4. Objectives
To provide the remote clinic nurse with an overview of potential
patient signs and symptoms and their management
5. Case Study
23 year old office worker, known diabetic type 1
Brought in by his colleague as he had been sick
Recently received bad news from family in Manila
Has been vomiting all night
He had been in Bahrain drinking alcohol with a family friend
yesterday to “cheer himself up”
7. Start as always with the …
ABC of resuscitation
History + examination
Pregnancy check?
Blood tests – FBC, U+E, LFTs, CRP, amylase if available
Blood glucose
Arterial blood gas (not available in RACs)
Urinary ketones
8. Assessment Results
A - patent
B - 29 breaths per minute, rapid shallow breaths, 100% on air
C – BP 102/68. Pulse 107. Cap refill 7 sec
History – as above
Examination – slightly tender abdomen
Bloods taken
Peripheral blood glucose 160 mg/dL
Urinary ketones +ve
15. Forming an Impression
DKA requires all 3 of the following:
High blood sugar
Glucose > 200 mg/dLl
(Finger-prick blood glucose can be normal)
• Ketones (blood or urine ≥ +++)
Acidosis (pH<7.30 or HCO3<15mmol)
16. Management
Consult
ABC – if impaired
Replace fluids
Monitor fluid balance (I/O chart)
Resolution of ketonaemia / insulin
Take care: electrolytes imbalance
Close monitoring
Transfer
17. Fluid Replacement
Initial management: 1 L 0.9% NaCl
Consult but expect:
30 mins (NB Age or
comorbidity)
1hr
2hr
4 hr
Then continue NaCl 0.9% as
dictated by fluid status
Subsequent management
In hospital
May include 10% Dextrose in
addition to 0.9% NaCl
Sliding scale insulin
Electrolyte replacement
18. Consider
• Absence of fever doesn’t mean absence of infection
• Alternative cause for acidosis if glucose and acidosis markedly
out of proportion
• Non specific abdominal does not mean DKA
Patients with frequent episodes are at increased risk of dying
and diabetic complications
19. Hyper-Osmolar Non-Ketotic (HONK)
Hyperglycaemic Syndrome (HHS)
Hallmark of type 2 DM
May occur in:
Newly diagnosed
Poor compliance with treatment
Concurrent illness – especially MI, Infection, CVA
Drugs – Steroids
Sugary drinks
20. Cause and consequences
Insulin production markedly reduced nut not absent
No switch to fat metabolism
No ketones or acidosis
Loss of intravascular volume
Mortality higher than DKA
Comorbidities
Longer diagnosis time, Electrolyte imbalance
Cerebral oedema and PE more common
21. Presentation & Outcome
Possibly osmotic symptoms
Dehydration around 10L deficit
Decreased level of consciousness
Signs of underlying infection in up to 50%
+/- thrombo-embolism in up to 30%
2/3 cases previously undiagnosed
As high as 50% mortality
22. Recognition
Diagnosis requires ALL of the following:
Raised blood glucose (usually >500 mg/dL)
Absence of ketones (or + or ++ only)
Serum osmolality >350mmol
23. Management
Consult
Fluid replacement
Electrolyte replacement
Caution:
pseudohyponatraemia
Insulin Search for cause
Anticoagulation
Monitor
Transfer
1 L 0.9% NaCl
1 hr
2 hr
4 hr
8 hr
Then continue NaCl 0.9%
as dictated by fluid status
26. Causes
Drug Induced
Insulin,
Sulphonylureas
Alcohol
Reactive Hypoglycaemia
Post prandial
Gastric surgery
27. Treatment
If able to eat
Glucose: Hypokit. Sweet fruit juice & lollipop
Long acting carbohydrate eg toast/ sandwich
In the community:
1mg glucagon IM and long acting carbohydrate on recovery
Hospital options-
IM glucagon 1mg
IV 20ml of 50% dextrose
Other: hypostop
28. Summary
Diabetic ketoacidosis.
Management of diabetic ketoacidosis.
Recognise and manage HONK (HHS)
Recognise and manage hypoglycaemia.
29. References
Hariman, C. (2011) Diabetic Emergencies [Online]. Available at:
https://www.mededcoventry.com/.../Diabetes%20lecture%202011%20-%... Accessed on: 28th July 2015
Editor's Notes
Recognise and participate in the management of diabetic ketoacidosis.
Recognise Hyperosmolar Non ketotic state
Recognise and manage hypoglycaemia.
ABG
pH 7.20
pO2 16.0
pCO2 2.70
HCO3- 13.8
Na 140
K 4.3
Insulin production markedly reduced but NOT absent.
No switch to fat metabolism and therefore no ketones or acidosis
Gluconeogenesis
Loss of intravascular volume
Gluconeogenesis (GNG) is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as pyruvate, lactate, glycerol, and glucogenic amino acids. While primarily odd-chain fatty acids can be converted into glucose, it is possible for at least some even-chain fatty acids.
Mortality markedly higher compared to DKA
Co-morbidities, longer time to diagnosis, electrolyte disturbances
Cerebral oedema and Pulmonary Embolism more common
Fluid replacement – SLOWER (may be a marker of population not pathology)
Electrolyte replacement (pseudohyponatraemia)
Insulin – ‘slower’ scale – normally very responsive to IV insulin
Search for cause
ANTICOAGULATION
Monitor
1L 0.9% NaCl
1 hr*
2 hr
4 hr
8 hr
Then continue NaCl 0.9% as dictated by fluid status
*half the rate of DKA
Neuroglycopenia is a medical term that refers to a shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia. Glycopenia affects the function of neurons, and alters brain function and behavior.
IV 50% must be given via a large bore securely placed catheter in to a large vein (ACF) to prevent extravasation and tissue loss.
