DKA/ HHS Flashcards
In DKA, _____________ is often the major finding
Plasma glucose is NOT excessively elevated <33.3
Plasma glucose CAN EVEN be normal/minimally elevated (<13.9) in pt with _____________
- Remember: normal plasma glucose < 11.1 mmol/L. However euglycaemia in this case refers to anything BELOW the plasma glucose cut-off for DKA
- Euglycaemic DKA seen in patients with ______, ______, _______, _______________.
Most common symptoms: ______________, __________
metabolic acidosis;
euglycemic DKA
poor oral intake, treatment with insulin prior to arrival in the emergency department, pregnant women, use of SGLT2 Inhibitors;
Hyperventilation, Abdominal Pain
In HHS main finding is ____________ and _____________ with little to no ketosis.
Neurologic abnormalities are frequently present (including coma in 25 to 50% of cases)
Most common symptoms: Neurological Symptoms
- More common in HHS than DKA due to ______________
- Eg: _________, _______, _________, __________
Serum glucose (>33.3mmol/L);
plasma osmolality (>320mOsm);
osmotic effects of glucose;
lethargy, focal signs (hemiparesis or hemianopsia, seizures), obtundation, coma
What are the electrolyte imbalances in DKA and HHS?
HypoK, HypoMg, HypoPi, Hypo/HyperNa
Sodium: HypoNa
- Hyperosmotic, Hypovolemic Hyponatraemia: due to high glucose in blood 🡪 pulls out water from cells 🡪 dilutional HypoNa
- Osmotic diuresis 🡪 loss of sodium-free water 🡪 causes Hypovolemia
- Corrected Na = Measured Na + (CBG – 5.5)/5*2
Potassium: total deficit, HyperK/ Normal K
- High loss of K via ROMK channels due to osmotic diuresis
- Lack of insulin leads to buildup to K extracellularly (main mech)
- May further HyperK in DKA due to acidosis shifting K extracellularly (smaller mech)
- Hence total K falls but plasma K can be normal/high
Why is there volume depletion in both DKA and HHS? What are the physical examination findings?
Despite ability of glucose to pull water out of cells, net movement of water is out from the plasma due to Osmotic Diuresis
Volume depletion is worsened in DKA (N&V from acidosis) and even more so in HHS (further osmotic diuresis)
Physical Examination Findings of dehydration common in both DKA and HHS
- Decreased skin turgor, dry axillae and oral mucosa
- Low jugular venous pressure, tachycardia
- Hypotension (if severe)
What events can precipitate DKA and HHS?
- Similar to the development of insulin resistance due to the imbalance between counter-regulatory hormones (cortisol, GH, catecholamines, glucagon) VS insulin
- In precipitating DKA/HHS: acute illness (AMI, pancreatitis), pneumonia, UTI will lead to surge of counter-regulatory hormones 🡪 tipping the balance 🡪 precipitating DKA/ HHS
What are the 4 pillars of DKA/ HHS treatment?
The 4 pillars of DKA/HHS treatment BOTH revolve around:
- IV fluids / Hydration
- IV insulin
- Potassium
- Treatment of trigger (infection/ AMI etc)
Monitor potassium, ketones, vitals
What would be the lab results in a patient with mild DKA?
- random plasma glucose (mmol/L)
- arterial pH
- serum serum beta- hydroxybutyrate (mmol/L)
- effective serum osmolality normal
- serum bicarbonate (mmol/L)
- anion gap
- Alteration in sensorium
- Urine ketones
- Random plasma glucose: > 14 mmol/ L except euglycaemic DKA due to SGLT2 inhibitor
- Arterial pH: 7.25- 7.30
- serum beta- hydroxybutyrate: 2-4
- Effective serum osmolality variable
- serum bicarbonate: 15- 18
- Anion gap: > 10
- Alert
- Urine ketones positive
What would be the lab results in a patient with moderate DKA?
- random plasma glucose (mmol/L)
- arterial pH
- serum serum beta- hydroxybutyrate (mmol/L)
- serum bicarbonate (mmol/L)
- anion gap
- Alteration in sensorium
- Urine ketones
- Random plasma glucose: > 14 mmol/ L except euglycaemic DKA due to SGLT2 inhibitor
- Arterial pH: 7.00- 7.24
- serum beta- hydroxybutyrate: 4-8
- serum bicarbonate: 10-14
- Effective serum osmolality variable
- Anion gap: > 12
- Alert/ drowsy
- Urine ketones positive
What would be the lab results in a patient with severe DKA?
