Template:DKA clinical features: Difference between revisions
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*May be the initial presenting of an unrecognized T1DM patient
*May be the '''initial presentation''' of unrecognized T1DM (6-21% of adults with T1D present with DKA as first diagnosis)
*OR symptoms/signs of inciting precipitant (e.g. history of med/dietary nonadherence, signs/symptoms of infection)
*OR symptoms/signs of an inciting precipitant (e.g. medication/dietary nonadherence, signs/symptoms of infection, insulin pump malfunction)
*Presenting features may include:
*Presenting features may include:
**Polydipsia, [[polyuria]] (initially) or decreased urine output (as volume depleted)
 
**Signs of [[dehydration]] (dry mouth, dry mucosa, etc.), [[hypotension]]
====Constitutional====
**+/- Weight loss
**[[Abdominal pain]], [[nausea/vomiting]]
**[[Tachypnea]] (Kussmaul's breathing)
**Acetone or fruity smell on breath
**Generally ill-appearance
**Generally ill-appearance
**[[Altered mental status]], drowsiness with decreased reflexes  
**[[Fatigue]], weakness, malaise
***[[Cerebral edema in DKA|Cerebral edema]] increases mortality significantly, especially in children
**+/- 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 in 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

Latest revision as of 12:12, 10 March 2026

  • 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

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
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