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

Transcript

Today, we are here to share a case which involves the hematological system.

We have a 55-year-old male who presented with persistent fatigue and intermittent dizziness. The doctor immediately noticed that he was pale. He reported no other symptoms such as loss of weight, fever, changes in bowel habit or bloody stool. The treating doctor started an anemia workout by ordering a complete blood count. While the results were consistent with a case of anemia, the team was taken aback with the platelet count. It was over approaching 1,000×10^9  /liter.

That is an extremely high platelet level!

In fact, it is referred as extreme thrombocytosis in a platelet count of more than 1000 x 109/L. An elevated platelet count is any value above 450 x 109/L, which we call thrombocytosis.

What can cause such a high platelet count?

To explore the causes of thrombocytosis, we can categorize them into two groups – clonal thrombocytosis and reactive thrombocytosis.

Clonal thrombocytosis refers to the autonomous proliferation of platelet cells in patients with myeloproliferative or myelodysplastic disorders, namely essential thrombocythemia, polycythemia vera, primary myelofibrosis and chronic myeloid leukemia

Reactive thrombocytosis is thrombocytosis secondary to a variety of medical or surgical conditions. Common examples are recent surgery, trauma, infection, malignancy and iron deficiency. The reactive form is usually self-limiting when the precipitating factor is resolved when possible.

How should we approach a case of high platelet count like what happened in this patient?

First and foremost, we would have to consider the possible complications of having a high platelet level and our number one concern will be thrombotic complications. Thrombotic events may manifest with symptoms such as headache, syncope, chest pain or more sinister complications such as stroke and myocardial infarction. Bleeker and Hogan, in 2011, reported that thrombotic complications are usually the major causes of morbidity & mortality in clonal thrombocytosis especially in essential thrombocytosis or polycythemia vera. Antiplatelet therapy may likely be initiated in these cases. On the other hand, thrombotic events are rare amongst patients with reactive thrombocytosis, and one large case series only reported an incidence of 1.6%.

I presume the risk will be higher in patients with other contributing risk factors such as recent surgery or trauma?

Yes. This is one of the reasons why it’s important to investigate for the cause so we can assess patient’s risk of developing a thrombotic event. If it’s a reactive thrombocytosis, we would have to just solve the underlying precipitating condition.

So, how did the medical team for this patient move forward from the result?

Due to the very high platelet count, the team was at one point determined to seek haematology referral and arrange bone marrow biopsy with a provisional diagnosis of essential thrombocytosis. In fact, the chief resident was already considering therapy with hydroxyurea, an anticancer drug. But then the senior consultant saw the case, and reminded his team that in any thrombocytosis, it’s important to rule out iron deficiency anemia.

This patient did have low haemoglobin

Yes, this patient had low hemoglobin. If we make a quick correlation with all the findings so far, one explanation is that the thrombocytosis is a reactive form and caused by iron deficiency. The team ordered iron studies and the patient was indeed deficient in iron. Iron therapy was initiated and both the hemoglobin and platelet levels gradually improved.

It was a case of extreme thrombocytosis due to reactive thrombocytosis. That was fortunate! The team managed to prevent an unnecessary invasive procedure in this case.

Yes. If we encounter a patient with thrombocytosis, it is suggested that we should always start with less invasive tests. A repeat platelet count and peripheral blood smear is advisable to confirm the result. If we recall the causes of reactive thrombocytosis; besides iron deficiency, other causes such as infection and tissue damage are inflammatory in nature. Thus, we can quickly send blood for inflammatory markers such as C-reactive protein & ESR; together with the iron studies. These blood tests do not take too much time for us to rule out these common causes. It’s usually not too late to only consider more invasive tests after reactive thrombocytosis has been ruled out.

Wow, I guess this case taught me that I should not be completely distracted from the initial presenting complaint simply because of a shocking and unexpected result. Once you’ve shared the information pertaining to the platelet count, I was drawn into it and didn’t realize I have neglected the issue of anemia. The patient’s presenting issue turned out to be the answer to the unexpected finding of thrombocytosis.

You’ve illustrated an important point right there. It’s justifiable for the team to be concerned of the high platelet level due to the possible complications and to manage that issue accordingly. But if the anaemia workout was continued concurrently, clinicians would be able to discover the case of iron deficiency and have the opportunity to correlate it with thrombocytosis.

That’s great! We found the cause and it’s a much treatable condition.

