4 Diabetic Ketoacidosis and HHNS Nursing Care Plans

DKA and HHNS are insulin-deficiency emergencies, and both land on your unit dehydrated, hyperglycemic, and circling the drain if you sit on them. The work is the same order every time: fluids first, then insulin, then potassium, while you hunt the trigger (usually infection, a missed insulin dose, or new-onset diabetes). Move fast, but do not crash the glucose or the potassium, because that is what kills these patients after you have already stabilized them.

What is diabetic ketoacidosis (DKA)?

Diabetic ketoacidosis is a life-threatening emergency from a relative or absolute lack of insulin. Without insulin, glucose cannot enter cells for fuel, so the liver breaks down fat into ketones instead. Those ketones pile up in blood and urine and turn the blood acidic. The result is the classic picture: hyperglycemia, acidosis, dehydration, and electrolyte losses including hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia, and hypophosphatemia. The earliest tells are creeping polydipsia and polyuria.

The common precipitants are infection (pneumonia, urinary tract infection), missed or disrupted insulin, and previously undiagnosed diabetes. Drugs that affect carbohydrate metabolism, including corticosteroids, thiazides, sympathomimetics, and pentamidine, can also tip a patient into DKA. Overall mortality runs 0.2 to 2%, highest in developing countries. Hypoglycemia is the most common complication, followed by hypokalemia, cerebral edema, acute respiratory failure, and even myocardial infarction or stroke.

What is hyperglycemic hyperosmolar nonketotic syndrome (HHNS)?

HHNS, also called hyperosmolar hyperglycemic state (HHS), is hyperglycemia plus hyperosmolarity plus dehydration. There is enough insulin to suppress ketosis but not enough to control glucose. Persistent hyperglycemia drives osmotic diuresis, which drains fluid and electrolytes. Patients present with hypotension, tachycardia, marked dehydration, and neurologic signs (seizures, hemiparesis, altered sensorium). DKA and HHS overlap in up to one-third of cases, but most HHS patients do not develop significant ketoacidosis.

Nursing Care Plans and Management

Care covers cardiovascular, pulmonary, renal, and CNS monitoring, reversing dehydration, correcting hyperglycemia, and teaching the patient enough self-care to avoid a repeat admission.

Nursing Problem Priorities

• Recognize the signs and symptoms of DKA and HHNS early.
• Give IV fluids and electrolytes to correct dehydration and restore volume.
• Monitor blood glucose and give insulin as prescribed.
• Manage acid-base and electrolyte disturbances.
• Monitor vital signs, including blood pressure and heart rate.
• Give supplemental oxygen if needed.
• Teach the importance of consistent diabetes management: medication adherence and glucose monitoring.
• Prevent future episodes through self-care and lifestyle changes.
• Schedule followup to monitor recovery, assess glycemic control, and adjust the plan.

Nursing Assessment

Assess for the following subjective and objective data:

• Diabetic Ketoacidosis (DKA):
• Excessive thirst and frequent urination
• Abdominal pain, nausea, and vomiting
• Rapid breathing (Kussmaul breathing)
• Fruity or acetone breath odor
• Confusion, lethargy, or altered mental status
• Dry or flushed skin
• High blood glucose levels (>250 mg/dL)
• Ketones in the urine or blood
• Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS):
• Extreme thirst and dehydration
• Excessive urination or low urine output
• Dry mouth and skin
• Weakness, fatigue, and dizziness
• Altered mental status or confusion
• Seizures or coma in severe cases
• Very high blood glucose levels (>600 mg/dL)
• Absence of significant ketones in the urine or blood

Nursing Goals

Goals and expected outcomes may include:

• The patient stays normovolemic: urine output greater than 30 mL/hr, normal skin turgor, good capillary refill, normal blood pressure, palpable peripheral pulses, and blood glucose between 70 to 200 mg/dL.
• The patient shows normal electrolytes and stable vital signs.
• The patient stays free of infection: normothermia, HR of 100 beats/minute or less, BP within normal range, WBC count of 11,000/mm³ or less, and negative cultures.
• The patient identifies ways to prevent and reduce infection risk and demonstrates them.
• The patient maintains a normal energy level and takes in adequate calories and nutrients.
• The patient maintains stable weight or gains toward the desired range with normal labs.
• The patient keeps blood glucose in the target range and names the factors that lead to unstable glucose and DKA.
• The patient verbalizes a plan for modifying those factors to prevent or minimize complications.

