I was called to A&E on a busy Monday shift to see an 18 year-old patient who had been bought in by her mother with drowsiness and abdominal pain. I entered her cubicle and saw that she looked unwell – she was breathing heavily and was pale. I was able to get some history from Catherine’s mother. Her symptoms had been present for 3 days and she was otherwise healthy with no medical problems. Hyperventilation And Hypoventilation

I had a look at her observation chart and saw that she was tachycardic and hypotensive for her age: her heart rate was 120bpm and blood pressure was 80/55 mmHg. She was breathing very deeply and her O2 sats were 100% on air. Her capillary refill time was prolonged at 4 seconds. Her GCS was 14/15 as she drowsy, but was opening her eyes in response to my voice. Her abdomen was mildly tender with no rebound or peritonism. Catherine’s mother mentioned that she had been drinking much more water and going to the toilet more often than normal. Cardiovascular Reflexes Hypovolaemia

Some of the bloods that the triage nurse had taken were back:

This set alarm bells ringing – she had deranged electrolytes (hyponatraemia/hyperkalaemia) and an acute kidney injury by the look of her urea and creatinine. Her haemoglobin was elevated which was probably because she was dehydrated. Hypernatraemia And Hyponatraemia Hyperkalaemia And Hypokalaemia Acute Kidney Injury

I took an arterial gas to assess her acid base status: Taking An Arterial Blood Sample Arterial Blood Gas Basics

Catherine had a partially compensated metabolic acidosis with elevated lactate and hyperglycaemia. I was pretty sure that Catherine had diabetic ketoacidosis and her deep breathing was ‘Kussmaul breathing’. I thought I could smell a pear-drop like odour in her breath, suggestive of ketoacidosis. Causes Of Metabolic Acidosis And Alkalosis Patterns Of Breathing

I put a wide bore intravenous cannula in, prescribed a bag of 0.9% normal saline stat to try and fill her fluids up and asked for the patient to be moved to resus. An ECG showed that Catherine had a sinus tachycardia. I quickly calculated her anion gap, confirming an elevated anion gap consistent with diabetic ketoacidosis: Anion Gap Fluid Challenge

This picture fitted well with Catherine's blood results. The hyponatreamia was dilutional due to her excess blood glucose, and her polyuria (leading to dehydration) was typical in type 1 diabetes mellitus as a result of osmotic diuresis. Hyperglycaemia Induced Hyponatraemia Osmotic Diuresis

I called my reg, Rob, to let him know the situation and asked his advice for ongoing management; he came straight to resus to see the patient. We got the DKA guidelines of the intranet and prescribed a fixed rate insulin infusion and more normal saline with potassium (since insulin drives potassium into cells, causing hypokalaemia). D K A Guidelines Insulin

Catherine's chest x-ray was normal (ruling out any serious infection - such as sepsis - as a trigger for her hyperglycaemia) and urine dip was positive for glucose and ketones, BHCG was negative. We explained to Catherine and her mum that she had diabetes - they were both really upset. Triggers Of Diabetic Ketoacidosis

Rob called the ITU registrar to let them know about the patient, they recommended we continued with resuscitation for now. My bleep went off and I was asked to review a patient with a temperature on the wards. I left my bleep number with the nurses in resus so they could contact me if there were any problems.

I finally got back to see Catherine an hour and a half later. She wasn’t drowsy anymore but her breathing seemed to be deeper still. Her capillary refill was also still prolonged. I became even more worried when the nursing staff told me she hadn’t passed much urine since coming into hospital . I took a venous blood gas: A B G Versus V B G

I was really concerned by this gas as her glucose wasn’t coming down and her acidosis was worsening. I asked the resus nurses to increase the rate of insulin by 1 unit per hour and insert a urinary catheter. I called Rob to let him know that Catherine’s VBG had deteriorated, he was busy with another sick patient on the ward – he asked me to call ITU again. I called the ITU registrar and explained the situation – he came to review the patient and she was transferred to ITU. The rest of my shift was frantic; I was on ward cover after 5 and didn’t stop until handover.

I popped up to ITU the next day before my consultant ward round. Catherine looked so much better! She had a central line in which had been really useful for her resuscitation, as central venous pressure monitoring and central venous sats had helped to guide fluid administration. Her blood glucose had normalised and the diabetes team (a specialist nurse and the endocrinology reg) were on their way to meet her and start her on subcut insulin. They would become Catherine's long term contact for the future, as she learned to control her blood glucose with insulin herself.



