Unsweetened vomit

Pregnant women vomit a lot. I don’t just mean morning sickness. Pregnancy can result in altered taste and smell, which means certain foods and smells make them feel violently sick. Although most cases of pregnancy induced vomiting get better after 20 weeks, there are some unlucky ladies who feel sick every single day until the birth of their you-are-lucky-you-look-cute-otherwise-I’d-bloody little bundle of joy.

A lady in her mid 30s was admitted at 39/40 with persistent vomiting. It had been going for two days and she was vomiting nearly every hour. There was no change in bowel habits. There was upper abdominal tightening that occurred with the vomiting, but no other abdominal pain. No one else was affected at home and she had not been travelling or eating unusual foods. She had no vertigo or hearing problems. She had a throbbing headache of about 5/10 severity, especially on being upright. There were no visual symptoms or other neurology.

She was unable to keep anything down, including fluids, for the past 24 hours.

On examination she was dehydrated, with dry mucous membranes. Her urine showed 5+ ketones. Her observations were stable. Her urine was dark, but the output was adequate. There was no abdominal tenderness.

During the admission, she was persistently hypoglycemic. Her BMs were around 3-3.5 despite 5% dextrose being used as rehydrating fluid.

There was no PMH of anything, and no access she could have had to antidiabetic medications/insulin.

Her U&Es, lactate, TFTs, LFTs and calcium were all normal.

Would it be reasonable to attribute her low glucose to 36 hours fasting in the absence of any other medical problems?

I’m thinking no. Here’s why:

  • The body responds to low glucose by first switching off insulin and increasing glucagon production. This has the effect of increasing gluconeogenesis and glycogenolysis in the liver.
  • Catecholamines are also released as the glucose continues to drop. Biochemically, this causes glycogenolysis in the liver and muscle and gluconeogenesis in the liver and kidney. Clinically, this produces the cathecholamine excess symptoms – sweats, tremors, tachycardia and a sense of hunger (and anxiety).
  • Finally, growth hormone is stimulated (which stimulate lipolysis) as well as ACTH (which increases lipolysis and muscle breakdown).
  • If glucose continues to stay low, the patient may develop neuroglycopenic symptoms (dizziness, inappropriate behaviour, poor concentration, confusion, blurred vision, stroke-like symptoms and eventually coma/death). The body prioritises glucose for the brain. If the body can’t supply the brain with glucose, this means something is failing in a big way.

So, in a patient with an otherwise intact endocrine system, a healthy liver and a decent glycogen store, fasting alone will rarely produce hypoglycemia. Hypoglycemia from malnutrition usually occurs when at least one of those three things are out e.g. Addison’s disease, liver disease or prolonged malnutrition depleting the glycogen stores.

What else could cause hypoglycaemia?

Hypoglycemia causes can be split into fasting (occurring at least 6 hours after a meal) and non-fasting. I’m just going to focus on the fasting ones for today.

The fasting hypoglycemias can be split into those with an appropriately low insulin level and those with an inappropriately high insulin level.

Appropriately low insulin

Alcohol – independent of any effect on liver function, alcohol inhibits hepatic gluconeogenesis

Endocrine – usually a problem in the CRH-ACTH-cortistol axis, but also rarely growth hormone deficiencies.

Liver disease – loss of gluconeogenesis ability and/or inability to store glycogen

Renal disease – the kidney does do some gluconeogenesis, but not as much as the liver. The most common clinical application of this is end stage diabetic nephropathy reducing kidney function and therefore a decrease in the insulin/antidiabetic dose requirements.

Sepsis – can lead to impaired gluconeogenesis. However, more commonly hypergylcemia. One of the SIRS criteria is actually raised glucose in a non diabetic.

Pregnancy – the foetus takes priority over resources. Mum’s stores are depleted. This leaves her at risk of hypoglycaemia.

Rare stuff – inborn errors of metabolism.

Inappropriately high insulin

Diabetic meds – by far the commonest. The body can’t ‘switch off’ insulin that is pushed into it. Insulin secretagogues can also cause hypogylcemia. A clinical possibility: An elderly diabetic patient with decreasing renal function has been on a sulfonylurea for ages. The sulfonylurea has reduced clearance because of the reducing renal function, so the patient ends up developing hypoglycaemia.

Insulinoma – classic MRCP case. A prolonged fast for 72 hours is the key test. Normally insulin should switch off. However, if the patient is hypogylcemia with a high insulin level (and raised C peptide to show it was endogenous insulin) then you are a diagnostic machine for spotting an insulinoma.

Bottom line: My patient probably had depleted glycogen stores from her baby which meant when she got into a fasting state, she didn’t have the reserves.