Nursing Interventions and Actions

1. Managing Hyperglycemia

Without insulin, less glucose enters cells and the liver keeps releasing more, driving hyperglycemia. Once blood glucose reaches about 180 mg/dL, the kidney's reabsorption capacity is saturated and glucose spills into the urine, dragging water and electrolytes with it.

Assess what triggered this episode. A young patient with new type 1 diabetes may present in DKA, often with a precipitating infection. More often DKA comes from a breakdown in management: diet, activity, or missed medication. In younger type 1 patients, watch for unaccounted-for changes such as a growth spurt or pregnancy.

Check the patient's and caregiver's ability to monitor glucose. Any meter reads accurately if used, maintained, and calibrated correctly. Unstable glucose often traces back to inconsistent monitoring.

Check insulin injection sites. Absorption varies day to day and drops in lipohypertrophied tissue. Repeated injections thicken the skin, which is why site rotation matters.

Auscultate bowel sounds. Hyperglycemia and electrolyte shifts slow gastric motility and cause gastroparesis, which changes what the patient can tolerate.

Weigh the patient regularly. Weight tracks intake, absorption, and utilization. A history of weight loss is common in newly diagnosed type 1 diabetes.

Review the patient's dietary program against recent intake. This exposes deviations from the plan that drive unstable glucose and uncontrolled hyperglycemia.

Watch for hypoglycemia. As carbohydrate metabolism resumes and insulin is adjusted, glucose can drop fast. In an unconscious patient, hypoglycemia can occur without an obvious change in LOC. Treat it quickly per protocol.

Resume oral nutrients and electrolytes once the patient tolerates fluids, then advance to solids. The oral route is preferred when the patient is alert and bowel function returns. Some HHS patients cannot eat for several days because of comorbidities.

Monitor serum glucose, acetone, pH, and HCO3. See Monitoring Results of Diagnostic and Laboratory Procedures.

Give rapid-acting insulin (regular, lispro, or aspart) by intermittent or continuous IV infusion. See Pharmacologic Support.

Give glucose solutions such as 5% dextrose and half-normal saline. See Pharmacologic Support.

Refer to a dietitian. A dietitian calculates and adjusts the diet to the patient's needs and, once HHS resolves, provides the counseling these patients need.

2. Promoting Infection Control and Preventing Infection

Infection is the most common trigger for a hyperglycemic crisis and the most common cause of death in DKA. The usual sites are respiratory, kidney, urinary tract, skin, and soft tissue. Poor glycemic control feeds severe infection, and the infection worsens the DKA, so the two drive each other.

Assess for signs of infection and inflammation. Look for fever, dysuria, cough, malaise, chills, chest pain, shortness of breath, and arthralgia.

Inspect the feet for ulcers, infected toenails, and other problems. Impaired circulation predisposes to poor wound healing. Screen for peripheral vascular disease and sensory neuropathy and gauge ulcer depth and severity.

Auscultate breath sounds. Rhonchi suggest retained secretions from pneumonia or bronchitis that may have precipitated the DKA. Lung infections trigger sepsis, which raises DKA risk.

Use aseptic technique for IV insertion and medication administration, and manage invasive lines carefully. High glucose blunts immunity. Rotate peripheral IV sites at least every 96 hours, change dressings per policy, and pull central lines as soon as feasible.

Give conscientious skin care. Intact skin protects against infection. Keep skin and linens dry and wrinkle-free. Impaired peripheral circulation raises the risk of breakdown.

Provide wound and foot care. Keep the wound bed moist but not wet. Wet-to-damp dressings support autolytic debridement, absorb exudate, and protect surrounding skin.

Provide a pressure-redistribution surface and off-loading devices for ulcers. These prevent breakdown. For a neuropathic plantar ulcer, a non-removable knee-high off-loading device (total contact cast, or a walker made irremovable) is preferred. Felted foam with appropriate footwear is an alternative.

Reinforce handwashing. These patients have a suppressed inflammatory response and are at higher infection risk. Hand hygiene breaks the chain of transmission.

Encourage two to three liters of oral fluid a day unless contraindicated. Hydration lowers infection susceptibility, supports wound healing, and keeps urine flowing to flush the urinary tract.

