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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

Episode 17: Right sided neck lump


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


There’s a buzz of excitement in the ward: it’s the grand round day. Every Wednesday Professor Azim, the head of Surgery, comes in to take a long, long round. All the housemen have been busy ensuring that the case records are complete. The Professor has a tendency to be slightly caustic, but there’s usually a lot of learning during the round.

It’s patient number seven, and you are it. “Who is presenting this patient?” the Professor asks.

“It’s me, Prof”, you answer

You start.

“This is a 41-year-old male who presents with weight loss and altered bowel habit for the past month.”

You go on to present the history in detail, then move on to the findings.

“There’s a mass in the right lower abdomen. It’s non-tender, firm, but not hard.”

“Supraclavicular nodes?” asks Professor Azim.

“No palpable nodes in the left supraclavicular region” you say, a little hopefully. This seems to be going well, and you are glad you remembered to examine the left neck.


“I’m thinking abdominal tuberculosis as my first diagnosis, and I’m keeping colon cancer as a possibility. He’s a little young for cancer, but after 40 we always want to rule it out.” This is a direct dig at the professor. One of his favorite aphorisms is “Rule out cancer in all patients above 40”.

“TB, huh? What does the chest show on examination?”

“It’s normal,” I say. I’ve looked at the respiratory system, the cardiovascular system, and have even done a neurological examination. I don’t want the professor to make his famous sarcastic crack about “In my days the head was part of the body. How the human being has evolved!”

“What’s your plan?” he asks.

“We will start with a workup for TB. Chest film, Mantoux. CT scan for the lump. If it’s consistent with TB we’ll start anti-tubercular therapy. If there’s evidence of a stricture we’ll plan surgery. If any node had been enlarged we would have biopsied it, but he has no enlargement of the axillary nodes or the left supraclavicular node.”

The professor moves forward to examine the patient, but I’m confident of my findings. This will go well. He looks carefully at the abdomen, then palpates it, percusses it, asks about auscultatory findings. Then he moves to the neck, and, after about fifteen seconds, his voice booms. My heart skips a beat.

“What’s this?” he asks.

You palpate the patient’s neck again. It feels like a node in the right supraclavicular fossa. Where did that come from? Should I pretend it’s a cervical rib? No, it’s clearly a node. Hard, malignant.

“What does this mean?” he asks.

I’m not sure,” I answer. “Maybe TB?” I know that’s the wrong answer. The node is too hard. But it’s on the right side!

“TB?” he asks.

“No, it’s too hard. Does he have a cancer in the head or neck? Maybe a laryngeal cancer? But there’s no hoarseness. And he’s not a smoker.”

“Could it have come from the abdominal mass?”

“No, abdominal masses metastasize up the thoracic duct to the Virchow’s nodes in the left supraclavicular fossa, not right.”

“Anybody comments from anyone else?”

The professor looks around. Nobody answers. The junior consultant too is quiet. The professor continues.

“Okay. What is the equivalent of the thoracic duct on the right?”

“There’s the right lymphatic duct. It drains into the right subclavian vein, corresponding to the drainage of the thoracic duct on the left side. But it’s not connected to the abdomen.”

” Actually, studies show that there IS a cross-communication between the thoracic duct on the left and the right lymphatic duct on the right in many persons. About 5% of the lymph from the thoracic duct crosses over and enters the right lymphatic duct. Which means that…?”

“Which means that in about 5% of cases mets from the abdomen can end up in the right supraclavicular nodes?”

“Yes. This means that in a patient with suspected abdominal cancer, always examine both the right and the left supraclavicular fossae.”

The registrar takes over, asking me to arrange a fine needle aspiration cytology of the lump.

The professor exchanges a glance with the junior consultant.

“Nobody reads anatomy these days,” he complains.



Davis HK. A statistical study of the thoracic duct in man. Developmental Dynamics, 1915;17 (2):211-44
Rabin ER, Meyer EC. Cardiopulmonary Effects of Pulmonary Venous Hypertension with Special Reference to Pulmonary Lymphatic Flow. Circulation research 1960;8:324-35
Ross KJ. A review of the surgery of the thoracic duct. Thorax 1961;16:12-21

Episode 16: Rapid Hyponatremia Correction


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


“Will my father be okay, Doctor?” Asks the young woman, pretty despite the worry. Her husband sits next to her, and, instinctively, she reaches for his hand.

