Category: Clinical Knowledge

Episode 2: Pulse Oximetry

Clinical KnowledgeEmergency

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Author: Thong Yi Kun
Script Editor: Dr Suneet Sood
Narrator: Thong Yi Kun

Transcript

The buzzer sounds as you are broken from your reverie. You are the sole registrar working in the red zone of a rural hospital emergency department. Major cases are infrequent but sometimes when it rains it pours.

A patient has arrived via ambulance. You rush out and greet the paramedic with an earnest look.

“What have you got for me today?”

“This lady attempted suicide. She put a pipe connecting the exhaust to her window”

“What are her saturations?”

“98%, but we have been manually ventilating her the whole way”

You quickly assess the patient. Her GCS is 3, appears pink but with minimal spontaneous breaths. You quickly make a provisional diagnosis of carbon monoxide poisoning. Despite her oxygen saturation of 98%, you decide for immediate endotracheal intubation in view of her impaired GCS.

Funny that, in carbon monoxide poisoning, the pulse oximeter shows high saturation levels of haemoglobin!

You decide to read up on how the pulse oximeter works.

The pulse oximeter works on two principles: first, by being able to take readings only the arterial blood, and second by being able to calculate the level of oxygenation.

How does the pulse oximeter take readings only from the arterial blood? Well, arteries are pulsatile, and the light absorbance changes from beat to beat, and the pulse oximeter is programmed to select these changes. Obviously, it will not work if the patient does not have a pulse! Also, in severe tricuspid regurgitation, the venous system acquires a pulse. This confuses the pulse oximeter, and it can read the venous blood, resulting in errors.

The pulse oximeter also calculates the level of oxygenation. Oxygenated haemoglobin absorbs more infrared light. Deoxygenated blood absorbs more red light. By comparing the ratio of absorbed infrared to red light, the percentage of oxyhaemoglobin can be worked out.

But why would a patient with severe CO poisoning have an artificially high SpO2?

The pulse oximeter reports the percentage oxygenation as the ratio of oxygenated haemoglobin to total haemoglobin. The total Hb of course is assumed to be the oxygenated plus deoxygenated Hb. Unfortunately, the pulse oximeter ignores non-functioning hemoglobins like methaemoglobin and carboxyhaemoglobin. Since it presumes the carboxyhemoglobin does not exist, the detected total haemoglobin falls drastically in patients with CO poisoning. This results in a falsely high percentage reading for oxygenated haemoglobin.

 

References:
Chan ED, Chan MM, Chan MM. Pulse oximetry: understanding its basic principles facilitates appreciation of its limitations. Respiratory medicine. 2013;107(6):789-99.

Stewart K, Rowbottom S. Inaccuracy of pulse oximetry in patients with severe tricuspid regurgitation. Anaesthesia. 1991;46(8):668-70.

Episode 1: Budd-Chiari Syndrome

Clinical KnowledgeGastroIntenstinalhaematology

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

Transcript

So what do you have for us today?

This is the story of a 30 year old man who presented with an upper gastrointestinal bleeding.

Last year, we received a patient who presented with hematemesis, hepatosplenomegaly, and ascites.

The surgeons carried out an endoscopy, and found esophageal varices, which they banded, and he stabilized.

I notice, your patient had hepatosplenomegaly. I can understand the splenomegaly in portal hypertension, but why the hepatomegaly?

That’s a good question. Portal hypertension may be prehepatic, intrahepatic, or posthepatic. The liver is quite normal in prehepatic portal hypertension, and ascites is not a feature. The liver is shrunken in intrahepatic portal hypertension, which usually results from cirrhosis. Ascites is common. The liver is enlarged in posthepatic portal hypertension, and ascites is common. In fact, subsequent MR angiograms showed hepatic vein thrombosis.

That’s interesting. What caused this hepatic vein thrombosis?

Initially we didn’t have proof, but made a guess. We had to take a very detailed history. This provided a clue to the cause of hepatic vein thrombosis.

What was the clue?

The patient gave a history of severe gastroenteritis and dehydration a year earlier, and needed admission and intravenous fluids. In susceptible persons, dehydration may provoke venous thrombosis at various sites, including the hepatic veins, mesenteric veins, cavernous sinus, and other sites.

You said “In susceptible persons, dehydration may provoke venous thrombosis”. What do you mean by susceptible persons?

I mean persons who are at risk of thrombosis, which means persons who have an underlying thrombophilia. The common causes are deficiencies of Protein C, Protein S, or antithrombin III, and the Leiden mutation of factor 5.

So did this patient have any of these?

Yes. Later we evaluated this patient for thrombophilia. Results showed that he had a significant deficiency of Protein C.

If he had a protein C deficiency, can’t he get this problem again?

Yes he can. We put him on a lifelong warfarin therapy.

Thanks. So you are saying two things. One, hepatomegaly with varices indicates posthepatic portal hypertension, not cirrhosis. And two, that dehydration can precipitate venous thrombosis in a patient with thrombophilia.

Partly true. If a patient with portal hypertension has a palpable liver, also think of hepatocellular cancer. Remember that hepatocellular cancer is commoner in cirrhosis, especially cirrhosis associated with Hepatitis B or C.

References

Burns PJ, Mosquera DA, Bradbury AW. Prevalence and Significance of Thrombophilia in Peripheral Arterial Disease. Eur J Vasc Endovasc Surg 22, 98–106 (2001).

Hassan KM, Kumar D. Reversible diencephalic dysfunction as presentation of deep cerebral venous thrombosis due to hyperhomocysteinemia and protein S deficiency: Documentation of a case. J Neurosci Rural Pract. 2013 Apr-Jun; 4(2): 193–196.

Hbibi M, Abourazzak S, Babakhouya A, Boubou M, Atmani S, Tizniti S, Bouharrou A. Severe hypernatremic dehydration associated with cerebral venous and aortic thrombosis in the neonatal period. BMJ Case Rep. 2012; 2012: bcr0720114426.

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