Yes, it turned out we were dealing with iron deficiency. But we should not rest on our laurels with this diagnosis. There must be a cause for the iron deficiency and we must explore further. In this patient’s age group for example, I would be worried about a chronic blood loss causing iron deficiency. Chronic GI bleed is a rather common cause of blood loss and a further investigation is integral. It’s a rather long process to get to the root of the problem but it’s all for the benefit of the patient.

So our final message is: if a patient has thrombocytosis, always exclude iron deficiency anemia.

References:

1.      Bleeker JS, Hogan WJ. Thrombocytosis: diagnostic evaluation, thrombotic risk stratification, and risk-based management strategies. Thrombosis. 2011 Jun 8; Article ID 536062
2.      Chandna A, Sharma J, Sangwaiya A, Samal S, Sankala M, Garg S. Case report: iron deficiency anaemia with thrombocytosis: a diagnostic challenge. IJHBR. 2014 Oct;3(1):43-6.

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

Transcript

You seem upset? What’s wrong?

I’ve just come from the wards. I have an elderly diabetic patient on clarithromycin and ketoconazole. This patient developed a runny nose, and my resident doctor started terfenadine, an anti-histamine.

I have to admit I cannot see what is wrong with that!

Well, clarithromycin is a macrolide antibiotic. Ketoconazole is an antifungal. Each of these drugs can prolong the QT interval in the cardiac cycle. When given together, the effect on the heart can be potent. On top of that, we have started terfenadine, an antihistamine that also prolongs the QT interval. Giving terfenadine to a patient who is elderly, diabetic, probably has some silent infarcts, and is already getting clarithromycin and ketoconazole, may cause a fatal cardiac complication.

I remember now. It’s called torsades de pointes, right?

Right. It’s a dangerous form of drug interaction

Is drug interaction really a common problem in clinical practice?

It certainly is. It deserves great attention, particularly since complications due to drugs are preventable. Let me give you an example of my own relative.

Okay.

So my uncle is an 80-year-old man with Parkinson’s disease. He was, naturally, getting the usual combination of carbidopa and levodopa, drugs that are associated with the risk of orthostatic hypotension. Well, he developed a urinary tract infection, and his GP started him on linezolid.

Linezolid? Isn’t that for gram positive infections?

Yes. It’s an oxazolidinone, a drug used for gram positive infections. It’s very safe, actually. But urinary infections are typically E coli, and we usually prefer ciprofloxacin or co-trimoxazole, or even co-amoxyclav. These are all bactericidal drugs, while linezolid is bacteristatic.

So why did the doctor choose linezolid?

I don’t know. I can only presume he had recently been visited by a very generous and persuasive drug representative for the pharma company.

So what happened?

Well, linezolid is a weak monoamine oxidase inhibitor, you know, a MAO inhibitor. And MAO inhibitors cause orthostatic hypotension, and are contraindicated in patients receiving carbidopa.

So this patient developed orthostatic hypotension?

Yes, very, very severe orthostatic hypotension. He thought his time was up. Somebody dragged him to a hospital, where he was seen by a senior physician.

And the linezolid was stopped?

No, can you imagine! The physician thought that this was urinary infection worsened by adrenal failure.

What sort of diagnosis is that?

And the physician stepped up the dose of linezolid, continued the anti-Parkinson’s medication, and started steroids.

Goodness!

Well, fortunately the patient called me. I noted that his symptoms started soon after starting linezolid, so I looked up the drug on the net to see if there were any side effects I didn’t know. I mean, I had known that linezolid was safe, but it’s always better to check it out. And it turned out that linezolid can cause severe drug interactions with carbidopa. So I told him, over the telephone, to stop linezolid immediately. Unfortunately, the nurse wouldn’t allow it, and she insisted that he should take the increased dose which had been prescribed by the physician. Finally he made a big ruckus, and the nurse relented.

Then he improved?

Yes, but it took him many days to properly recover.

Well, if it’s a lesser-known side effect, I don’t know that you can blame the GP who started the linezolid.

I don’t agree. I don’t blame the GP for not knowing. I do blame her for not looking it up before prescribing.

What you are saying is that all doctors should check for drug interactions every time they prescribe?

Yes. I am saying that all doctors should check for drug interactions every time they prescribe.

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

Transcript

Today’s case will touch on a hematological topic which I believe is familiar and feared by medical students at the same time – haemostasis and the coagulation pathway.

I’m sure it’ll be a good opportunity for us to revise and clear up any doubts in this topic. Let us start with the patient’s story.

