The design of the new psychiatry unit was so damn mathematical. Everything was coloured in single hues and with the minimum number of edges possible. It was as if someone had designed it on an original PSOne and needed to keep the textures and polygon count simple, and was sponsored by a consortium of Euclid, Pythagorus and MS Paint.
It was a welcome change from the surgical attachment. Towards the end of the surgical placement we needed cover for the twilight period from pm to midnight, as the doctor down for that shift had called in sick. I decided to go for it. I was getting tired of all things surgical but thought that on my next job I might come to miss all this. How wrong I was.
At 6pm I was called to see a man in his late 40s day 5 post abdominal surgery. I was asked to review his capillary glucose around the 20-23 mark. He had a background of Type 2 diabetes.
The first thing I asked for was his ketones, which came back as 0.1. This excluded DKA for now.
My next priority was to consider the possibility of hyperosmolar hypgerglycemia state (HHS), previously known as HONK. I checked the Diabetes UK Guidance, which stated three criteria for HHS:
- Glucose > 30mmol/L
- Hyperosmolar (>320 mosm/kg)
So now I knew my patient was not in DKA, and not in HHS. I could relax just a little. However, he could still be dehydrated from hyperglycemia, and so a fluid status assessment was needed. I also needed to look for an underlying cause.
I see fluid status assessment as a 3 part process:
- How is the patient clinically
- How are the patient’s observations
- How is the patient biochemically
If you feel the patient is shocked, you want to be able to work out which type of shock is most likely.
It’s usually possible to work out the type of shock (hypovolemic, cardiogenic or distributive) from the history, clinical status, the obs and the biochemistry.
(For completeness, there’s also obstructive shock in say massive PE, and hypoadrenal shock as in an Addisonian crisis).
I will go through fluid balance in more detail in a future post. In this patient’s case, there was an increased pulse, and the rest of his observations were normal. He was not catheterised, but was passing some urine every few hours. He complained of no new pain, and in particular no abdominal pain (anastomotic leak is the concern here at this time in the postoperative period). His mucous membranes seemed a little dry.
His chest was clear and a urine dipstick was normal. He had no lines.
I looked at his blood results from that morning.
|White cell count||20.2||8.3|
There were no medications to explain the AKI, or any recent intravenous contrast. He had no features of obstruction. The most likely cause was pre-renal. This is problem #1.
Problem #2 is the glucose. Although not a medical emergency in itself yet, this was an acute rise and needed to be explained. He had taken his medications as normal, and had reasonably well controlled glucose before admission. His post operative recovery until then was plain sailing, and his post op glucose had never been above 13 until today.
In addition to medications, the four causes we must always consider for sudden hyperglycaemia in a diabetic are ACS, stroke, pancreatitis and infection.
In terms of ACS, he had no chest pain. However, we must be cautious about the lack of chest pain in diabetics, the elderly and females. In fact, one third of all ACS cases have no chest pain. In addition, a patient over the age of 85 who is having an MI is more likely to complain about shortness of breath than chest pain. Have a listen to the amazing Canadian Emergency Medicine Cases podcasts, free to F1s and medical students. In this case the ECG showed no changes and initial and 12 hour troponins were negative.
I then looked at the rest of his obs, and mentally overlaid the glucose chart with the obs chart. This is what I saw:
Hmm. Was there a unifying diagnosis to explain the AKI, the hyperglycemia, the pulse and the acutely elevated WCC in a patient with no fever, no pain and no localising signs of infection?
This patient met SIRS criteria (pulse, WCC). Even though there were no localising signs, it was still clinically justified to consider the abdomen as a source of sepsis given the history (SIRS + source = sepsis). In addition, there was end-organ damage (AKI). I felt that this patient therefore had severe sepsis.
It was a handy coincidence that just the day before I had written a question for my iPhone app about osteomyelitis in a diabetic patient. I was looking up information about how osteomyelitis presents in diabetic patients compared to the classic textbook description, and found the following:
“Elevated serum glucose can be a marker of systemic and less often local infection in the diabetic patient. In their history, the compliant patient will often complain of long-standing difficulty with elevated blood sugars roughly corresponding with the time frame of the presence of their ulcer. Often, recalcitrant hyperglycemia is the only systemic manifestation of osteomyelitis in these patients.” – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884907/#r23132-16
I read around some more, and found that sepsis and hyperglycemia are well associated. It’s probably part of the acute stress response. Whether or not treating the hyperglycemia improves outcomes in sepsis seems to be less clear.
Edit – 10/4/13 The patient turned out to eventually have an ischaemic bowel after all that. This would explain the raised lactate, and the SIRS criteria. In ischaemic bowel, the physical findings are classically out of proportion to the degree of pain. In the early stages, there may be minimal or no tenderness and no signs of peritonitis. In the later stages typical symptoms of peritonism develop, with rebound guarding and tenderness.