I was called to A&E on a busy Monday shift to see an 18 year-old patient who had been bought in by her mother with drowsiness and abdominal pain. I entered her cubicle and saw that she looked unwell – she was breathing heavily and was pale. I was able to get some history from Catherine’s mother. Her symptoms had been present for 3 days and she was otherwise healthy with no medical problems. Hyperventilation And Hypoventilation

I had a look at her observation chart and saw that she was tachycardic and hypotensive for her age: her heart rate was 120bpm and blood pressure was 80/55 mmHg. She was breathing very deeply and her O2 sats were 100% on air. Her capillary refill time was prolonged at 4 seconds. Her GCS was 14/15 as she drowsy, but was opening her eyes in response to my voice. Her abdomen was mildly tender with no rebound or peritonism. Catherine’s mother mentioned that she had been drinking much more water and going to the toilet more often than normal. Cardiovascular Reflexes Hypovolaemia

Some of the bloods that the triage nurse had taken were back:

This set alarm bells ringing – she had deranged electrolytes (hyponatraemia/hyperkalaemia) and an acute kidney injury by the look of her urea and creatinine. Her haemoglobin was elevated which was probably because she was dehydrated. Hypernatraemia And Hyponatraemia Hyperkalaemia And Hypokalaemia Acute Kidney Injury

I took an arterial gas to assess her acid base status: Taking An Arterial Blood Sample Arterial Blood Gas Basics

Catherine had a partially compensated metabolic acidosis with elevated lactate and hyperglycaemia. I was pretty sure that Catherine had diabetic ketoacidosis and her deep breathing was ‘Kussmaul breathing’. I thought I could smell a pear-drop like odour in her breath, suggestive of ketoacidosis. Causes Of Metabolic Acidosis And Alkalosis Patterns Of Breathing

I put a wide bore intravenous cannula in, prescribed a bag of 0.9% normal saline stat to try and fill her fluids up and asked for the patient to be moved to resus. An ECG showed that Catherine had a sinus tachycardia. I quickly calculated her anion gap, confirming an elevated anion gap consistent with diabetic ketoacidosis: Anion Gap Fluid Challenge

This picture fitted well with Catherine's blood results. The hyponatreamia was dilutional due to her excess blood glucose, and her polyuria (leading to dehydration) was typical in type 1 diabetes mellitus as a result of osmotic diuresis. Hyperglycaemia Induced Hyponatraemia Osmotic Diuresis

I called my reg, Rob, to let him know the situation and asked his advice for ongoing management; he came straight to resus to see the patient. We got the DKA guidelines of the intranet and prescribed a fixed rate insulin infusion and more normal saline with potassium (since insulin drives potassium into cells, causing hypokalaemia). D K A Guidelines Insulin

Catherine's chest x-ray was normal (ruling out any serious infection - such as sepsis - as a trigger for her hyperglycaemia) and urine dip was positive for glucose and ketones, BHCG was negative. We explained to Catherine and her mum that she had diabetes - they were both really upset. Triggers Of Diabetic Ketoacidosis

Rob called the ITU registrar to let them know about the patient, they recommended we continued with resuscitation for now. My bleep went off and I was asked to review a patient with a temperature on the wards. I left my bleep number with the nurses in resus so they could contact me if there were any problems.

I finally got back to see Catherine an hour and a half later. She wasn’t drowsy anymore but her breathing seemed to be deeper still. Her capillary refill was also still prolonged. I became even more worried when the nursing staff told me she hadn’t passed much urine since coming into hospital . I took a venous blood gas: A B G Versus V B G

I was really concerned by this gas as her glucose wasn’t coming down and her acidosis was worsening. I asked the resus nurses to increase the rate of insulin by 1 unit per hour and insert a urinary catheter. I called Rob to let him know that Catherine’s VBG had deteriorated, he was busy with another sick patient on the ward – he asked me to call ITU again. I called the ITU registrar and explained the situation – he came to review the patient and she was transferred to ITU. The rest of my shift was frantic; I was on ward cover after 5 and didn’t stop until handover.

I popped up to ITU the next day before my consultant ward round. Catherine looked so much better! She had a central line in which had been really useful for her resuscitation, as central venous pressure monitoring and central venous sats had helped to guide fluid administration. Her blood glucose had normalised and the diabetes team (a specialist nurse and the endocrinology reg) were on their way to meet her and start her on subcut insulin. They would become Catherine's long term contact for the future, as she learned to control her blood glucose with insulin herself.