Encourage deep breathing, coughing, and incentive spirometry; keep the patient in semi-Fowler's. Deep breaths and IS expand alveoli and mobilize secretions; coughing clears them. Semi-Fowler's aids lung expansion and reduces aspiration risk.

Obtain cultures as indicated. See Monitoring Results of Diagnostic and Laboratory Procedures.

Limit indwelling urethral catheters to patients who cannot void or who need continuous output measurement. Catheters raise infection risk. If one is placed, aim to remove it within 48 hours.

Give antibiotics as indicated. See Pharmacologic Support.

Refer to podiatry and promote properly fitted shoes. About 85% of diabetic foot ulcers are preventable with good preventive care, including shoe inspection for support and fit. A podiatrist can correct high-risk foot deformities.

3. Enhancing Nutritional Balance

Diet and lifestyle contribute to DKA and severe hypoglycemia even though insulin adherence is the biggest factor. Nutritional support holds a stable metabolic state and helps prevent complications such as abnormal glucose, water metabolism disorders, ketosis, infection, and nerve damage.

Determine the patient's dietary program and usual pattern. This finds deviations from therapeutic needs that drive unstable glucose.

Monitor weight daily or as indicated. Weight tracks intake, absorption, and utilization. Eating disorders contribute to 20% of recurrent DKA in young patients. Rapid weight loss is a symptom of newly diagnosed type 1 diabetes.

Auscultate bowel sounds; note abdominal pain, bloating, nausea, or vomiting; keep NPO as indicated. Fluid, electrolyte, and glucose imbalances slow gastric emptying. Nausea and vomiting often come with diffuse abdominal pain and anorexia.

Identify food preferences, including ethnic and cultural needs. Building preferences into the meal plan improves adherence after discharge. For example, patients who observe Ramadan may face higher risk of acute complications.

Involve the family in meal planning. Family involvement supports the patient and teaches caregivers the nutritional needs. Options include carbohydrate counting, the exchange list, the point system, and preselected menus.

Recognize hypoglycemia. It can occur from reduced carbohydrate metabolism while insulin is still on board. Hypoglycemia carries a twofold to threefold increased mortality, rising with age and with a history of severe episodes.

Monitor serum glucose, pH, HCO3, and acetone, and perform fingerstick glucose and urine ketone checks. See Monitoring Results of Diagnostic and Laboratory Procedures.

Give glucose solution (dextrose and half-normal saline). Add glucose-containing fluid after insulin and fluids bring glucose to about 400 mg/dL. Once glucose falls below 250 mg/dL (14 mmol/L), add 10% glucose so the fixed-rate insulin infusion can continue without causing hypoglycemia.

Give regular insulin by intermittent or continuous IV. IV is the route of choice: rapid onset and short duration let you match insulin to fast-changing glucose. Larger volumes of insulin in isotonic saline work when no infusion pump is available, as long as the insulin dose is the same.

Collaborate with a dietitian to resume oral intake. The dietitian adjusts the timing, size, frequency, and composition of meals to avoid hypoglycemia and postprandial hyperglycemia. Every patient on insulin needs a comprehensive diet plan.

Provide a diet of 60% carbohydrates, 20% fats, and 20% proteins in set meals. Complex carbohydrates (peas, beans, whole grains, vegetables) lower glucose and cholesterol. Schedule food to insulin action. A workable caloric distribution is 20% at breakfast, 35% at lunch, 30% at dinner, and 15% as a late-evening snack.

Teach three meals a day at set times plus a bedtime snack. Consistent timing keeps glucose level instead of swinging between highs and lows. Tie meals to insulin, especially with mealtime analogues such as Humalog, NovoLog, or Apidra, which act faster than regular insulin.

Balance sugar-containing beverages with water. Maintain carbohydrate intake unless the insulin dose changes, and drink water to hold intravascular volume. Juice and soda carry too much carbohydrate to use as a primary fluid source.

Give prochlorperazine, diphenhydramine, and metoclopramide as prescribed. These treat GI symptoms such as diabetic gastroparesis to improve intake and absorption. See Pharmacologic Support.

4. Managing Fluid Volume

Without insulin, glucose climbs and the kidneys dump it along with water and electrolytes. That osmotic diuresis drives the dehydration and electrolyte loss you are correcting.