“ Miss Chandra, I have to admit that the outlook looks somewhat grave,” “Professor Lee here is one of the leading neurologists in the state. says Dr. Chan, pointing towards me

“Oh.. He seemed to be getting better in the beginning, then…”

Dr. Chan is clearly uncomfortable. I feel a little sympathy for him.

I think of our conversations a few minutes ago.

Dr. Chan had called me in to see a 70-year-old man who had come in with disorientation following a history of diarrhoea. The man had been living alone, and his daughter had come by after a long absence. She found him disoriented, and rushed him to hospital when Dr. Chan had seen him.

Dr. Chan is a young man of about 30. He is sharp, but is just a little too confident for my liking. He had actually made a good clinical diagnosis. He said to me that he had thought of hyponatremia, and the lab reports had confirmed that the patient had sodium levels of only 118 millimoles per liter.  So he started an intravenous line with hypertonic saline.

“In fact, I had brought the hyponatremia back to normal by the evening! The patient’s orientation initially improved, then he started to worsen. The next day the patient developed quadriparesis. I checked his sodium levels, but they were within the normal range of 135-145 millimoles/L. I even tried to raise them, keeping the sodium close to 145, but the patient didn’t improve. Now I don’t know what’s going on.”

He hadn’t seen the look of horror on my face as he explained how quickly he corrected the sodium. Still, we all make mistakes.

I said, “This patient obviously had chronic hyponatremia, which is when hyponatremia lasts more than 48 hours. The hyponatremia was the cause of the symptoms, and your diagnosis was right, the patient needed sodium.”

Dr. Chan nodded vigorously, happy that I seemed to be with him, but I continued. “But, you see, we don’t replace sodium too quickly.”

Dr. Chan looked confused. “Too quickly?” he asked, not understanding.

“Yes, “I think we replaced his sodium levels too fast.”

“So, er, how long should we have taken?”

“Well, sodium levels should be raised by not more than 8 millimoles/24 hours. In this patient, the sodium was raised by over 20 mmol in less than a day.”

“How does this matter?”

“Sodium is responsible for most of the osmotic activity of the blood. Low sodium tends to produce brain edema, so the brain compensates by losing extracellular water, and by losing some intracellular sodium. If we replace all the sodium in the blood, the blood osmotic activity returns to normal, but the brain cells are unprepared. There is rapid demyelination in the brain, particularly in the region of the pons, but also in the cerebellum and other areas. Patients get dysphagia, dysarthria, quadriparesis, lethargy, even coma.”


“It’s called the Osmotic Demyelination Syndrome (ODS).”

“Will he recover?”

“The outlook is bad, but some degrees of recovery are possible.”

“What should I tell the patient’s relatives?”

“The truth,” I said.

“But they’ll sue me!”

“We’ll take the chance. Come, I’ll sit with you while you tell them. That way you’ll feel more confident,”



Hegazi MO, Nawara A (2016) Prevention and Treatment of the Osmotic Demyelination Syndrome: A Review. JSM Brain Sci 1(1): 1004.

Koul PA, Khan UH, Jan RA, Shah S, Qadri AB, Wani B, Ashraf M, Ahmad F, Bazaz SR. Osmotic demyelination syndrome following slow correction of hyponatremia: Possible role of hypokalemia. Indian J Crit Care Med. 2013 Jul-Aug; 17(4): 231–233.

Lin S-H, Jsu Y-J, Chiu J-S, Davids MR, Halperin ML. Osmotic demyelination syndrome: a potentially avoidable disaster. QJM: An International Journal of Medicine, Volume 96, Issue 12, 1 December 2003, Pages 935–947,

Simon EE. Hyponatremia. Medscape, updated 6 Jan 2016, accessed 24 Mar 2018, accessible at

Episode 15: Blood transfusions


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


You hurry past the patient diagnosed with intrabdominal bleeding in Bed 1. Extra beds have been placed in the Emergency Department, making the already packed ED even more crowded. Finding your way to the back entrance amongst the crowd of medical staff, your spot your patient, who is just being wheeled back from radiology.

