Introduction
Navigating the complexities of acute medicine for the UKMLA can be challenging, but understanding the differences between Diabetic Ketoacidosis (DKA) vs HHS is non-negotiable. As a medical student or junior doctor, encountering a patient with hyperglycemia is an inevitability, and distinguishing between these two conditions is a high-stakes, high-yield topic that requires a nuanced understanding of pathophysiology, clinical presentation, and, most importantly, management. Mistakes here can have life-threatening consequences.
This definitive guide will cut through the confusion and provide a clear, practical framework to help you confidently differentiate between these two hyperglycaemic emergencies. We will break down the core definitions, compare their clinical features and lab findings side-by-side, and give you a step-by-step approach to management that is tailored to the UKMLA and your future practice. This falls under your Endocrinology essentials.
Understanding Diabetic Ketoacidosis (DKA)
Diabetic Ketoacidosis is a life-threatening complication of diabetes mellitus, primarily affecting people with Type 1 Diabetes, but it can also occur in Type 2 Diabetes, particularly in periods of severe stress. At its core, DKA is a state of severe insulin deficiency that leads to three major issues: hyperglycaemia, ketosis, and acidosis.
Without insulin to allow glucose into cells, blood sugar levels rise dramatically. The body, starved of glucose, begins to break down fatty acids for energy. This process produces ketones, which are acidic. The accumulation of ketones in the blood lowers the pH, leading to a metabolic acidosis. The combination of these three factors creates a profoundly unwell patient.
Triggers for DKA are often an infection (e.g., pneumonia or a UTI), poor medication compliance, a new diagnosis of diabetes, or a traumatic event like a myocardial infarction. Sepsis is a common trigger for both DKA and HHS, so it’s important to be familiar with Sepsis Management.
Clinically, a patient with DKA will present with symptoms of both hyperglycaemia and acidosis. They will be dehydrated, thirsty, and passing large amounts of urine. Critically, you will also find signs of ketosis, such as abdominal pain, vomiting, and the classic “pear drop” smell on their breath (due to acetone). They may also have Kussmaul respirations—deep, gasping breaths—as the body attempts to compensate for the acidosis by “blowing off” carbon dioxide.
Understanding Hyperosmolar Hyperglycaemic State (HHS)
Hyperosmolar Hyperglycaemic State, often referred to as HONK (Hyperosmolar Non-Ketotic Coma), is another serious complication of diabetes, most commonly seen in older adults with Type 2 Diabetes. The pathophysiology is distinct from DKA, and this is where most UKMLA candidates get confused.
In HHS, there is enough insulin present to prevent the breakdown of fatty acids and subsequent ketosis. However, it is not enough to prevent severe hyperglycaemia. This leads to an enormous osmotic diuresis—the kidneys try to excrete the excess glucose, pulling water with it. The result is profound dehydration and a dangerously high serum osmolality. This can also lead to Acute Kidney Injury (AKI).
The hallmark of HHS is a gradual onset over days or even weeks, leading to severe dehydration and neurological symptoms. The patient may present with confusion, lethargy, focal neurological deficits, and even coma. They will have a history of polyuria and polydipsia, but unlike DKA, they will not have the signs of ketosis like vomiting or abdominal pain. Their breath will not have the characteristic fruity smell.
Diabetic Ketoacidosis DKA vs HHS: Key Differences at a Glance
For the UKMLA, the ability to rapidly distinguish between these two conditions based on a clinical vignette and lab results is non-negotiable. While both involve elevated blood glucose, their underlying mechanisms and defining features are different. Interpreting clinical data and lab values is a crucial skill here.
Table 1: DKA vs. HHS – A Side-by-Side Comparison for the UKMLA
| Feature | Diabetic Ketoacidosis (DKA) | Hyperosmolar Hyperglycaemic State (HHS) |
|---|---|---|
| Typical Patient | Younger, often with Type 1 Diabetes | Older, often with Type 2 Diabetes |
| Onset | Rapid (hours to 1-2 days) | Gradual (days to weeks) |
| Blood Glucose | >11 mmol/L | >30 mmol/L (often much higher) |
| Ketones | Present and high (>3.0 mmol/L) | Absent or small (usually <3.0 mmol/L) |
| pH | Acidosis (pH <7.3) | Normal or near-normal (pH >7.3) |
| Bicarbonate | Low (<15 mmol/L) | Normal (>15 mmol/L) |
| Osmolality | Variable, usually not severely elevated | Severely elevated (>320 mOsm/kg) |
| Presentation | Thirst, polyuria, abdominal pain, vomiting, fruity breath, Kussmaul breathing | Severe dehydration, altered consciousness, confusion, focal neurology |
| Triggers | Infection, missed insulin dose, new diagnosis | Infection, poor compliance, dehydration, medications (e.g., steroids) |
The 5-Step Management of DKA and HHS
Management for both conditions is an emergency and follows a similar, but not identical, path. It is crucial to follow the NICE guidance and the Joint British Diabetes Societies (JBDS) guidelines, as these are the gold standard for UK practice. This falls under the remit of Emergency Medicine.
