DKA & HHS Study
DKA and HHS Study Notes
Purpose of this module
Understand etiology, pathophysiology, diagnosis, clinical manifestations, and interprofessional/nursing management of Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic Syndrome (HHS).
Review Type 1 Diabetes (T1DM) and Type 2 Diabetes (T2DM) as context for DKA/HHS presentations and care.
Prepare for nursing care, patient education, and NCLEX-style questions.
DKA: Epidemiology, Etiology, and Onset
Epidemiology
Formerly known as juvenile-onset or insulin-dependent diabetes.
Accounts for about 5–10% of all diabetes cases; incidence increasing.
More common in people <40 years old, but can occur at any age.
Autoimmune component; genetic predisposition and viral triggers.
Global context: ~38.4M with diabetes; ~1.8M adults with T1DM; ~304k children with T1DM.
Etiology
Autoimmune destruction of β-cells → insulin deficiency (absolute lack of insulin).
Genetic predisposition and viral exposure implicated.
Other diabetes syndromes: Latent autoimmune diabetes in adults (LADA), MODY (maturity-onset diabetes of the young).
Onset and honeymoon phase → 3 P’s (polydipsia, polyuria, polyphasia)
Islet cell autoantibodies may be present months to years before symptoms.
Rapid onset once insulin production is insufficient, leading to ketoacidosis.
Honeymoon period after initial treatment (usually 3–12 months) with temporary insulin independence before β-cell destruction progresses.
Long-term: most patients require permanent insulin therapy.
DKA: Diagnostic Criteria
Diabetes diagnosis criteria (reference baseline)
A1C > 6.5% (lab method NGSP certified and DCCT-based).
Want below 7% in diabetics
Fasting plasma glucose (FPG) > 126mg/dL (fasting defined as no caloric intake for ≥8 hours).
2-hour plasma glucose > 200 ext{ mg/dL} during an OGTT (75-g glucose load).
In patients with classic hyperglycemia symptoms (polyuria, polydipsia, polyphagia), random plasma glucose > 200 ext{ mg/dL}.
DKA diagnosis (key features)
Hyperglycemia, ketosis, metabolic acidosis, dehydration.
Typically occurs in T1DM; can occur in T2DM under stress/insulin deficiency.
DKA: Pathophysiology (Overview and Significance)
Core defect
Insulin deficiency and relative (or absolute) insulin resistance lead to decreased glucose utilization and increased hepatic glucose production.
Catabolic state driven by counterregulatory hormones
Glucagon, epinephrine, cortisol, and growth hormone promote gluconeogenesis and lipolysis.
Metabolic consequences
Increased lipolysis → free fatty acids → ketogenesis → ketone bodies (acetoacetate, beta-hydroxybutyrate).
Ketosis causes metabolic acidosis; accumulation of ketone bodies leads to ↓ pH.
Osmotic diuresis from hyperglycemia causes dehydration and electrolyte losses.
Key consequence loop (simplified)
Insulin deficiency + ↑ counterregulatory hormones → ↑ glucose production and ketogenesis → hyperglycemia + ketosis + acidosis → osmotic diuresis → dehydration and electrolyte imbalance.
DKA lab hallmarks
Hyperglycemia, ketonemia/ketonuria, metabolic acidosis (low pH, low bicarbonate).
Electrolyte disturbances common (especially potassium shifts during treatment).
DKA: Clinical Manifestations and Initial Laboratory Findings
Early clinical features → 3 P’s (polydipsia, polyphasia, polyuria)
Lethargy, weakness, dehydration (dry mucous membranes, poor skin turgor).
Signs of dehydration: tachycardia, orthostatic hypotension.
Abdominal pain, anorexia, nausea/vomiting.
Sweet, fruity breath odor (acetone).
Kussmaul respirations as a compensatory mechanism for metabolic acidosis.
Laboratory and bedside findings
Blood glucose commonly ≥ 250{ mg/dL} with ketones.
Blood pH < 7.30.
Serum bicarbonate < 16 ext{ mEq/L} .
Moderate to high ketone levels in urine or serum.
Volume depletion with elevated hematocrit and electrolyte abnormalities.
Anion gap context
Anion gap helps identify the cause of acidosis.
Calculated as: ext{Anion Gap} = ( ext{Na}^+ + ext{K}^+) - ( ext{Cl}^- + ext{HCO}_3^-).
