth power of the radius? So even a small decrease in radius causes a marked increase in the pressure within the renal vein.”

“Hm,” I said. That makes a lot more sense than the right angle theory.

The next day Perminder said, “I’ve worked out the Palomo-tumor contradiction.”

“Which one?” I asked. I had already forgotten yesterday’s class.

“Why a tumor can block the left testicular vein and cause varicocele, and yet a ligation of the testicular vein can cure it.”

“Oh that one!” I said. Now I was interested. “Tell.”

“Let’s first talk about a tumor. When a tumor blocks the testicular vein, the vein and its tributaries will dilate. That’s to be expected. The blood from the testes has nowhere to go. It’s the same principle as development of varices in cirrhosis.”

“Makes sense,” I said.

“Now let’s talk about ligation of the veins. Idiopathic varicoceles develop because of dilatation of the left testicular vein. Remember, the left testicular vein drains into a high-pressure area? In these varicoceles, there is a retrograde blood flow from the renal down the testicular vein into the Pampiniform plexus. So in patients with idiopathic varicoceles, the testes cannot be draining into the renal vein. In fact, they are draining into the collaterals.”

“So why can’t the testicular vein drain into the collaterals in a tumor?”

“Because the collaterals take long to develop. In an idiopathic varicocele the time span is very long, and good collaterals have developed.”

“Makes sense,” I said, impressed. “Where do these collaterals go?”

“These collaterals connect the testicular veins with some retroperitoneal veins, the inferior epigastric vein, and some others. When you tie off the testicular vein, you block off a high-pressure vein that is retrogradely flowing from the renal towards the testis. This cures the varicocele. And after blocking off the testicular vein, the collaterals happily carry the blood away from the testis!”

“Ahhh, now I get it! In an idiopathic varicocele, the cause is the retrograde flow from the kidney, and the collaterals from the testis have already developed. So you can easily tie off the testicular vein. In a tumor, the cause of the varicocele is the high pressure in the testicular vessels because of inability of the blood to flow into the renal vein. In tumor patients operative ligation of the testicular vein will not help, because the testicular vein is already blocked.”

“True. But if you are going to operate on a patient with a tumor, you may as well remove the tumor.”

“There’s that, too”, I said.

Take home message: The pressure in the renal vein is higher than the pressure in the vena cava, causing varicoceles being commoner on the left than on the right. The high pressure is because of an important law of physics: Poisuille’s law, which states that pressure is inversely proportional to the fourth power of the radius.



Gendel V, Haddadin I, Nosher JL. Antegrade pampiniform plexus venography in recurrent varicocele: Case report and anatomy review. World J Radiol 2011; 3(7): 94-198 Available from: URL: 94.htm DOI: 94