I was called to A&E on a busy Monday shift to see an 18 year-old patient who had been bought in by her mother with drowsiness and abdominal pain. I entered her cubicle and saw that she looked unwell – she was breathing heavily and was pale. I was able to get some history from Catherine’s mother. Her symptoms had been present for 3 days and she was otherwise healthy with no medical problems. Hyperventilation And Hypoventilation

I had a look at her observation chart and saw that she was tachycardic and hypotensive for her age: her heart rate was 120bpm and blood pressure was 80/55 mmHg. She was breathing very deeply and her O2 sats were 100% on air. Her capillary refill time was prolonged at 4 seconds. Her GCS was 14/15 as she drowsy, but was opening her eyes in response to my voice. Her abdomen was mildly tender with no rebound or peritonism. Catherine’s mother mentioned that she had been drinking much more water and going to the toilet more often than normal. Cardiovascular Reflexes Hypovolaemia

Some of the bloods that the triage nurse had taken were back:

This set alarm bells ringing – she had deranged electrolytes (hyponatraemia/hyperkalaemia) and an acute kidney injury by the look of her urea and creatinine. Her haemoglobin was elevated which was probably because she was dehydrated. Hypernatraemia And Hyponatraemia Hyperkalaemia And Hypokalaemia Acute Kidney Injury

I took an arterial gas to assess her acid base status: Taking An Arterial Blood Sample Arterial Blood Gas Basics

Catherine had a partially compensated metabolic acidosis with elevated lactate and hyperglycaemia. I was pretty sure that Catherine had diabetic ketoacidosis and her deep breathing was ‘Kussmaul breathing’. I thought I could smell a pear-drop like odour in her breath, suggestive of ketoacidosis. Causes Of Metabolic Acidosis And Alkalosis Patterns Of Breathing

I put a wide bore intravenous cannula in, prescribed a bag of 0.9% normal saline stat to try and fill her fluids up and asked for the patient to be moved to resus. An ECG showed that Catherine had a sinus tachycardia. I quickly calculated her anion gap, confirming an elevated anion gap consistent with diabetic ketoacidosis: Anion Gap Fluid Challenge

This picture fitted well with Catherine's blood results. The hyponatreamia was dilutional due to her excess blood glucose, and her polyuria (leading to dehydration) was typical in type 1 diabetes mellitus as a result of osmotic diuresis. Hyperglycaemia Induced Hyponatraemia Osmotic Diuresis

I called my reg, Rob, to let him know the situation and asked his advice for ongoing management; he came straight to resus to see the patient. We got the DKA guidelines of the intranet and prescribed a fixed rate insulin infusion and more normal saline with potassium (since insulin drives potassium into cells, causing hypokalaemia). D K A Guidelines Insulin

Catherine's chest x-ray was normal (ruling out any serious infection - such as sepsis - as a trigger for her hyperglycaemia) and urine dip was positive for glucose and ketones, BHCG was negative. We explained to Catherine and her mum that she had diabetes - they were both really upset. Triggers Of Diabetic Ketoacidosis

Rob called the ITU registrar to let them know about the patient, they recommended we continued with resuscitation for now. My bleep went off and I was asked to review a patient with a temperature on the wards. I left my bleep number with the nurses in resus so they could contact me if there were any problems.

I finally got back to see Catherine an hour and a half later. She wasn’t drowsy anymore but her breathing seemed to be deeper still. Her capillary refill was also still prolonged. I became even more worried when the nursing staff told me she hadn’t passed much urine since coming into hospital . I took a venous blood gas: A B G Versus V B G

I was really concerned by this gas as her glucose wasn’t coming down and her acidosis was worsening. I asked the resus nurses to increase the rate of insulin by 1 unit per hour and insert a urinary catheter. I called Rob to let him know that Catherine’s VBG had deteriorated, he was busy with another sick patient on the ward – he asked me to call ITU again. I called the ITU registrar and explained the situation – he came to review the patient and she was transferred to ITU. The rest of my shift was frantic; I was on ward cover after 5 and didn’t stop until handover.

I popped up to ITU the next day before my consultant ward round. Catherine looked so much better! She had a central line in which had been really useful for her resuscitation, as central venous pressure monitoring and central venous sats had helped to guide fluid administration. Her blood glucose had normalised and the diabetes team (a specialist nurse and the endocrinology reg) were on their way to meet her and start her on subcut insulin. They would become Catherine's long term contact for the future, as she learned to control her blood glucose with insulin herself.




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