# Situation: A 76-year-old woman with type 2 diabetes mellitus is brought from home after three days of increasing drowsiness and poor oral intake during a febrile illness. She weighs 60 kg. The provider diagnoses hyperosmolar hyperglycemic state (HHS). Her glucose is far higher than is usual in ketoacidosis, yet her blood ketones are only mildly raised. Which mechanism explains this difference?

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=630226  
> language: ko  
> subject: Nursing Practice V — Care of Clients with Maladaptive Patterns of Behavior; Care of Clients with Life-Threatening Conditions, Acute Multi-Organ Problems, High Acuity and Emergency Situations

## 문제

Situation: A 76-year-old woman with type 2 diabetes mellitus is brought from home after three days of increasing drowsiness and poor oral intake during a febrile illness. She weighs 60 kg. The provider diagnoses hyperosmolar hyperglycemic state (HHS).

Her glucose is far higher than is usual in ketoacidosis, yet her blood ketones are only mildly raised. Which mechanism explains this difference?

## 보기

1. Very high glucose suppresses glucagon release, so the liver has no signal to make ketones
2. Ketones are lost in the urine by osmotic diuresis as fast as the liver produces them
3. Dehydration diverts liver metabolism toward lactate production instead of ketones
4. Enough insulin is still secreted to restrain fat breakdown, though not to control glucose **✔ 정답**

**정답: 4**

## 해설

In HHS the pancreas still secretes some insulin. Far less insulin is needed to suppress lipolysis and ketogenesis than to move glucose into cells, so the remaining insulin restrains fat breakdown while glucose keeps rising. Profound dehydration then drives glucose far higher than in DKA.

## 심화 해설

Core mechanism

In HHS, the pancreas retains a small but clinically meaningful amount of endogenous insulin secretion. The metabolic pathways that produce ketones are far more sensitive to insulin than the pathways that move glucose into cells. Suppression of lipolysis and hepatic ketogenesis requires much lower insulin concentrations than stimulation of peripheral glucose uptake. Therefore, in HHS the residual insulin is enough to restrain adipose tissue breakdown and keep ketone production low, but not enough to lower blood glucose effectively.

Why glucose climbs so high

Because insulin cannot drive glucose into muscle and adipose tissue normally, hyperglycemia worsens. At the same time, osmotic diuresis caused by glucosuria produces profound dehydration and a falling glomerular filtration rate. Dehydration further reduces urinary glucose excretion, allowing glucose to accumulate to levels far higher than those typically seen in DKA. The result is marked hyperglycemia with hyperosmolality but only mild ketosis.

Comparison of DKA and HHS

| Feature | DKA | HHS |
| --- | --- | --- |
| Residual insulin | Very low or absent | Small amount still present |
| Lipolysis and ketogenesis | Markedly activated | Partially suppressed |
| Ketone production | High | Low or mild |
| Glucose elevation | Usually 250–600 mg/dL | Often >600 mg/dL |
| Dehydration severity | Moderate | Profound |
| Acidosis | Present | Usually absent or mild |

Why the other options are incorrect

Option 1 is incorrect because glucagon is not suppressed in HHS. In fact, elevated glucagon contributes to ongoing hepatic glucose output and hyperglycemia. Option 2 is incorrect because ketones are not lost in urine at a rate that matches hepatic production; ketonuria reflects excess production, not a disposal mechanism that prevents ketosis. Option 3 is incorrect because dehydration does not divert hepatic metabolism toward lactate instead of ketones. The primary determinant of ketogenesis is the insulin-to-glucagon ratio, not hydration status.

Key point! HHS and DKA exist on a spectrum of relative insulin deficiency. The presence of even small amounts of insulin in HHS is sufficient to block ketogenesis but insufficient to control glucose, which is why hyperglycemia and hyperosmolality dominate the clinical picture. Watch out! Do not assume that very high glucose always means severe ketosis; the degree of ketosis depends on how much insulin action remains.

## 임상 시나리오

Why HHS Has Mild Ketones Despite Extreme HyperglycemiaInsulin sensitivity differs by pathway
In HHS, the pancreas still secretes a small amount of insulin. Suppression of lipolysis and ketogenesis requires far lower insulin levels than stimulation of peripheral glucose uptake.

Residual insulin is enough to restrain fat breakdown and keep ketone production low, but not enough to move glucose into cells. Glucose rises, often above 600 mg/dL, while ketones remain only mildly elevated.

Profound dehydration from osmotic diuresis reduces glomerular filtration and urinary glucose loss, driving glucose far higher than in DKA.

CautionDo not assume absent insulin in HHS. Aggressive insulin dosing must be balanced with fluid resuscitation to avoid overly rapid osmolarity shifts.

## 핵심 개념

- **HHS** — Hyperosmolar hyperglycemic state with profound hyperglycemia, dehydration, and minimal ketosis due to residual insulin.
- **ketogenesis** — Hepatic production of ketone bodies from fatty acids, highly sensitive to suppression by low insulin levels.
- **lipolysis** — Breakdown of adipose tissue triglycerides into free fatty acids, inhibited by small amounts of insulin.
- **osmotic diuresis** — Glucosuria-driven water loss causing dehydration and reduced renal glucose clearance.
- **DKA** — Diabetic ketoacidosis with near-absent insulin, marked ketosis, acidosis, and usually lower glucose than HHS.

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