The “In my own experience” block: In my own clinical practice, I have seen first-hand the chaos that can ensue in a busy A&E department when a DKA or HHS patient arrives. The key to a calm and effective response is to immediately assess the patient using the ABCDE approach. Don’t get fixated on the blood glucose level alone. You must check their ketones, their blood gas, and their potassium level immediately. These are the parameters that truly dictate the severity and guide your management. I’ve seen junior doctors miss a critical potassium derangement because they were only focused on the glucose reading—a mistake that could be fatal.
Step 1: A-B-C-D-E Assessment
Regardless of the diagnosis, the first step is always to assess the patient using the ABCDE approach.
Airway: Is the airway patent? Is the patient conscious and able to protect their airway?
Breathing: Is their breathing laboured? Are they using accessory muscles? Check for Kussmaul respirations (deep, rapid breathing) in DKA. Obtain an arterial blood gas (ABG) to assess for acidosis.
Circulation: Are they tachycardic or hypotensive? This indicates severe dehydration. Insert two large-bore IV cannulas and obtain bloods, including a baseline HbA1c.
Disability: Assess their GCS. Are they confused or obtunded? Check blood glucose and ketones at the bedside.
Exposure: Look for a source of infection, such as a urinary catheter or skin infection.
Step 2:Â Fluid Management: The Cornerstone of Treatment
This is a key area where DKA and HHS management diverge. While both require aggressive fluid resuscitation, the volume and type of fluid differ.
Fluid Management in DKA: Start with a fluid bolus of 500-1000 mL of 0.9% saline over 30-60 minutes. Subsequent fluid infusions should be based on the patient’s hydration status and a strict fluid balance chart. The goal is to replace lost fluid and improve tissue perfusion.
Fluid Management in HHS: HHS patients are often much more profoundly dehydrated than DKA patients. The fluid deficit can be massive, sometimes exceeding 10 litres. The goal is a more gradual fluid replacement to avoid cerebral oedema. Give 0.9% saline initially, but once the blood glucose drops to a certain level, switch to 0.45% saline to correct the hypertonicity more slowly.
Step 3: Insulin Infusion: The Insulin vs. Fluid Debate
Insulin is the cornerstone of DKA treatment. However, in both DKA and HHS, fluid resuscitation must always be started first. Starting insulin prematurely can worsen hypokalaemia and cause life-threatening arrhythmias.
Insulin in DKA: Use a fixed-rate intravenous insulin infusion. The standard starting dose is 0.1 units/kg/hour. Do not stop the insulin infusion until the acidosis is resolved and the patient is stable enough for a subcutaneous regimen.
Insulin in HHS: Insulin is also used in HHS but with a lower threshold and a more cautious approach. The primary management is fluid resuscitation. Insulin is often started at a lower rate (e.g., 0.05 units/kg/hour) to avoid a rapid drop in osmolality and the risk of cerebral oedema.
Step 4: Potassium Replacement
Potassium is a tricky electrolyte in both DKA and HHS. While a patient may present with a normal or even high serum potassium level, their total body potassium is depleted due to the osmotic diuresis. As you start fluid and insulin therapy, potassium will shift back into the cells, and the serum level will plummet.
Rule of thumb: If the initial potassium is <5.5 mmol/L, you must start potassium replacement with your first bag of fluid. If the level is >5.5 mmol/L, recheck in an hour and add potassium once it falls below this threshold.
Step 5: Monitoring
Both conditions require meticulous monitoring. You will need to check blood glucose, ketones (DKA only), and electrolytes (especially potassium) hourly. The fluid balance chart must be accurate. This is a topic where the UKMLA loves to test your ability to spot a deteriorating patient and act accordingly.
