Foundations, Part 9

Hyperglycaemia: Why Glucose Goes High

Three hours after a meal, the CGM still reads 14.8 mmol/L with the arrow flat. The correction bolus from an hour ago has not done anything. Some highs come and go on their own; some are telling you the insulin is not getting in. Knowing which is which is what this page is for.

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Common causes of high glucose in type 1 diabetes

Glucose goes high for a small set of recurring reasons. Recognising which one is in play is one of the most useful things CGM data can reveal. Tap to expand any cause for the detail.

Missed or late bolus

The single most common cause of post-meal highs. Even a few minutes’ delay changes the insulin-to-carb timing significantly.

Underestimated carbohydrate

Particularly with meals that are difficult to count, or foods with hidden carbohydrate content.

Infusion site or cannula failure (pump users)

A kinked or dislodged cannula can silently stop insulin delivery. One of the most important causes to recognise quickly because the time-to-ketones clock starts the moment delivery stops.

Illness and infection

Counter-regulatory hormones rise during illness, increasing insulin resistance and hepatic glucose output. Many people find they need substantially more insulin when unwell, even if appetite is low.

Stress hormones

Cortisol and adrenaline raise blood glucose independently of food. Includes physical stress, emotional stress, and poor sleep.

Dawn phenomenon

An early-morning glucose rise driven by growth hormone and cortisol, which increase hepatic glucose output before waking.

Rebound from hypo treatment

Overtreating a low can produce a sharp rise, particularly when glucose tabs, juice, and the liver’s own counter-regulatory response all arrive at once. Covered in detail on the Hypoglycaemia page.

High-fat and high-protein meals

Fat slows gastric emptying and protein stimulates glucagon. The result is a delayed glucose rise that arrives hours after the meal, often after the bolus insulin has worn off.

Insufficient basal insulin

If background insulin is not covering hepatic glucose output between meals, glucose drifts upward even without food.

What is happening physiologically

In type 1 diabetes, the beta cells that produce insulin have been destroyed. Without sufficient insulin action, two things happen at once: glucose cannot enter muscle and fat cells efficiently (insulin is the signal that lets them take it up); and the liver continues to produce glucose, because in the absence of insulin, hepatic glucose output is not suppressed.

There is an important nuance. In someone without diabetes, insulin is secreted directly into the portal vein, reaching the liver first at high concentration. This efficiently suppresses hepatic glucose output. Injected or pumped insulin enters peripheral circulation and reaches the liver at much lower concentration. This portal vein mismatch means that exogenous insulin is inherently less effective at switching off liver glucose production than endogenous insulin.

Portal vs peripheral insulin delivery in T1DSide-by-side comparison of native insulin (released into the portal vein, hits the liver first at high concentration) versus injected or pumped insulin (enters peripheral circulation, reaches the liver at much lower concentration). Names the portal-vein mismatch as the reason exogenous insulin is inherently less effective at switching off liver glucose production. Without diabetes (the natural route) Pancreas secretes insulin Portal vein high insulin concentration Liver output suppressed Muscle & fat lower insulin, balanced THE GRADIENT REVERSES IN T1D In T1D (subcutaneous insulin) Injection / pump into subcutaneous tissue Peripheral circulation muscle & fat see it first Muscle & fat over-insulinised on activity Liver low insulin The mismatch: liver under-insulinised, muscle/fat over-insulinised. Source of post-meal spikes and exercise hypos.
The natural gradient (top) reverses in T1D (bottom).

Persistent highs and the action framework

A brief spike after a meal is one pattern. A glucose level that stays above 14 mmol/L (250 mg/dL) for 90 minutes or more is a different situation entirely, and it shifts the likely cause.

When glucose is persistently high and not responding to correction insulin, the most common explanation is a delivery or site problem. For pump users, this means the insulin may not be reaching the subcutaneous tissue at all. The priority in this situation is consistent: check the infusion site for redness, swelling, a kinked cannula, or air in the tubing; change the site if there is any doubt; correct with a reliable delivery route, typically an insulin pen injection. The Hyper Treatment Explorer walks through this action framework with system-specific guidance.

Glucose and ketone timeline after a pump site failureTwo stacked traces over four hours from a kinked or dislodged cannula. Glucose rises gradually as basal delivery silently stops; beta-hydroxybutyrate (BHB) rises in parallel as fat is broken down without insulin to interrupt it. The trace names the BHB 1.5 mmol/L threshold for switching from a correction bolus to an injection plus site change. Hours since the pump cannula stopped delivering 5 10 15 20 Glucose mmol/L 0 1.0 2.0 3.0 Ketones mmol/L 0 1 2 3 4 5 6 hours 14 mmol/L (correction threshold) Glucose rising Ketones rising Action point: persistent > 14 mmol/L not responding to correction. Check site, inject by pen, test ketones.
Schematic curves; individual variation can be substantial. The pattern is the point: ketones lag glucose, then accelerate.

Persistent highs that do not respond to correction are an early ketone warning. When the trace stays above 14 mmol/L for ninety minutes after a correction, treat the site as suspect, switch the delivery route to a pen, and test ketones. The full physiology and treatment routing live on the Ketones page.

Ketones, when highs become dangerous

When there is not enough insulin for cells to use glucose, the body switches to breaking down fat for energy. This produces ketones, acidic byproducts that accumulate in the blood. In small amounts ketones are normal (they are produced during fasting and exercise); in type 1 diabetes the danger arises when ketone production accelerates because of true insulin deficiency, and the body cannot clear them fast enough.

Diabetic ketoacidosis (DKA) occurs when ketone levels become high enough to make the blood acidic. It is a medical emergency that requires hospital treatment. DKA can develop within hours, particularly during illness or after a pump failure that stops insulin delivery completely.

The four-band ketone level table, the correction framework, and the paediatric ISPAD Chapter 13 sick-day routing live on the Ketones page (the next part of Foundations). The Hyper Treatment Explorer surfaces a population-average ketone correction estimate at your total daily insulin and routes paediatric high-ketones via ISPAD rather than adult DAFNE or BERTIE pathways.

Sick day rules, why illness changes everything

Illness is one of the most common triggers for persistent hyperglycaemia and ketone development. The mechanism is straightforward: infection and inflammation cause the body to release counter-regulatory hormones (cortisol, glucagon, adrenaline, growth hormone), all of which increase insulin resistance and stimulate hepatic glucose output.

Many people find they need significantly more insulin during illness, not less. This can feel counterintuitive, especially when appetite is reduced and food intake is low. But the increased insulin resistance means that even without eating, glucose and ketone levels can rise rapidly.

Never stop taking insulin during illness. Even when not eating, basal insulin is needed to suppress hepatic glucose output and prevent ketone production. Stopping insulin during illness is one of the most common pathways to DKA.

The key principles during illness tend to be consistent: continue all insulin (basal and correction); monitor blood ketones every 2 to 4 hours when glucose is persistently above 14 mmol/L; stay hydrated, dehydration accelerates ketone accumulation; and many people find they need to increase basal rates or add additional correction doses. The Hyper Treatment Explorer includes sick-day protocols and shows a population-average ketone correction estimate at your total daily insulin, age band, and AID system. Worth exploring with your care team before you need it.

This content is for educational exploration only. It describes average responses and general principles. It is not medical advice and cannot replace individual clinical guidance from your diabetes care team.

Part 9 of 12

Hyperglycaemia

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