You are a registrar in a small town surrounded by palm oil plantations. You are four hours away from the nearest major hospital. An hour earlier, a bus full of plantation workers had crashed into a tree at high speed. The tens of injured workers were brought to the nearest hospital – your hospital.

Your patient, Halim, is a 23-year-old male. Flipping through his X-rays confirms your diagnosis of bilateral femur fractures. When you first saw him, his thighs were obviously deformed. After assessing him and excluding other serious injuries, you send him off to radiology, asking for immediate X-rays. Before sending him off, you start a saline infusion at high speed, insert an indwelling urethral catheter, splint the fractures, give painkillers, and send an urgent requisition for blood. Halim’s wife stands by, sick with worry.

Coming out of radiology fifteen minutes later, Halim seems more confused and lethargic than before. His heart rate has risen from 110 to 150. He is tachypnoeic, cold and clammy, and capillary refill is obviously prolonged. His blood pressure has dropped from 120/80 to 80/50. By your estimation, this is class 4 haemorrhagic shock.

Just then, your intern comes running up. She has been talking to the blood bank.


“The patient’s blood group is A-. The blood bank says there’s no A- blood.”

“Tell them to give me O negative blood then. Hurry.”

“I asked. We’re out of that too. Our last unit was given to the patient with intraabdominal bleeding. We are left with A+, B+ and B- blood only. The blood bank technician says they’ve called the national blood bank for more, but it’ll take at least 4 hours to get more blood.”


You look at Halim’s wife.


“ What’s going to happen doctor?”

“Has he ever received a transfusion before?”



You turn to the intern.


“There’s no option. Get me four units of the A+ blood then”, you order.

“What! But the patient is A-?”

“I’ll explain later. Just hurry.”


Four hours later Halim has been stabilized, and has come out of surgery for internal fixation of the femur fractures. As you sit in the doctors’ room, coffee in hand, your intern tries her luck.


“How come you gave A+ blood to an A- patient? Won’t he get a transfusion reaction?”

“Will he?”

“I, er, think so,”


“Well, er, mismatched transfusion results in reactions.”

“Mismatched ABO transfusion results in reactions. This is because persons with blood group A already have antibodies to B antigens, and vice versa. If you had transfused B blood to this man, the anti-B antibodies in his blood would have destroyed all the transfused blood. In contrast, mismatched Rh transfusions do not cause reactions, at least not the first time. This man has no anti-Rh antibodies, because he has never been exposed to the Rh antigen.”

“So, he will develop antibodies to Rh now?”

“Yes, of course. This means that now, he can never ever receive an A+ transfusion. If he does, he will have a severe transfusion reaction.”

“So how come he has anti-B antibodies in the blood, if he has never received a transfusion?”


You start thinking about the reasons:

Shared antibodies with food and bacterial polysaccharide antigens that result in the development of anti-A and anti-B in infancy. You start thinking how fortunate it is that it was Halim who received the A+, not his wife. If she had been A- and had received an A+ transfusion, her chances of bearing babies would have been affected.


You smile and give your usual reply;


“I don’t know. Why don’t you look it up and tell me?”



Kruskall MS, Mintz PD, Bergin JJ, Johnston MF, Klein HG, Miller JD, et al. Transfusion therapy in emergency medicine. Annals of emergency medicine. 1988;17(4):327-35.
Venkata Raman B, Sravani B, Phani Rekha P, Lalitha KVN, Narasimha Rao B. Effect of plant lectins on human blood group antigens with special focus on plant foods and juices. International Journal of Research in Ayurveda and Pharmacy 2012;3(2):255-63, available at

Episode 14: A Hypernatremic Child


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


I’ve just remembered a fascinating clinical problem we encountered a few weeks ago.

What was that?