We have a 45-year-old lady who had developed painful right lower leg swelling. The swelling developed suddenly four days before she came to us. Recently, she had had a greenstick fracture on her left tibia. Although no surgery was needed, she was resting in bed at home for a few days. An important risk factor to note would be her obesity and current use of oral contraceptive pills.

Ahha! A unilateral swollen leg which is sudden and after a period of immobility – sounds like deep vein thrombosis to me.

Spot on! DVT should be on top of our list but we should always quickly consider other causes of leg swelling. Anyhow, the swelling was unilateral, and calf circumference was markedly larger on the affected leg. A Doppler ultrasound revealed a blood clot in her superficial femoral vein. The D-dimer levels were very high.

She did have several important risk factors which predisposed her to blood clots, didn’t she?

Yes. Let us review the Virchow’s triad – the main theory which highlights the three primary factors contributing to the formation of clot. No. 1 – stasis in blood flow; which occurred with the patient’s prolonged immobility in this case; No. 2 – vascular endothelial injury from the tibial fracture, and No. 3 – hypercoagulability; probably related to her OCP use altering the blood viscosity.

She fulfilled all three components! How did she do after the confirmation of diagnosis?

Here comes the highlight of this case. As she presented a few days after the onset of swelling, her doctor decided that the presentation was not so acute. Perhaps he decided that the clot was already stable, and the probability of ongoing thrombosis was low.

Probably true, no, that the risk of ongoing thrombosis was low?

Yes, probably true. Anyhow, the doctor started her on oral warfarin instead of first starting with intravenous heparin.

So?

And then her clotting worsened, and she developed gangrene on the leg after two days.

Wow. Instead of being anticoagulated, new clots formed? How is that possible?

To understand this, it’s time for us to revisit the coagulation pathway and the pharmacology of Warfarin. To put it simply, there are two initial pathways, namely extrinsic and intrinsic pathways, which start the whole cascade of events in which one factor is involved in activating a subsequent factor. The two pathways meet in the final common pathway as factor Xa is activated, followed by the activation of thrombin and ultimately the formation of fibrin plug. Besides these direct factors in the cascade, we have important cofactors to regulate the process. One which is pertinent to our case will be Vitamin K. Vitamin K is essential in the activation of Factors II, VII, IX & X. Warfarin is a Vitamin K antagonist. It inhibits the activation of these factors which are directly involved in the coagulation pathway.

Yup, then why did the anticoagulation therapy for this patient not work?

What we often forget is Vitamin K ALSO catalyses the production of Proteins C and S. These two proteins prevent coagulation. Warfarin interferes with Vitamin K. The levels of proteins C and S fall.

For a time, therefore, the blood may become hypercoagulable.

Later, the procoagulant proteins, that is factors II, VII, IX, X are blocked, leading to anticoagulation. But in the beginning there may be a short phase where the blood is actually hypercoagulable.

But tell me: if the inhibition should affect both the coagulation factors and the anti-coagulant Proteins S & C, why is this patient experiencing the hypercoagulating effect of the inhibition of Protein S & C only?

Good question. Proteins C and S have shorter half-lives compared to the clotting factors. As Protein C and S will be depleted first, Warfarin intake during the initial phase poses a hypercoagulable state.

Thanks for the explanation and the quick revision. Tell me: is the complication of gangrene common?

No, it’s a rare complication, with a prevalence of 0.01 to 0.1%. Still, all physicians should be aware of this complication. A relatively more common warfarin-induced complication is skin necrosis.

How should we prevent this?

To prevent these complications, initial therapy with heparin is recommended. The mechanism of action of heparin is different. It directly inhibits the activation of thrombin and factor Xa in the coagulation pathway thus its anticoagulation effect is almost immediate. The starting dose of warfarin should be a low maintenance dose rather than a high initial dose to minimize the transient hypercoagulable state induced by the rapid decline in protein C levels. This means we should firstly start with both heparin and warfarin, and later stop the heparin when the effect of anticoagulation is achieved by warfarin. We use INR as a marker to determine if a patient is adequately warfarinised.

I presume she needed an amputation?

Yes, she did. This was an avoidable complication. Doctors should remember: start heparin first, then warfarin.

