A woman in her early 40s is referred by her GP to the Acute Medical Unit feeling generally unwell.
“What’s the main problem?”
Me too, I thought.
“I’m sorry to hear that. Why do you think you are depressed?”
“My fiancé broke up with me a year to the day last week, and I lost my job yesterday (details slightly changed)”
Adjustment disorder then. I had 7 patients to clerk, and it was only 10:30am. A part of me wanted to simply screen for serious problems and discharge if possible. However, I had a feeling that quite a few more open questions would be needed to ensure we get the full history in a patient in this frame of mind. I also needed to make sure she did not get the feeling of time pressure to ensure she really spoke her mind.
“I’m sorry to hear that. How have you been since?”
“I’ve not eaten for the past 7 days. And for the last 5 days, every time I eat, it comes back up. Dark brown with black specks.”
Hold on. Poor appetite goes with depression, but possible coffee ground vomit? I had another look at her obs:
- Pulse 103
- BP 130/70
- RR 18
- Sats 100 on air
- Temp 36.4
The tachycardia concerned me in light of her possible GI bleed. I decided to get some IV access and take some bloods while taking the rest of the history. There were no other abdominal signs, other evidence of a GI bleed or risk factors apart from the alcohol use described later. She also reported heavy periods recently, but no other coagulation deficit symptoms. She had been suffering with extreme fatigue, poor motivation and poor sleep as well as low mood. She had no suicide ideation. Her past medical history was remarkable for a period a year ago where she would drink 1 bottle of vodka a day. She said she only drank a bottle a week now. No other drug use.
I was still thinking depression/adjustment, but wanted reassurance from the bloods that there was no evidence of a bleed.
I sent FBC, U&E, Clotting, TSH, LFT and Bone Profile, including Magnesium. I gave 1L Hartmann’s over 8 hours whilst I awaited her results.
I was phoned by the lab regarding the following results. The rest of the bloods were normal, including LFTs and coagulation. (Although BMJ learning has produced an excellent e-learning module highlighting that in alcoholic liver disease, the main problem is synthetic function, and it is not unusual for LFTs to be entirely normal).
- Hb 10.7
- WCC 8.4
- Plt 20
- Na 128
- K 2.3
- Urea 1.8
- Creatinine 34
- eGRF >90
I switched her fluids to 1L N Saline with 40mmol KCl over 4 hours, then 8 hours, and informed my registrar. An ECG showed no changes.
Hypokalemia could be explained by her vomiting, which would also explain her hyponatremia (1L of gastric fluid contains 20-80 mmol Na and 5-20 mmol K according to the BNF). I thought back to her history and realised something else may be going on.
To reiterate the risk factors for this condition:
Very poor intake for 7 days
Previous alcohol misuse
What I was thinking of was Refeeding Syndrome.
I recently prepared a brief presentation on this case. To cut to the essentials, the longer the patient has been starved and the worse the patient’s pre-existing glycogen/lipid stores, the more the patient will switch to using proteins and ketones.
When you reintroduce glucose to a patient who has primed their body to preserve glucose at every possible opportunity, there is a massive surge of insulin.
This insulin shifts the intracellular electrolytes even more intracellularly. In particular, phosphate, potassium and magnesium levels drop alarmingly. In addition, insulin stimulates glycogen, fat, and protein synthesis. This requires phosphate, magnesium and thiamine.
Our patient was given 200mg thiamine and 2 Vitamin B Strong tablets before anything else. This is because when we do refeed her, the surge of glucose will deplete the thiamine reserves. (Or so we are taught, and NICE guidelines suggest. Have a look at the flip side). Whether or not this is actually true, 200mg of thiamine doesn’t do harm.
I advised her to avoid high glucose foods, and to eat about 50% of her normal amount of food per day. I informed the nurses of this plan.
The next day, her electrolytes came back as:
- Na 131
- K 2.7
- Ca 2.0 (adj)
- Mg 0.31
- Phosphate 0.33
This was getting quite serious. Magnesium deficiency causes torsades de pointes and seizures. Phosphate deficiency causes weakness and dysphagia, which is the last thing you need in a starved patient.
We had to now prioritise the IV fluids. We could only get two cannulas in. Hypomangesia in itself leads to hypokalemia through a renal mechanism and causes torsades as described. Hypokalemia causes many arrhythmias. These two needed to be corrected first. We also started cardiac telemetry.
We started a 20mmol phosphate infusion after 30mmol of magnesium had been given. We infused these electrolytes at the maximum recommended rates in the BNF. A repeat electrolyte count later in the day showed similar results, despite the IV fluids. She seemed to be in normal fluid balance, with an improving urine output and stable obs. The nurse did mention visible haematuria (plts = 20, Hb 10.1).
Our management plan, and what happened next, will be revealed in the next post.