Template:DKA clinical features

• May be the initial presentation of unrecognized T1DM (6-21% of adults with T1D present with DKA as first diagnosis)
• OR symptoms/signs of an inciting precipitant (e.g. medication/dietary nonadherence, signs/symptoms of infection, insulin pump malfunction)
• Presenting features may include:

Constitutional

• • Generally ill-appearance
  • Fatigue, weakness, malaise
  • +/- Weight loss (may be significant in new-onset T1D)

Volume Depletion

• • Polydipsia, polyuria (initially) → decreased urine output (as volume depleted)
  • Signs of dehydration: dry mucous membranes, poor skin turgor, sunken eyes, delayed capillary refill
  • Hypotension, tachycardia
  • Most adults are 3-6 liters depleted at presentation

Gastrointestinal

• • Abdominal pain — present in up to 50% of DKA; can mimic an acute abdomen (appendicitis, pancreatitis, mesenteric ischemia)
    • ED Pearl: Abdominal pain that does not improve with correction of acidosis and hydration warrants further workup for intra-abdominal pathology — do not assume it is "just DKA"
    • Abdominal pain correlates with severity of acidosis; more common with pH <7.2
  • Nausea/vomiting (present in >75% of cases)
  • Anorexia
  • Ileus / decreased bowel sounds (from electrolyte derangements and acidosis)
  • Gastroparesis — increases aspiration risk, especially if intubation is being considered

Respiratory

• • Tachypnea — compensatory for metabolic acidosis
  • Kussmaul breathing (deep, labored breathing pattern) — classic finding in moderate-severe DKA; represents maximal respiratory compensation
  • Acetone / fruity smell on breath — from exhaled ketones; may be subtle or absent; not all clinicians can detect it
  • ED Pearl: A DKA patient who is no longer tachypneic despite persistent acidosis is decompensating — respiratory compensation is failing and the patient may need emergent airway management

Neurologic

• • Altered mental status — ranges from drowsiness and lethargy to confusion, stupor, and coma
    • Severity correlates with serum osmolality more than glucose level or pH
    • AMS is present in ~15-25% of DKA patients at presentation
  • Decreased reflexes
  • Headache
  • Seizures (uncommon; more frequent in pediatric DKA)
  • Cerebral edema — significantly increases mortality, especially in children; suspect if neurologic status worsens during treatment (see Cerebral edema in DKA)

Cardiovascular

• • Tachycardia (from dehydration, acidosis, and catecholamine surge)
  • Hypotension / shock (from severe volume depletion)
  • Arrhythmia — from hyperkalemia (at presentation) or hypokalemia (during treatment); obtain ECG early
  • Chest pain — may represent ACS as a precipitant or consequence

Other

• • Hypothermia — DKA patients may be normothermic or hypothermic even in the presence of infection; absence of fever does NOT exclude infection as a precipitant
  • Blurred vision (from osmotic lens swelling)
  • Muscle cramps (from electrolyte derangements)
  • Deep vein thrombosis / pulmonary embolism — DKA is a hypercoagulable state; consider VTE in patients with unexplained tachycardia, hypoxia, or chest pain disproportionate to presentation