References:

1.       Pourdeyhimi N, Bullard Z. Warfarin-induced skin necrosis. Hosp Pharm. 2014 Dec 1;49(11):1044-8.
2.       Hostetler SG, Sopkovich J, Dean S, Zirwas M. Warfarin-induced venous limb gangrene. J Clin Aesthetic Dermatol. 2012 Nov 1;5(11):38-42.
3.       Kakagia DD, Papanas N, Karadimas E, Polychronidis A. Warfarin-induced skin necrosis. Ann Dermatol. 2014 Feb 1;26(1):96-8.
4.       Lipe B, Ornstein DL. Deficiencies of natural anticoagulants, protein C, protein S, and antithrombin. Circulation. 2011 Oct 4;124(14):e365-8.

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

Transcript

So, what case do you have today?

I have this case of a common symptom presenting from an uncommon condition, which highlights the importance of taking a proper history, examining well, and keeping an open mind.

So tell us.

Well, this 64 year old gentleman, diabetic, hypertensive, presented to the emergency department with dysphagia. Dysphagia means surgical referral; surgical referral for dysphagia means upper gastrointestinal endoscopy.

It sounds reasonable. What did the scope show?

Nothing! In fact, a senior surgeon came along and repeated the scope. Still nothing!

That’s funny, but if I remember right, dysphagia due to early achalasia may easily be missed by endoscopy.

True, but wait for the complete history, which was taken some days later by a smart undergraduate student, even as the symptoms were improving. The patient had dysphagia for only five days. Careful examination showed hoarseness, along with reduced sensation on the right face, right upper limb, and right lower limb. The left ninth, tenth, and twelfth nerves were also affected. He had an unsteady gait, but there was no limb weakness. The student looked up the books and came up with a diagnosis of Wallenberg’s syndrome, also known as the lateral medullary syndrome. She kept a CNS tumour as a differential.

What’s Wallenberg’s syndrome?

Wallenberg’s syndrome is a lower brainstem lesion that results from an occlusion of the vertebral artery. The patient develops sensory deficits of the face on the same side as the infarct, and sensory deficits of the trunk and extremities on the opposite side. Other typical features include dysphagia, dysarthria, hoarseness, and ipsilateral cerebellar signs–that means that patient falls to side of lesion. An MRI is diagnostic.

What did the neurologist say?

The neurologist confirmed the Wallenberg’s syndrome. He said that the ipsilateral features of ataxia were due to damage to the inferior cerebellar peduncle and cerebellum, while the contralateral features of loss of pain and temperature sense in the body and extremities indicated involvement of the anterior spinothalamic tract. The prognosis is good, and, in fact, the patient had already recovered largely within a couple of weeks. The neurologist also commented that acute neurological symptoms are caused by vascular or demyelinating disorders, almost never by tumours. And the MRI was consistent.

What’s your message to our listeners?

As always, take a good history. Examine carefully. And, I think, the main message is “not all dysphagia arises from the esophagus”.

References

Saha DK, Saha M, Nazneen S. Lateral Medullary Syndrome. Bangladesh Critical Care Journal. 2017;5(1):72-3.

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

Transcript

Hi! Thank you for having me. Through today’s case, we will look back at a topic in basic anatomy and its clinical relevance. This case is particularly interesting because we have a patient who had undergone a surgical procedure in one region but later presented with a problem in a different anatomical region.

Wow, let us start and learn.

We have a 55-year-old man who underwent an abdominoperineal resection for the diagnosis of rectal carcinoma. Soon after the surgery, he reported weakness in his left foot and had difficulty walking. He described that he would ‘catch his toes’ whenever he walked.

Ok, so the patient had pelvic surgery and later had a problem with his foot. That seems unfortunate and unexpected. You’ve mention his toes will get ‘caught’, mind explaining more about this presentation?

He had what we usually call a foot drop. There is weakness in the muscles responsible for dorsiflexion. Patients compensate by lifting their feet higher than usual to prevent their toes from scraping the ground when walking. We call it a high steppage gait.

Upon examination, eversion of the foot was weak. Ankle plantarflexion and foot inversion was normal.

Did the patient have a nerve injury? Are we looking at a case of inadvertent nerve injury at the hip region perhaps due to the surgery?

You get it right for the first part. We are indeed exploring a case of peripheral neuropathy. The next step is to use our clinical skills to localize the site of lesion to answer your second question. A foot drop can be caused by injury anywhere in the peripheral nervous system. The entire nerve root can be affected, such as an L5 radiculopathy.  Or the sciatic nerve can be affected. Or the common fibular nerve at the leg.