Assess precipitating factors (other illness, new-onset diabetes, poor adherence). This sets the baseline for teaching once hyperglycemia resolves. UTI and pneumonia are the most common infectious triggers in older patients. Missed insulin doses, often from poor education or psychological stress, are common in adolescents.

Assess skin turgor, mucous membranes, and thirst. Turgor decreases and tenting appears as hydration drops. Oral mucosa goes dry and thirst becomes extreme.

Monitor hourly intake and output. Oliguria or anuria reflects reduced glomerular filtration and renal blood flow. Hyperglycemia exceeds the renal glucose threshold and causes glucosuria, osmotic diuresis, dehydration, and hyperosmolarity; severe dehydration can impair renal function.

Monitor vital signs, especially for orthostatic hypotension and Kussmaul's respirations. Reduced blood volume shows as a falling systolic pressure and orthostatic hypotension. Acetone breath comes from acetoacetic acid breakdown. Kussmaul's respirations (rapid, deep breathing) blow off carbon dioxide to raise arterial pH. Fever with flushed, dry skin points to dehydration, and peripheral vasoconstriction gives a weak, thready pulse.

Assess neurologic status every two hours. A decreased level of consciousness comes from volume depletion, glucose extremes, hypoxia, or electrolyte imbalance. Mild disorientation or confusion is common; frank coma is uncommon but appears with neglect or severe dehydration or acidosis.

Weigh the patient daily. Weight tracks fluid status and the adequacy of replacement. A loss of 2.2 lbs (1 kg) over 24 hours equals about a liter of fluid lost. Typical free water loss in DKA is about six liters, or nearly 100 mL/kg of body weight.

Assess for nausea and vomiting. These often come with diffuse abdominal pain and anorexia. Ketones, especially beta-hydroxybutyrate, drive nausea and vomiting that worsen fluid and electrolyte loss.

Maintain a fluid intake of at least 2500 mL/day within cardiac tolerance once oral intake resumes. Hydration lowers counterregulatory hormones, improves renal glucose clearance, and boosts insulin sensitivity, cutting hyperglycemia, hypertonicity, and acidemia. Hydration alone has reduced glucose by 17 to 80% over 12 to 15 hours.

Watch for fluid overload, especially in older adults and patients with heart or renal failure. Jugular venous distention, dyspnea, crackles, or a CVP over 12 mm Hg can follow rapid infusion. Replace volume aggressively up front, but guard against cerebral and pulmonary edema in patients with renal failure or congestive heart failure.

Monitor blood glucose, serum ketones, potassium, sodium, creatinine, and BUN, and monitor ABG for metabolic acidosis. See Monitoring Results of Diagnostic and Laboratory Procedures.

Insert an indwelling urinary catheter as indicated. It gives accurate output, especially with neurogenic bladder and urinary retention. Remove it once the patient is stable to lower infection risk.

Give isotonic 0.9% NaCl first. The first goal is correcting the circulatory volume deficit. Isotonic saline expands extracellular volume without dropping plasma osmolality too fast. Patients typically need one to three liters in the first two hours, then a liter every four hours depending on dehydration and CVP.

Follow with a hypotonic solution such as 0.45% normal saline. After stabilizing with isotonic saline, switch to half-normal saline at 200 to 1000 mL/hour to match osmotic-diuresis losses. Continuation depends on the fluid deficit, urine output, and serum electrolytes.

Add dextrose when serum glucose is less than 180 mg/dL in DKA. Below 180 mg/dL, replace isotonic saline with 5 to 10% dextrose in half-isotonic saline. Dextrose prevents hypoglycemia and the rapid osmolality drop that can cause cerebral edema.

Give IV potassium, other electrolytes, and bicarbonate as indicated. See Pharmacologic Support.

Give IV insulin by continuous infusion using a pump. Regular insulin's rapid onset moves glucose intracellularly fast. A low-dose regimen avoids the severe hypoglycemia and hypokalemia seen with high-dose regimens.

Before starting, flush the tubing with at least 30 mL of the insulin-containing solution. Insulin binds to the container and tubing. Flushing saturates that binding so the patient gets the intended dose.

5. Initiating Patient Education and Health Teachings

DKA is an acute complication of diabetes, and about one-third of cases occur in newly diagnosed patients. Most deaths come from cerebral edema. Knowledge drives prevention, so assess and build what the patient understands.

Assess knowledge of DKA and complication prevention. In one study, 38% of DKA patients had poor awareness of complications and 67% had poor management knowledge. Gaps shape how the patient engages in care.