Common UKMLA Pitfalls and How to Avoid Them
The UKMLA is designed to test your clinical reasoning, not just your memorisation. Here are some common traps and how to navigate them.
Pitfall 1: Assuming a High Blood Glucose Always Means DKA
This is the most common mistake. A patient with a blood glucose of 40 mmol/L and an alert GCS is highly likely to have HHS, not DKA. Always remember to check ketones and pH to confirm the diagnosis. A lack of ketones and a normal pH rules out DKA, regardless of the blood sugar level.
Pitfall 2: Neglecting Potassium Management
As discussed, hypokalaemia is a silent killer in these conditions. The UKMLA will often present a case where a patient’s potassium is dropping. You must recognise this as a medical emergency and intervene by adding potassium to the fluid bags.
Pitfall 3: Not Looking for the Underlying Cause
Both DKA and HHS are symptomatic of an underlying trigger. In the UKMLA, you will be expected to demonstrate an ability to find this trigger. Ask about fever, signs of infection, missed medication doses, or recent illness. The station will often give you clues in the history. This is where your History Taking skills are tested.
Pitfall 4: Mismanaging Fluids
Giving too much fluid too quickly in HHS can lead to serious complications. Remember, HHS is a state of severe dehydration but requires gradual rehydration to prevent cerebral oedema. This distinction is a hallmark of good clinical judgment and a favourite UKMLA question.
Frequently Asked Questions (FAQ) about DKA and HHS
The defining difference is the presence of significant ketosis and acidosis in DKA, which is absent or minimal in HHS. This is due to the complete lack of insulin in DKA, allowing for fatty acid breakdown, while in HHS there is enough insulin to prevent ketosis but not to control blood glucose.
Both conditions are characterised by severe dehydration. Fluid resuscitation is the immediate priority to restore circulatory volume, improve tissue perfusion, and in the case of DKA, to help lower blood glucose levels and clear ketones. Starting insulin before fluids can lead to dangerous electrolyte shifts.
Patients with DKA have a total body potassium deficit. When insulin is administered, it drives potassium from the bloodstream back into the cells, which can cause a sudden, life-threatening drop in serum potassium levels. This is why close monitoring and early potassium replacement are essential.
The most common triggers for both are infection and poor medication adherence. Other triggers can include a new diagnosis of diabetes, a traumatic event like a heart attack, surgery, or certain medications like steroids.
DKA has a more rapid onset with symptoms of acidosis such as nausea, vomiting, abdominal pain, and the characteristic “pear-drop” breath smell. HHS has a more gradual onset, with profound dehydration and neurological symptoms like confusion and lethargy being more prominent.
Serum osmolality is a measure of the concentration of solutes in the blood. In HHS, the extreme hyperglycaemia and dehydration lead to a dangerously high osmolality, which can cause cerebral oedema if corrected too quickly.
Yes, this is known as a mixed picture. For example, a patient with Type 2 Diabetes might present with a high blood glucose level and some degree of ketosis. In these cases, the management should be guided by the dominant features, but it’s important to be aware of the complexity.
DKA is most common in children with newly diagnosed Type 1 Diabetes. The disease is often aggressive, leading to a rapid and complete absence of insulin, which precipitates DKA more quickly.
The acidosis in DKA is caused by ketones, not a simple acid-base imbalance. The body will correct the acidosis naturally as the ketones are cleared with insulin therapy. Giving bicarbonate can cause a dangerous shift in potassium and carbon dioxide, leading to rebound alkalosis and cerebral oedema.
Treatment for DKA is complete when the patient’s blood glucose is less than 14 mmol/L, their pH is greater than 7.3, their bicarbonate is greater than 15 mmol/L, and their ketones are less than 0.6 mmol/L. Only when all of these are met can you consider stopping the insulin infusion.
Conclusion:
Distinguishing between Diabetic Ketoacidosis DKA vs HHS is one of the most clinically relevant skills you will learn as a doctor. The UKMLA assesses not just your knowledge of the differences but your ability to apply a systematic, safe, and effective approach to management.
By focusing on the core principles of fluid resuscitation, appropriate insulin therapy, and meticulous electrolyte monitoring, you will not only be well-prepared for your exam but also for the realities of managing these critical patients on the wards. Remember, the difference in a UKMLA question—and in real life—can be a single lab value. Your ability to spot that detail is the hallmark of a confident and competent clinician.