- random plasma glucose (mmol/L)
- arterial pH
- serum serum beta- hydroxybutyrate (mmol/L)
- serum bicarbonate (mmol/L)
- anion gap
- Alteration in sensorium
- Urine ketones
- Random plasma glucose: > 14 mmol/ L except euglycaemic DKA due to SGLT2 inhibitor
- Arterial pH: <7.00
- serum beta- hydroxybutyrate: >8
- serum bicarbonate: <10
- Effective serum osmolality variable
- Anion gap: > 12
- stupor/ coma
- Urine ketones positive
What would be the lab results in a patient with HHS?
- random plasma glucose (mmol/L)
- arterial pH
- serum serum beta- hydroxybutyrate (mmol/L)
- serum bicarbonate (mmol/L)
- anion gap
- Alteration in sensorium
- Urine ketones
- Random plasma glucose: > 33 mmol/ L
- Arterial pH: <7.30
- serum beta- hydroxybutyrate: <0.6
- serum bicarbonate: >15
- Effective serum osmolality > 320
- Anion gap: <12
- stupor/ coma
- Urine ketone small
What are the clinical features of DKA?
DKA develops more acutely within 24-48 hours
Hyperglycaemia: Polydipsia, Polyuria
Acidosis: Hyperventilation (Kussmaul breathing), N&V, Altered Mental State (lethargy, confusion, delirium)
- Kussmaul breathing deep gasping breathing due to respiratory compensation
Severe generalised abdominal pain
- One of the defining features of DKA: ½ of pt with DKA, none of pt with HHS
- A/w severity of metabolic acidosis
- Pathophysiology: delayed gastric emptying and ileus induced by the metabolic acidosis and associated electrolyte abnormalities; due to N&V
Dehydration (from Vomiting + Osmotic diuresis)
Other features: less common / less defining of DKA
- Hyperkalaemia: arrhythmia. Due to acidosis 🡪 shifts K out of cells
- Fruity odour: due to exhaled ketones (similar to scent of nail polish)
What are the triggers of DKA/ HHS?
Infection (especially pneumonia, UTI)
Dehydration from underlying medical issue
Acute illness - AMI, pancreatitis, sepsis 🡫, stroke
Pregnancy (may present with euglycemic DKA)
Drugs – Antipsychotics, steroids
Wrong insulin dose / compliance issues 🡪 lack of BASAL insuli
What are the investigations to perform to diagnose and monitor DKA/ HHS?
ABG for acid-base status, Serum HCO3-
Serum glucose and electrolytes (calculate anion gap: Na – Cl – bicarb) 🡪 to determine HAGMA!
Urinalysis and dipstick for urinary ketones. Serum ketones if urine ketones not found, then serum BOHB 🡪 to determine cause of HAGMA + monitor treatment
Renal panel for dehydration 🡪 renal impairment is possible in severe dehydration, for monitoring hydration status
Plasma osmolality (2Na + glucose)🡪 to determine HHS or DKA
What are the investigations to perform to confirm aetiology of DKA/ HHS?
Blood tests
- FBC (leucocytosis common due to pro-inflammatory state in hyperglycemia)
- Blood culture/UFEME if suspected infection or patient septic 🡪 to determine aetiology
- LFTs: if caused by liver abscess
- Amylase, lipase: pancreatitis
- Thyroid function tests
Cardiac enzymes + ECG for complication (hyperkalaemia) or aetiology (AMI)
CXR – pneumonia
CT brain/ MRI stroke protocol
What is the management of DKA?
1) Immediate fluid resuscitation:
- If SBP < 90mmHg: IV 500ml 0.9% NS over 10-15 minutes
- If SBP > 90mmHg (remember: 1,2,4,6): IV 1L 0.9% NS/ 0.45% NS within 1st hour, THEN 1L over next 2 hrs, THEN 1L over next 4 hrs, THEN 1L over next 6-8 hrs
2) IV Insulin infusion to suppress production of ketone bodies in the liver – note: not bolus!
- Decrease in CBG of 3 to 4 mmol/L per hour
- Decrease in BOHB of 3 mmol/L per hour
- Keep CBG between 8 to 12 mmol/L for DKA and 12 to 16 mmol/L for HHS
- DO NOT STOP insulin until DKA/HHS has resolved
3) Potassium Replacement
- K < 3.3: Do NOT start IV insulin. Replace K+ first before giving insulin
- K 3.3- 5.2: Give 10 to 20mmol of KCl per 500mls of IV Fluid
- K >5.2: Do not give K replacement. Recheck K in 2 hours
4) Treatment of underlying cause
5( Bicarbonate therapy ONLY IN SEVERE ACIDOSIS – as bicarbonate has not been proven to work / shown to be a/w increased ketosis
- If pH < 6.9, repeat every 2 hours
- If pH persistently < 6.9 after IV hydration, administer NaHCO3
