Diabetic emergencies Flashcards
A 17-year-old girl presents to the emergency department with abdominal pain and vomiting. On examination, she appears dehydrated and is hypotensive. The collateral history reveals that over the last 3 months she has been losing weight and urinating more frequently. Possible diagnosis?
Diabetic ketoacidosis (DKA)
Pathophysiology of DKA
- DKA is associated with a net reduction in insulin and a relative increase in counter hormones (cortisol, glucagon, catecholamines, growth hormone)
- This leads to reduced glucose entry into cells → metabolism of lipids as an alternate energy source
- Uncontrolled lipolysis → elevated free fatty acids + ketone bodies → a state of ketoacidosis
DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies.
2 main ways that DKA presents
- First presentation of T1DM
- Pt has established T1DM and triggered by a precipitating factor such as infection
What are the 3 key features of DKA?
- Ketoacidosis
- Dehydration
- Potassium imbalance
Signs and symptoms of DKA
Symptoms:
* Abdominal pain
* N + V
* Polyuria + polydipsia
* Inability to tolerate oral fluids
* Lethargy + confusion
* Weight loss
Signs:
* Fruity smell of acetone on the breath
* Dehydration (mild → only just detectable; moderate → dry skin + mucus membranes; reduced skin turgor; shock → tachycardia, hypotension (late), drowsiness, reduced urine output)
* Kussmaul respiration (deep, laboured breathing associated with metabolic acidosis)
Diagnostic criteria of DKA
A diagnosis requires all three:
* Hyperglycaemia (e.g. blood glucose > 11 mmol/L)
* Ketosis (> 3 mmol/L or 2+ on urine dipstick)
* Acidosis (pH below 7.3)
- Bicarbonate < 15 mmol/l
Management of DKA
FIG-PICK
* F – Fluids – IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)
* I – Insulin – fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)
* G – Glucose – closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L
* P – Potassium – add potassium to IV fluids and monitor closely (e.g., every hour initially)
* I – Infection – treat underlying triggers such as infection
* C – Chart fluid balance
* ** K – Ketones** – monitor blood ketones, pH and bicarbonate
In terms of drugs: FIGP
Primary investigations of DKA
- Urine dip: glycosuria + ketonuria
- Bedside ketone and capillary glucose
- ABG/VBG: quickest way to ascertain pH and HCO3 levels.
- U&Es: electrolyte derangement + acute kidney injury due to dehydration
- FBC and CRP: raised inflammatory markers may suggest underlying infection as a precipitant
- Infection screen: if an infection is the suspected trigger
ABG may be used as the initial blood gas sample for diagnosis, but later samples should be venous if possible
Define the resolution of a DKA
- pH >7.3 and
- Blood ketones < 0.6 mmol/L and
- Bicarbonate > 15.0mmol/L
What are the complications of DKA treatment?
- Hypoglycaemia (low blood sugar)
- Hypokalaemia (low potassium) → arrhythmias
- Cerebral oedema (particularly in children)
- Pulmonary oedema secondary to fluid overload or acute respiratory distress syndrome
- Gastric stasis
A 75-year-old obese gentleman with type 2 diabetes is found by his niece in a confused state on her fortnightly visit. She takes him to the emergency department where his BM is 30.6 mmol/L, and BP is 94/59 mmHg. Possible diagnosis?
Hyperosmolar hyperglycaemia state (HHS)
What is HHS?
It is characterised by:
* Hyperosmolality (water loss leads to very concentrated blood) - (>320 momsol/kg)
* High sugar levels (hyperglycaemia) (>30 mmol/L)
* Absence of ketones - distinguishing it from ketoacidosis.
OR
- Hyperglycaemia drives an osmotic diuresis with subsequent fluid + electrolyte loss → hyperosmolality + hypovolaemia
- Due to the presence of small amounts of circulating insulin in T2DM , lipolysis does not occur and hence ketoacidosis is not seen - unlike in diabetic ketoacidosis (DKA)
Clinical features of HHS
Signs:
* Reduced GCS
* Dehydration (tachycardia + hypotension, dry mucous membranes, reduced skin turgor)
* Seizures
Symptoms:
* Generalised weakness and leg cramps
* Confusion, lethargy, hallucinations, headache
* Visual disturbance
* Polyuria
* Polydipsia
* N + V
* Abdominal pain
Patholophysiology of HHS
Hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion (+ electrolyte disturbances)
Precipitating factors of HHS
- Intercurrent illness
- Dementia
- Sedative drugs
Clinical features of HHS - categorise into:
* Consequences of volume loss
* Systemic
* Neurological
* Haematologcial
Consequences of volume loss:
* Clinical signs of dehydration
* Polyuria
* Polydipsia
Systemic:
* Lethargy
* N +V
Neurological:
* Altered level of consciousness
* Focal neurological deficits
Haematological:
* Hyperviscosity (→ may result in MI, stroke, peripheral arterial thrombosis)
Management of HHS
- Fluid replacement → IV 0.9 % NaCl solution
- Insulin should NOT be given - UNLESS blood glucose stops falling while giving IV fluids
- VTE prophylaxis (those at risk due to hyperviscosity)
- Monitor potassium levels (can be given with K+)
Complications of HHS
Vascular complications due to hyperviscosity:
* Stroke
* MI
* Peripheral artery thrombosis
