Barry Renal Acid Base Regulation Anion Gap Paracetamol Poisoning Salicylate Poisoning Reflex Control Of Breathing Arterial Blood Gas Basics Basic Questions About Barry Causes Of Metabolic Acidosis And Alkalosis Renal Pharmacology Respiratory

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It had been a long night in A&E when I was called into resus to review a patient who had just been brought in by the paramedics. He was confused and acting strangely. A friend with him was able to provide me with a limited history.

The friend told me that Barry was 48 years old and had a long history of depression, which has resulted in multiple drug overdoses over the years and extensive self-harm marks over his left forearm. A tearful and distressed Barry called him approximately 2 hours ago and told him that this time he had enough of everything and had taken an overdose. He would not disclose which tablets he had taken and when the friend and paramedics arrived they were unable to find any empty packets or bottles of medication.

“Barry, Barry, can you hear me?” I shouted. “I want to die, leave me alone” he slurred back.

On examination his BP was 107/82, pulse 90bpm, temperature 37.4C, respiratory rate 28, and oxygen saturations 98% on room air. Reflex Control Of Breathing

I calculated his GCS to be E3, V4, M5 (12/15). Heart sounds were normal, lungs clear and his abdomen was soft and non-tender. Barry’s pupils were equal bilaterally at 4mm and reactive. I was unable to complete a full neurological examination, as he was agitated and particularly uncooperative. Some days it feels as if everyone who presents to A&E doesn’t want our help at all.

I sent bloods for FBC, U&Es, LFTs, glucose, calcium, magnesium, INR, and paracetamol and salicylate levels. Due to the increased respiratory rate and to get early information about the acid base balance I performed an arterial blood gas analysis of a sample from his radial artery:Arterial Blood Gas Basics


The results showed a respiratory alkalosis with partial metabolic (HCO3-) compensation.Renal Acid Base Regulation

So far, this seemed quite typical of aspirin overdose, but there is usually a metabolic acidosis as well. To explore the possibility of a metabolic acidosis typical of aspirin poisoning, I went on to calculate the anion gap: Salicylate Poisoning Anion Gap


The anion gap was elevated. Therefore, he had a primary respiratory alkalosis and a high anion gap metabolic acidosis as well. This combination is so characteristic of salicylate overdose in the context of his confusion and agitation I knew I had my diagnosis. Causes Of Metabolic Acidosis And Alkalosis

More than an hour had passed since he had called his friend, so gastric lavage and oral activated charcoal were not an option, particularly in the presence of his reduced GCS and uncooperative attitude. I started IV 0.9% saline with 40 mmols of potassium chloride knowing that the compensatory renal excretion of bicarbonate, sodium, potassium and water results in dehydration and electrolyte imbalance.

It was at this point that the laboratory results came back confirming what I suspected. Paracetamol level <10mg/L and salicylate level 76mg/dL. It was good to see that this was not a combined paracetamol overdose alleviating the need to commence N-Acetylcysteine, but the salicylate level was higher than I’d ever seen. Paracetamol Poisoning

I went on to Toxbase, an online database of the national poisons information service, for information about how to proceed next. For salicylate levels this high Toxbase suggested giving 1.5L of 1.26% sodium bicarbonate over 2 hours. This is to alkalinise the urine to a pH of 7.5-8 to enhance the elimination of salicylates and reduces CNS effects.

Barry had taken a significant aspirin overdose with acid base disturbances, electrolyte abnormalities and CNS effects. I contacted the ICU registrar to organise transfer to level 2 care, as he needed regular monitoring of observations and two hourly blood gases and salicylate levels, with continuation of the bicarbonate infusion and electrolyte replacement until his acid base status was improving and the salicylate levels were falling.

Fortunately, with this management he improved and did not require additional renal, respiratory or cardiovascular support He was reviewed by psychiatry and transferred for in-patient psychiatric management 3 days later.

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It had been a long night in A&E when I was called into resus to review a patient who had just been brought in by the paramedics. He was confused and acting strangely. A friend with him was able to provide me with a limited history.

The friend told me that Barry was 48 years old and had a long history of depression, which has resulted in multiple drug overdoses over the years and extensive self-harm marks over his left forearm. A tearful and distressed Barry called him approximately 2 hours ago and told him that this time he had enough of everything and had taken an overdose. He would not disclose which tablets he had taken and when the friend and paramedics arrived they were unable to find any empty packets or bottles of medication.

“Barry, Barry, can you hear me?” I shouted. “I want to die, leave me alone” he slurred back.

On examination his BP was 107/82, pulse 90bpm, temperature 37.4C, respiratory rate 28, and oxygen saturations 98% on room air. Reflex Control Of Breathing

I calculated his GCS to be E3, V4, M5 (12/15). Heart sounds were normal, lungs clear and his abdomen was soft and non-tender. Barry’s pupils were equal bilaterally at 4mm and reactive. I was unable to complete a full neurological examination, as he was agitated and particularly uncooperative. Some days it feels as if everyone who presents to A&E doesn’t want our help at all.