Normal gap typically ~3–11; >11 suggests acid gain (e.g., ketoacids).
DKA: Pathophysiology Details (Deeper Dive)
Circulating insulin deficiency → decreased tissue glucose utilization → hyperglycemia with ketones
Ketogenesis and metabolic acidosis
Increased lipolysis → free fatty acids → ketogenesis in liver → ketone bodies.
Ketones lower blood pH → metabolic acidosis.
Electrolyte disturbances (depletion and shifting)
Electrolytes depleted by vomiting, osmotic diuresis, and poor intake.
Potassium shifts: insulin deficiency and acidosis cause K+ to move out of cells; treatment with insulin and gradual pH correction drives K+ back into cells.
Osmotic diuresis also causes losses of Na+, Cl-, and other electrolytes.
Clinical course implications
Without prompt treatment, progression to severe dehydration, renal failure, shock, coma, and potentially death within ~24 hours.
DKA: Interprofessional Care – Initial and Ongoing Management
Initial interventions (emergency phase)
Ensure airway and give supplemental O2 as needed.
Establish IV access and begin fluid resuscitation with normal saline (NaCl).
Fluid choice: 0.9% NaCl or 0.45% NaCl; typically start at about 1 L/hour in adults.
Initiate continuous regular insulin infusion: 0.1 ext{ U/kg/hr} IV.
Plan to reduce glucose by about 36 ext{-}54 ext{ mg/dL/hr} safely.
As glucose approaches ext{≈} 250 ext{ mg/dL}, add dextrose-containing fluids (e.g., 5% dextrose) to prevent hypoglycemia while resolving acidosis.
Collect important history: time of diabetes, last meal, last insulin dose.
Ongoing monitoring and adjustments
Monitor vitals, level of consciousness, ECG, oxygen saturation, urine output.
Assess breath sounds for fluid overload.
Frequent glucose monitoring; monitor potassium and bicarbonate; assess need for bicarbonate if pH < 7.0–7.0.
Electrolyte management (key focus during DKA correction)
Potassium: monitor closely; potassium replacement to correct hypokalemia as needed.
Bicarbonate: consider bicarbonate replacement if pH < 7.0–7.1 (severe acidosis).
Goals of therapy
Restore intravascular volume, reverse dehydration, correct electrolyte abnormalities, and suppress ketogenesis.
Prevent hypoglycemia, cerebral edema, and other complications during treatment.
DKA: Nursing Management and Patient Education
Nursing management responsibilities
IV fluids/volume assessment and management.
Initiate and titrate insulin therapy according to protocol.
Monitor electrolytes and renal function; monitor ECG changes.
Monitor blood glucose every 1–2 hours; monitor vital signs and neurological status.
Assess renal status, cardiopulmonary status, and level of consciousness.
Vigilance for signs of electrolyte imbalance, fever, hypovolemic shock, tachycardia, and Kussmaul respirations.
Patient education topics (self-management)
Disease process: what caused DKA, how it is treated, and how to prevent recurrence.
Glucose monitoring: keep a daily log; use a glucometer; recognize signs/symptoms of hypo-/hyperglycemia.
Medication education: insulin administration, timing, and dose adjustments; use of glucagon for severe hypoglycemia.
A1c testing: purpose and frequency.
Exercise, meal planning, and food choices.
Foot care, eye exams, immunizations.
Smoking cessation and psychosocial support.
Nursing education should emphasize recognition of early symptoms and action steps.
DKA: Type 1 Diabetes – Brief Review (Context)
Type 1 Diabetes (T1DM) overview (brief)
Autoimmune destruction of pancreatic β-cells leading to absolute insulin deficiency.
Typically presents with polyuria, polydipsia, polyphagia, weight loss, fatigue.
Requires lifelong insulin therapy.
Honeymoon period after initial insulin treatment; may last months to a year.
HHS: Epidemiology, Etiology, and Pathophysiology
Epidemiology and patient population
Hyperosmolar Hyperglycemic Syndrome (HHS) occurs predominantly in patients >60 years old.
Common in Type 2 diabetes or new-onset T2DM.
Etiology and pathophysiology (core concepts)
Relative or absolute deficiency of effective circulating insulin plus elevated counterregulatory hormones (glucagon, epinephrine, cortisol).