Assess family history of diabetes or DKA. A first-degree relative with diabetes is linked to better DKA-management awareness.

Assess health literacy (language, reading, comprehension) and cultural information needs. This ensures teaching is pitched at the right level.

Establish rapport and trust. The patient has to trust you before they engage in learning.

Explain the signs and symptoms of DKA. Hyperglycemia shows as polyuria, polydipsia, polyphagia, flushed skin, and malaise. GI symptoms (nausea, vomiting, generalized abdominal pain) occur in more than 60% of patients, and abdominal pain mimicking an acute abdomen is common in children and severe acidosis.

Cover risk factors, disease process, and complications. Explain the normal glucose range against the patient's level, the type of diabetes, and the link between insulin deficiency and high glucose. Acute and chronic complications include visual disturbances, neurosensory and cardiovascular changes, renal impairment, and hypertension.

Demonstrate glucose testing and teach the patient to check urine ketones once glucose reaches 250 mg/dL or higher. Checking three to four times a day is essential. Glucose over 250 mg/dL with high urine ketones goes to the provider immediately. Frequent home monitoring catches the rise before it becomes DKA.

Review target glucose levels. The ideal adult range is about 80 to 120 mg/dL. During treatment, the optimal rate of glucose decline is 100 mg/dL/hour, and glucose should not fall below 200 mg/dL in the first four to five hours, since improved insulin sensitivity can drop it fast.

Teach the signs of hypoglycemia. These signal excessive insulin. Letting glucose fall to hypoglycemic levels is a common mistake that triggers rebound ketosis and prolongs treatment.

Teach that polyuria, polydipsia, and polyphagia signal hyperglycemia needing more insulin. Untreated, this leads to coma and death. Osmotic diuresis depletes sodium, potassium, phosphates, and water, driving severe dehydration, thirst, tissue hypoperfusion, and possibly lactic acidosis or renal impairment.

Teach sick-day management. Keep the same insulin regimen, never stop insulin or skip doses, and monitor glucose more often. The key rule: never eliminate insulin when nausea and vomiting hit. Take the usual dose and try frequent small carbohydrate portions.

Explain the dietary plan. Limit simple sugar, fat, salt, and alcohol; increase whole grains, fruits, and vegetables. A high-fiber diet slows glucose absorption and lowers lipids; cutting saturated fat lowers coronary and peripheral vascular risk. A consistent carbohydrate diet typically runs 69% carbohydrates, 20 to 30% fats, and 12 to 20% proteins.

Stress fluid intake during illness. Anorexia or nausea limits food, but the patient should keep drinking to avoid dehydration and hypotension. If vomiting, diarrhea, or fever persists, take a half cup of regular cola or orange juice, a half cup of broth, or sports drinks every 30 minutes to one hour for calories.

Teach glucose monitoring around exercise and insulin adjustment. Adjust the insulin dose after changes in food intake and before exercise, since exercise increases glucose use. Monitor glucose and urine ketones during emotional stress too, which can raise hepatic glucose release and insulin resistance.

Stress daily foot inspection and foot care. Reduced peripheral circulation hides foot injuries. Routine self-inspection, appropriate shoes, and avoiding barefoot walking lower the risk of ulceration and amputation.

Stress routine eye exams. Poorly controlled diabetes changes vision and can lead to blindness. Diabetic retinopathy changes have been reported before and after DKA treatment.

Review the insulin regimen (onset, peak, duration). Understanding the medication lets the patient adjust doses and food to avoid swings. Dose algorithms account for inpatient-established dosages, usual activity, and meal plans.

Review self-administration and equipment care; have the patient demonstrate. Watch them draw up and inject insulin, use a pen, or run a pump. This catches problems like memory gaps so you can build workarounds. Skill development lowers HbA1c.

Discuss insulin timing and meals. Regular insulin works best 30 minutes before eating; insulin lispro (Humalog) works best within 15 minutes, with onset twice as fast as regular and about half the duration. If a reading is over 80 mg/dL, inject rapid-acting insulin after eating rather than before.

Discuss a medical alert bracelet. It speeds entry into the health system. The American Diabetes Association recommends one for everyone with diabetes, especially on glucose-lowering medication that can cause hypoglycemia.