I sent bloods for FBC, U&Es, LFTs, glucose, calcium, magnesium, INR, and paracetamol and salicylate levels. Due to the increased respiratory rate and to get early information about the acid base balance I performed an arterial blood gas analysis of a sample from his radial artery:Arterial Blood Gas Basics


The results showed a respiratory alkalosis with partial metabolic (HCO3-) compensation.Renal Acid Base Regulation

So far, this seemed quite typical of aspirin overdose, but there is usually a metabolic acidosis as well. To explore the possibility of a metabolic acidosis typical of aspirin poisoning, I went on to calculate the anion gap: Salicylate Poisoning Anion Gap


The anion gap was elevated. Therefore, he had a primary respiratory alkalosis and a high anion gap metabolic acidosis as well. This combination is so characteristic of salicylate overdose in the context of his confusion and agitation I knew I had my diagnosis. Causes Of Metabolic Acidosis And Alkalosis

More than an hour had passed since he had called his friend, so gastric lavage and oral activated charcoal were not an option, particularly in the presence of his reduced GCS and uncooperative attitude. I started IV 0.9% saline with 40 mmols of potassium chloride knowing that the compensatory renal excretion of bicarbonate, sodium, potassium and water results in dehydration and electrolyte imbalance.

It was at this point that the laboratory results came back confirming what I suspected. Paracetamol level <10mg/L and salicylate level 76mg/dL. It was good to see that this was not a combined paracetamol overdose alleviating the need to commence N-Acetylcysteine, but the salicylate level was higher than I’d ever seen. Paracetamol Poisoning

I went on to Toxbase, an online database of the national poisons information service, for information about how to proceed next. For salicylate levels this high Toxbase suggested giving 1.5L of 1.26% sodium bicarbonate over 2 hours. This is to alkalinise the urine to a pH of 7.5-8 to enhance the elimination of salicylates and reduces CNS effects.

Barry had taken a significant aspirin overdose with acid base disturbances, electrolyte abnormalities and CNS effects. I contacted the ICU registrar to organise transfer to level 2 care, as he needed regular monitoring of observations and two hourly blood gases and salicylate levels, with continuation of the bicarbonate infusion and electrolyte replacement until his acid base status was improving and the salicylate levels were falling.

Fortunately, with this management he improved and did not require additional renal, respiratory or cardiovascular support He was reviewed by psychiatry and transferred for in-patient psychiatric management 3 days later.

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Key Facts & Figures

It had been a long night in A&E when I was called into resus to review a patient who had just been brought in by the paramedics. He was confused and acting strangely. A friend with him was able to provide me with a limited history.

The friend told me that Barry was 48 years old and had a long history of depression, which has resulted in multiple drug overdoses over the years and extensive self-harm marks over his left forearm. A tearful and distressed Barry called him approximately 2 hours ago and told him that this time he had enough of everything and had taken an overdose. He would not disclose which tablets he had taken and when the friend and paramedics arrived they were unable to find any empty packets or bottles of medication.

“Barry, Barry, can you hear me?” I shouted. “I want to die, leave me alone” he slurred back.

On examination his BP was 107/82, pulse 90bpm, temperature 37.4C, respiratory rate 28, and oxygen saturations 98% on room air. Reflex Control Of Breathing

I calculated his GCS to be E3, V4, M5 (12/15). Heart sounds were normal, lungs clear and his abdomen was soft and non-tender. Barry’s pupils were equal bilaterally at 4mm and reactive. I was unable to complete a full neurological examination, as he was agitated and particularly uncooperative. Some days it feels as if everyone who presents to A&E doesn’t want our help at all.

I sent bloods for FBC, U&Es, LFTs, glucose, calcium, magnesium, INR, and paracetamol and salicylate levels. Due to the increased respiratory rate and to get early information about the acid base balance I performed an arterial blood gas analysis of a sample from his radial artery:Arterial Blood Gas Basics


The results showed a respiratory alkalosis with partial metabolic (HCO3-) compensation.Renal Acid Base Regulation

So far, this seemed quite typical of aspirin overdose, but there is usually a metabolic acidosis as well. To explore the possibility of a metabolic acidosis typical of aspirin poisoning, I went on to calculate the anion gap: Salicylate Poisoning Anion Gap


The anion gap was elevated. Therefore, he had a primary respiratory alkalosis and a high anion gap metabolic acidosis as well. This combination is so characteristic of salicylate overdose in the context of his confusion and agitation I knew I had my diagnosis. Causes Of Metabolic Acidosis And Alkalosis

More than an hour had passed since he had called his friend, so gastric lavage and oral activated charcoal were not an option, particularly in the presence of his reduced GCS and uncooperative attitude. I started IV 0.9% saline with 40 mmols of potassium chloride knowing that the compensatory renal excretion of bicarbonate, sodium, potassium and water results in dehydration and electrolyte imbalance.

It was at this point that the laboratory results came back confirming what I suspected. Paracetamol level <10mg/L and salicylate level 76mg/dL. It was good to see that this was not a combined paracetamol overdose alleviating the need to commence N-Acetylcysteine, but the salicylate level was higher than I’d ever seen. Paracetamol Poisoning

I went on to Toxbase, an online database of the national poisons information service, for information about how to proceed next. For salicylate levels this high Toxbase suggested giving 1.5L of 1.26% sodium bicarbonate over 2 hours. This is to alkalinise the urine to a pH of 7.5-8 to enhance the elimination of salicylates and reduces CNS effects.

Barry had taken a significant aspirin overdose with acid base disturbances, electrolyte abnormalities and CNS effects. I contacted the ICU registrar to organise transfer to level 2 care, as he needed regular monitoring of observations and two hourly blood gases and salicylate levels, with continuation of the bicarbonate infusion and electrolyte replacement until his acid base status was improving and the salicylate levels were falling.

Fortunately, with this management he improved and did not require additional renal, respiratory or cardiovascular support He was reviewed by psychiatry and transferred for in-patient psychiatric management 3 days later.

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