Result: severe hyperglycemia and hyperosmolarity with dehydration; ketogenesis is minimal or absent due to some residual insulin activity.
Increased serum osmolality leads to intracellular dehydration and neuro symptoms.
Common clinical picture and precipitating factors
Major precipitating conditions: infections, sepsis, pneumonia, UTIs, acute illness, or new-onset T2DM.
Symptoms evolve more subtly than DKA; marked dehydration and neurologic symptoms (somnolence, confusion, seizures, coma) can occur.
HHS: Diagnostic and Therapeutic Considerations
Diagnostic features
Very high blood glucose: typically > 600 ext{ mg/dL} (may be much higher).
Serum osmolality elevated; ketones minimal or absent in serum/urine.
No significant ketoacidosis (pH usually not markedly acidotic; bicarbonate may be normal or mildly reduced).
Interprofessional care – key elements
Aggressive IV fluid resuscitation to restore volume (typical initial fluids: normal saline, then adjust to 0.45% NS or 0.9% NS based on clinical status and Na levels).
Insulin therapy to correct hyperglycemia and prevent ongoing osmotic diuresis (often IV regular insulin infusion).
Transition to subcutaneous insulin when stable and able to take PO; monitor for hypoglycemia.
Electrolyte management: correct potassium, sodium, magnesium, and phosphate as needed.
Monitor glucose every 1–2 hours; monitor electrolytes, fluid status, and neurologic status.
Specific treatment targets and notes
For glucose reduction: goal is a slow decrease (approximately 50–100 mg/dL per hour) to avoid cerebral edema.
When using dextrose-containing fluids is indicated (e.g., to prevent hypoglycemia while correcting hyperosmolar state), transition to D5-containing fluids when glucose approaches 250–300 ext{ mg/dL}.
Correct fluid volume deficit in the first hour, then continue with maintenance fluids (typical ranges: 500–1000 mL/h depending on weight and state).
HHS: Nursing Management and Patient Education
Nursing assessment and monitoring
Frequent checks: glucose every 1–2 hours, vitals, mental status, fluid status, and I&O.
Monitor electrolytes and renal function; monitor for rise in osmolality-related neurological symptoms.
Watch for signs of electrolyte imbalances: hypokalemia, hyponatremia, hypomagnesemia, hypophosphatemia; correct as indicated.
Patient education and discharge planning
Long-term management of T2DM to prevent HHS episodes: diet, exercise, medication adherence, and regular monitoring.
Recognize triggers: infections, dehydration, poor fluid intake, nonadherence to therapy.
Type 2 Diabetes (T2DM): Brief Review and Context
Epidemiology
Type II diabetes accounts for 90–95% of all diabetes cases.
Increasing incidence, including in adults younger than 45 and in children, with obesity trends.
Etiology and metabolic abnormalities (four major issues)
Insulin resistance in muscle, liver, and adipose tissue.
Decreased pancreatic production of insulin (β-cell dysfunction).
Increased hepatic glucose production (glucose output).
Altered adipokines and inflammatory cytokines affecting glucose metabolism.
Normal physiology (how insulin normally works)
Insulin binds to receptors, enabling glucose uptake into cells; energy production largely occurs in cells that rely on insulin.
Insulin-dependent tissues: skeletal muscle, adipose tissue.
Insulin-independent tissues: brain, kidneys, intestinal lining.
Pathophysiology when things go wrong
Insufficient insulin production or insulin resistance prevents glucose from entering cells efficiently.
This leads to hyperglycemia and compensatory hyperinsulinemia may occur with progressive β-cell failure.
Risk factors
Overweight/obesity, age >45, sedentary lifestyle, family history, history of gestational diabetes, certain ethnic groups.
Type 2 Diabetes: Clinical Manifestations and Complications
Clinical manifestations
Nonspecific symptoms early on; classic T1DM symptoms may be present (polyuria, polydipsia, polyphagia).
Fatigue, recurrent infections, recurrent vaginal yeast infections, slow wound healing, visual changes.
Complications (high-level overview)
Cardiovascular disease and stroke risk
Dyslipidemia (LDL often ≥100 mg/dL or on lipid-lowering therapy)
Diabetic retinopathy and kidney disease (nephropathy)
Peripheral neuropathy and erectile dysfunction; increased risk of infections.