If we look back at the examination findings, plantarflexion was normal. Radiculopathy or sciatic nerve injury will cause weakness to both dorsiflexion and plantarflexion. Thus, we are looking at a fibular nerve injury in this man because only dorsiflexion and eversion were affected. The fibular nerve, of course, is a branch of the sciatic. It comes out of the sciatic just above the knee.

So the cause is a lesion at the knee when the surgery is at the pelvic region. Please explain.

Firstly, the fibular nerve travels very superficially near the fibular head. As it is superficial slightly below the knee level, at this site it is more prone to injury.

It can be injured during knee surgery or during a fracture of the knee or the fibula.

That’s understandable. But how can surgery on the pelvis cause injury to the fibular nerve at the knee?

To explore this case, we should take a few steps back. If we stop focusing on the site of surgery but other factors such as – the positioning of the procedure, we may find the answer.

Ah, then I would have to understand how abdominoperineal resection is performed.

Abdominoperineal resection is a procedure to remove the anus, rectum and sigmoid colon. For this operation, the patient has to be placed in a lithotomy-Trendelenburg position. To adopt the lithotomy position, the patients’ legs are spread apart to gain access to the anal region – hips flexed and abducted while the knees were flexed and supported by stirrups. You can see this position in gynecological procedures, labour and of course, lithotomy, which is the removal of stones from bladder, urinary tract or kidney.

Here comes the solution for the puzzle, the culprit seems to be the stirrups! Stirrups are metal devices that support the legs at the knee level. Picture this –  patient was laid supine. The table was tilted, head down, so that the intestines would fall towards the diaphragm, and away from the site of the surgery. This is the Trendelenburg position. In this position, the metal stirrups press on the side of the knee, directly over the fibular nerve. If the procedure is long, and abdominoperineal resections take several hours, the nerve damage can be irreversible. Proper padding of the stirrup can prevent the problem.

Thank you Dr!

References

Marciniak C. Fibular (Peroneal) Neuropathy – Electrodiagnostic Features and Clinical Correlates. Phys Med Rehabil Clin N Am. 2013; 24: 121–137. Available from: https://depts.washington.edu/neurolog/images/emg-resources/Fibular_Peroneal_Neuropathy.pdf

Rutkove SB. Overview of lower extremity peripheral nerve syndromes [database on the Internet]. In: Shefner JM, Dashe JF, ed. Waltham, MA: UpToDate Inc; 2017 Aug 29 [cited 2017 Sep 1]. Available from: http://www.uptodate.com

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

Transcript

Ryan had just finished with his rounds and stood in front of the elevator, on the way to the operating theatre. He was looking forward to operating on a challenging stomach cancer. The elevator had just pinged when he heard a voice.

“Doctor, may I ask you about a case?”

Ryan turned around. In front stood a zealous medical student hoping to get his logbook signed. Ryan didn’t really have the time, but, hey, as the chief resident in surgery he had some teaching responsibilities also. “What’s your name,” he asked.

“Jon.”

“Okay, Jon, make it quick.”

Jon began rattling off the full patient history,

“This patient is a 46 year old Chinese policeman. He presents with pain in the right upper abdomen. I thought he probably has gallstones, but he also has a long background of Crohn’s disease. The symptoms don’t fit with Crohn’s disease, but I don’t like to make a second diagnosis.”

“Maybe he does have gallstones? Does he have any risk factors?” Asked Ryan briskly.

Jon was taken aback for a second, trying hard to remain calm. Right-o, the 5 Fs: Female, fat, fertile, fair, forty. Jon was about to blurt out the magical F words when he realised the male policeman had almost none of those risk factors. He panicked, sweat is rolling down his cheeks as his silence became longer and longer.

Ryan asked, a little more kindly, “Maybe Crohn’s can lead to gallstone formation?”

Jon hung his head.

“Crohn’s disease is a form of inflammatory bowel disease that can affect any part of your GI tract, from the mouth to the anus. Crohn’s can cause a severe ileitis there. What’s absorbed in the ileum?”

“Vitamin B12?” asked Jon, knowing fully well that that wasn’t the correct answer.

“Well, of course, B12 is absorbed in the terminal ileum, but B12 has nothing to do with gallstones,” said Ryan, a little curtly. When Jon looked blank, Ryan continued, “Have you thought of bile salts?”

Bile salts! Jon didn’t know where bile salts fit in, but he did know about them. “You mean like sodium taurocholate and sodium cholate and so on?”

“Yes,” said Ryan, “any others?”

“Er, I can’t think of any” said  Jon

“Well,” said Ryan, “What will happen if the bile salts are not absorbed?”