This three week baby was admitted to the paediatrics ward with a history of not feeding for two days. The mother said the baby was sleeping excessively, and couldn’t be woken up for feeds. The baby passed urine once in the last 24hrs, and didn’t pass stool for 3days. This is her first baby, and she was careful to follow the advice everybody gives: breast feed only! So the baby was exclusively breast fed. At birth the baby had weighed 3.5 kg, and had been fine except for a physiological jaundice. At admission we found that the baby’s weight had dropped to 2.5 kg.

Isn’t a little loss of weight usual in the first few days of life?

It is. Babies lose up to 10% of their body weight in the first 5 days of life due to physiological diuresis. They regain the birth weight by day 14. This child has lost about a third of its weight. Any loss of weight of more than 10% is pathological and should be investigated.

On examination?

On examination except mild jaundice and absence of fat in the buttocks area no abnormality was found. The baby’s blood tests were normal except for two changes. The bilirubin was 135 micromoles/liter, consistent with physiological jaundice that’s elevated by dehydration. The second change was in the electrolytes. The baby’s serum sodium level was 165 millimoles/L.

That’s a significant hypernatremia!

That’s right; for a baby the normal values are 135-140

So what was the cause?

Simply that the mother was producing insufficient breast milk! She refused to provide supplementation, so the baby started getting dehydrated.

That doesn’t make sense. How can a baby get dehydrated so quickly? And I know that milk is a low-sodium fluid, so insufficient feeding would simply worsen the hyponatremia, not cause hypernatremia.

Good questions. Let’s break these into two parts. One, why does dehydration occur? And two, how does hypernatremia occur? The answers are simple. One, babies lose a lot of water by insensible loss. In addition to the water lost during respiration, a lot of water is lost through the skin, so they get dehydrated quickly. Two, insensible water loss is pure water loss. That’s why hypernatremia occurs.

Two more questions. Why do babies lose so much water? Isn’t there sodium loss during insensible fluid loss?

In response to question one, newborns lose a lot of water through insensible losses because they have a high surface area in proportion to their weight. Adults have a skin surface area of 250 square cm/kg. In comparison, infants have a  skin surface are of seven HUNDRED square cm/kg. Compared to adults, that’s an enormously increased surface area per kg.

In response to question two, no, the sodium loss during insensible losses is low. In such a setting the best replacement for a neonate is  milk. For an older child or an adult dehydrated due to excessive insensible losses the best replacement is water or intravenous dextrose.

What happened to the baby?

We just fed the baby with formula milk via a nasogastric tube. The baby recovered quickly. I’ve brought up this case because there are several important messages here. One, though breast is best, it sometimes just isn’t enough. Two, babies have a very high surface area in relation to their weight, and, consequently, can dehydrate surprisingly fast. Three, insensible losses should be considered to be water losses, not water and electrolyte losses.



Myers RS. Pediatric fluid and electrolyte therapy. J Pediatr Pharmacol Ther 2009 Oct-Dec; 14(4): 204–211

Episode 13: Drugs in dialysis


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


How are you? Glad to be here in another podcast entry. Shall we get to the case right away?

Yes! The mic is yours.

A 45-year-old man, a known alcohol abuser, was being treated for necrotizing pancreatitis. He also had a long-standing diabetes, with end-stage renal failure. A necrosectomy was carried out.

The patient’s condition sounded serious indeed.

Yes. The reason this case was chosen was due to the valuable learning points which we can learn from what happened to this patient post-surgery. He was actually recovering well after surgery. He was on ticarcillin-tazobactam and had undergone dialysis once after surgery.


Then, about a week after surgery, he developed convulsions. He had no past history of seizure.

A seizure? That seems unexpected. How should we approach such a case?

First and foremost, we have to determine if it is a case of seizure. Histories from both the patient and witnesses are equally important: is this epilepsy?

Then, one should consider other causes, such as hypoglycaemia, stroke, and meningitis. Drug history is essential as both toxicity and withdrawal can provoke a seizure episode.

Drugs? Are they the culprit in this case? The antibiotic?

Yes. This patient was given Ticarcillin. It is one of the penicillins. Convulsions may occur in very high doses, a side effect known in all penicillins. Patients on dialysis are particularly susceptible. It is important to realize that in the three days between successive sessions of hemodialysis, the drug levels rise steeply, unlike in persons with normal kidneys, where drugs are excreted constantly.