Autonomic neuropathy (including cardiovascular autonomic dysfunction) and higher mortality in some settings.
Notable health statistics (from the slides)
Numerous ER visits for hypoglycemia and hyperglycemic crises; eyes, kidney, and cardiovascular complications are prominent.
Type 2 Diabetes: Risk Factors and Lifestyle Implications
Key risk factors listed
Overweight/obesity; age; sedentary lifestyle; family history; history of gestational diabetes.
Higher prevalence in some ethnic groups (e.g., African American, Native American, Hispanic, Pacific Islander).
Management implications
Emphasis on lifestyle modification (weight loss, physical activity) alongside pharmacotherapy.
Regular monitoring for dyslipidemia, hypertension, and microvascular complications.
Education on self-management and early recognition of hyper/hypoglycemia.
Practical Nursing Considerations and Self-Care Education
Nursing priorities for DKA and HHS
Early recognition of symptoms and prompt initiation of protocol-based treatment.
Frequent monitoring of glucose, electrolytes, fluid status, and neurologic status.
Prevent complications such as hypoglycemia, cerebral edema (DKA risk), and electrolyte disturbances.
Patient education themes (reiterated for practical recall)
How to monitor glucose; how to administer insulin; recognizing signs of hypo-/hyperglycemia.
Understanding A1c testing and its significance.
Importance of hydration, meal planning, and exercise.
Foot care, eye exams, immunizations, and psychosocial support.
NCLEX-Style Practice Questions (with answers)
Question 1
Prompt: Polydipsia and polyuria related to diabetes mellitus are primarily due to?
Answer: B) fluid shifts resulting from the osmotic effect of hyperglycemia
Question 2
Prompt: A client with DKA is being treated in the ED. Which findings would confirm the diagnosis? (Select all that apply)
Correct: C) deep, rapid respirations (Kussmaul respirations), E) elevated blood glucose level, F) low plasma bicarbonate level, D) decreased urine output
Rationale: DKA features include hyperglycemia, metabolic acidosis with low bicarbonate, ketosis, and dehydration with compensatory Kussmaul breathing and often decreased urine output.
Question 3
Prompt: In the acute phase of DKA, the priority intervention is?
Answer: D) administer short-duration insulin IV (along with fluids per protocol; fluid resuscitation typically precedes insulin in real-world protocols)
Question 4
Prompt: A patient with DKA has an initial glucose of 450 mg/dL; after NS resuscitation the glucose is 240 mg/dL. What is the next step?
Answer: C) IV fluids containing dextrose (D5 NS or D5 0.45% NS) to prevent hypoglycemia while continuing correction
Question 5
Prompt: For a patient with newly diagnosed type I diabetes preparing for discharge, which items are essential in teaching? (Select all that apply)
Answers: A) insulin administration, D) use of a portable glucose monitor, E) hypoglycemia prevention, symptoms, and treatment
Key Formulas and Numerical References
Diagnostic thresholds
ext{A1C} > 6.5 ext{ extperthousand}
ext{FPG} > 126 ext{ mg/dL}
2 ext{-hour PG} > 200 ext{ mg/dL} during OGTT
Random glucose > 200 ext{ mg/dL} with classic symptoms
DKA lab criteria
Blood glucose: typically ≥ 250 ext{ mg/dL}
pH < 7.30
HCO3− < 16 ext{ mEq/L}
Ketones: moderate to high in urine/serum
Anion gap calculation
ext{Anion Gap} = ( ext{Na}^+ + ext{K}^+) - ( ext{Cl}^- + ext{HCO}_3^-)
Normal: roughly 3–11; >11 suggests acid gain (e.g., ketoacids)
Treatment-related targets (DKA)
Insulin drip: 0.1 ext{ U/kg/hr} IV
Glucose decline rate: 36–54 rac{ ext{mg}}{ ext{dL} ext{ per hour}}
Add dextrose when glucose ≈ 250 ext{ mg/dL} to prevent hypoglycemia while resolving acidosis
Fluid management cues
Initial fluids: NaCl 0.9% or 0.45% at about 1 ext{ L/hr} (adult)
Potassium management: monitor and correct; insulin shifts K+ into cells; replace as needed to avoid hypokalemia during therapy
DKA honeymoon period
Approximate duration: 3–12 ext{ months} after initial treatment