“I know this!” exclaimed Jon, seeing the light.

“Go on then.” Dr Ryan replied

“Bile salts are expelled into the duodenum in the bile, and are reabsorbed in the ileum,” Jon explained

“And when there is extensive Crohn’s ileitis?” prompted Ryan

“Because of the ileal inflammation, bile salts are not reabsorbed effectively. The bile acid pool decreases,” said Jon, and “the bile acid to Cholesterol ratio in your biliary system decreases, leading to the precipitation of cholesterol stones.”

“Similarly, the ileum is responsible for absorption of fat. Thus, patients with Crohn’s tend to be deficient in vitamins A, D, E, and K.” added Ryan, turning away.

“Er, can I get my logbook signed” asked Jon, hopefully?

“I think you need to read up the names of the other bile salts, don’t you?” asked Ryan

“Ah yes, of course” said Jon, faking a smile as Ryan walked off.

To summarise: Diseases of the terminal ileum such as in Crohn’s disease, can cause not only malabsorption of nutrients, but also disrupt the enterohepatic circulation, resulting in gallstones.

References
Heaton K, Read A. Gall stones in patients with disorders of the terminal ileum and disturbed bile salt metabolism. Br Med J. 1969;3(5669):494-6.

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

Today we have an obstetrics case for discussion.

This 30-year-old woman had been seeing us in the antenatal clinic. She had three healthy babies, all delivered by caesarean section. This pregnancy had been uneventful. We admitted her at 37 weeks for an elective caesarean.

Why caesarean? Why not a trial of normal labour?

If a woman has had three previous caesareans it is virtually mandatory that future pregnancies should be delivered operatively. In these patients we do not recommend a trial of labour.

Okay.

At admission she was quite stable. She had mild abdominal pain and lower abdominal tenderness. She also complained of frequency of micturition.

Sounds like an infection!

Yes. The medical officer diagnosed urinary infection, and sent off the urine for microscopy and culture. He also started antibiotics.

Okay.

A few hours after admission, she developed a tachycardia. Uterine contractions were infrequent and irregular. Then the senior specialist came along. She saw the patient and said, this is impending uterine rupture.

Impending uterine rupture?

Yes. An immediate caesarean section was carried out. At surgery the senior specialist was proved right. The patient had marked thinning of the uterine scar, and in a few hours the uterus would have ruptured, with loss of the baby and a serious threat to the mother’s life. As it turned out, the patient had an unremarkable postoperative course.

That was a smart diagnosis by the specialist!

In actual fact, the medical officer’s mistake is bigger. Any patient who has had a previous caesarean section is at risk of uterine rupture through the previous scar. The urinary features and the abdominal tenderness should have alerted the medical officer.

Why does impending uterine scar rupture cause urinary symptoms?

There are three reasons why impending scar rupture causes urinary symptoms.

First cause: the operated uterus often becomes adherent to the bladder anteriorly. When the uterus stretches too much, this stretch involves the bladder, with the development of frequency.

Okay, adhesions between uterus and bladder cause frequency. Second cause?

Secondly, abnormal stretching of the uterine scar causes local inflammation. Inflammatory peptides diffuse through to the bladder, causing a mild cystitis. That causes frequency.

Okay, scar stretching causes inflammation, which cases adjacent cystitis. Third cause?

Thirdly, the afferents of the lower urinary tract travel along two regions: T11 to L2, and S2 to S4.1 Afferents from the uterus also travel up T11- L1. You can see that there is considerable overlap. In this setting sensation from the uterus may easily be referred to the bladder. [SLOW]

Oh, so the cause of the frequency is a sensation from the uterus referred to the bladder, causing a sort of spurious frequency?

Yes.

Nice! Thank you. So, the bottom line is: sensations from the uterus can be referred to the urinary bladder causing a desire to pass urine. Doctors should remember that in a patient with previous caesarean, frequency of micturition may be a sign of impending scar rupture.

References:
de Groat WC, Yoshimura N. Afferent nerve regulation of bladder function in health and disease. Handb Exp Pharmacol. 2009;(194):91-138.

Here at Basic Medcast, we create podcasts that link clinical scenarios with basic sciences. We hope that it will be a valuable resource for medical undergraduates to integrate the clinical and basic science aspects of the art of medicine.

The first two podcast episodes have already been published:

Episode 1: Budd-Chiari Syndrome

Episode 2: Pulse Oximetry

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Regards,
Thong Yi Kun
BMedSc candidate