Stress strict followup care. Tighter control prevents exacerbations and delays systemic complications. An endocrinologist may help manage care after stabilization.

Address complementary therapies that alter glucose. Some herbal preparations change metabolism and raise or lower glucose, so report all of them to the provider. Plant-based therapies studied for anti-diabetic effects include aloe vera, bitter melon, cinnamon, fenugreek, ginger, and okra, but they can drop glucose dangerously low.

Review smoking's effect on insulin and encourage cessation. Nicotine constricts small vessels and delays insulin absorption while they stay constricted.

Set a regular exercise schedule and address insulin timing. Exercise should not coincide with peak insulin action. Take a snack before or during exercise as needed, and rotate injection sites away from the muscle group being used to avoid accelerated insulin uptake.

6. Administer Medications and Provide Pharmacologic Support

DKA treatment rests on IV insulin to lower glucose, IV fluids to correct dehydration and electrolytes, and potassium for hypokalemia. HHNS relies on IV fluids to restore hydration and normalize glucose, with insulin as needed. Antiemetics or antibiotics are added based on the patient's complications.

Rapid-acting insulin (regular, lispro, or aspart) by intermittent or continuous IV infusion. The IV route is first choice because subcutaneous absorption is erratic in a crisis. Continuous infusion eases the transition to carbohydrate metabolism and reduces hypoglycemia.

Glucose solutions such as 5% dextrose and half-normal saline. Add after insulin and fluids bring glucose to about 400 mg/dL. The optimal rate of glucose decline is 100 mg/dL/hour, and glucose must not fall below 200 mg/dL in the first four to five hours, since hypoglycemia can develop rapidly with improved insulin sensitivity.

Antibiotics. Early antibiotics help prevent sepsis. Guide therapy by culture and sensitivity, but starting empiric antibiotics on suspicion of infection until cultures return may be advisable.

Prochlorperazine. For nausea and vomiting. It is about as effective as metoclopramide, ondansetron, promethazine, and droperidol, with generally mild side effects.

Diphenhydramine. A first-generation antihistamine used for motion sickness.

Metoclopramide. FDA-approved for nausea and vomiting in diabetic gastroparesis; it increases gastric motility.

Potassium IV and other electrolytes. If potassium is greater than 6 mEq/L, do not supplement; monitor until it falls to 4.5 to 6 mEq/L, then give 10 mEq/hour of potassium chloride. Insulin drives potassium intracellularly, so stop the infusion if potassium exceeds 5 mEq/L.

Sodium bicarbonate. Infuse only when decompensated acidosis threatens life, especially with sepsis or lactic acidosis. When indicated, give 100 to 150 mL of 1.4% concentration initially. Rapid early correction can worsen hypokalemia and cause paradoxical cellular acidosis.

7. Monitoring Results of Diagnostic and Laboratory Procedures

DKA labs commonly include blood glucose, arterial blood gas for acid-base balance, serum ketones to confirm ketosis, electrolytes, and a CBC for infection or dehydration. HHNS adds serum osmolality to gauge dehydration severity and renal function tests. Blood and urine cultures are drawn if infection is suspected.

Serum glucose, acetone, pH, and HCO3. With controlled fluids and insulin, glucose falls steadily, glucose re-enters cells for energy, acetone drops, and acidosis corrects. Watch for traps: high glucose can cause dilutional hyponatremia, high triglycerides can falsely lower glucose readings, and high ketones can falsely elevate creatinine.

Urine and blood culture and sensitivity. These identify infectious organisms and guide the antibiotic.

Fingerstick glucose and urine ketone testing. Fingerstick monitoring supports tight glycemic control. Illness alters metabolism and glucose uptake, so monitor closely.

Arterial blood gas (ABG) analysis. DKA shows metabolic acidosis with low bicarbonate and a pH less than 7.3. Venous pH can be used for repeat measurements, and guidelines favor venous over arterial blood for monitoring unless respiratory problems require arterial sampling.

Blood glucose, serum ketones, potassium, sodium, creatinine, and BUN. DKA occurs when glucose is greater than 250 mg/dL, with elevated ketones. Hyperkalemia appears first in response to metabolic acidosis, then potassium falls as the fluid deficit progresses, leaving hypokalemia. Rising glucose shifts water out of cells and depletes serum sodium. Elevated BUN and creatinine indicate dehydration-driven cellular breakdown or acute renal failure.