While we are on the topic of drug-induced seizures, a number of medications may cause them. The major ones are analgesics (fentanyl, meperidine), antibiotics (ampicillin, imipenem, metronidazole, ciprofloxacin), antidepressants (Amitriptyline, bupropion), antipsychotics (Chlorpromazine, haloperidol) and bronchial agents such as Aminophylline.

I see. What can we learn from this case?

Penicillins in high doses, particularly in patients with renal failure, can cause convulsions.


1.       Smyth B, Jones C, Saunders J. Prescribing for patients on dialysis. Aust Prescr. 2016 Feb;39(1):21.
2.       Longmore M, Wilkinson IB, Baldwin A, Wallin E. Oxford handbook of clinical medicine. 9th ed. New York: Oxford University Press; 2014. 7, Renal Medicine; p. 297.
3.       Munar M, Singh H. Drug Dosing Adjustments in Patients with Chronic Kidney Disease.  American Academy of Family Physicians. 2007. 75(10).
4.       Schachter SC. Evaluation and management of the first seizure in adults [database on the Internet]. In: Garcia P, Wilterdink JL, ed. Waltham, MA: UpToDate Inc; 2017 Sep 8 [cited 2017 Oct 8]. Available from:

Episode 12: Ceftriaxone and gallstones


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


Doctor, you are looking smug today, if you don’t mind my saying so!

Yes! I achieved an easy diagnosis today, but my colleagues think I’m brilliant!

Lucky you! What happened?

Well, I was having a much-needed post-surgery coffee with a group of other surgeons today, and this neurologist walks in. So a urologist sitting next to me asks him, why are you looking so glum, and the neurologist says, I’ve got a gallstone! I had some vague epigastric pain, and the radiologist picked up a small stone in my gall bladder! So the urologist says, that’s bad luck, that means surgery!

And my colleague, a general surgeon, pipes up. “Yup,” she says, “abdominal pain plus gallstone equals surgery.”

Then one of the gynaecologists adds, “And you’ve just recently come back from a bout of typhoid fever. Now you’ll be out for some more time.”

Oh, he had had typhoid! That’s not very common, is it?

No, but this chap has family in India, and had picked it up during a trip there. Anyway, the doctors start commiserating with this neurologist, and somebody turns to me and says, why are you so silent?

And, why were you so silent?

Ah! So I put on a thoughtful look, and asked the neurologist, “You had typhoid, didn’t you? They must have given you ceftriaxone?” And the neurologist says “Yes.” So I said, “Well, ceftriaxone causes gallstones. But if you wait, the gallstone will disappear.”


That’s exactly what everybody said, “Really?”. And they Googled it, and sure enough, the literature confirms that ceftriaxone causes gallbladder sludge, which often, but not always, disappears with time. It may form stones, and, indeed, cause gallstone disease.

What did the neurologist say?

Well, he thought I was brilliant, and so did the others.

The truth is, about six months ago a relative from India had called for this same problem. I had, I must admit, advised surgery. Luckily, before he was operated, somebody there told him to wait it out, and sure enough, after some time ultrasound confirmed that the gallstone had disappeared.

Ah, hence the smugness!

Yes. It was pure luck that I knew about this complication of ceftriaxone.

Why does ceftriaxone cause gallstones?

Ceftriaxone is excreted unchanged in the urine and bile, in roughly equal proportions. The gall bladder concentrates the bile, and if the patient is receiving ceftriaxone, a sludge may form. This sludge contains ceftriaxone and calcium, and small amounts of cholesterol and other compounds.

But sludge is not the same as actual gallstones.

No, but there are reports that the sludge may progress to stones in the gall bladder. There may even be stones in the bile duct. But overall, ceftriaxone precipitates are less of a problem than cholesterol or pigment stones.



  1. Bickford CL, Spencer AP. Biliary sludge and hyperbilirubinemia associated with ceftriaxone in an adult: case report and review of the literature. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy. 2005;25(10):1389-95.
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