Diabetic and endocrine emergencies, Richard Keshi, Emergency Physician

1. DIABETIC EMERGENCIES
BY
DR RICHARD KESHI
SPECIALTY REGISTRAR,EMERGENCY MEDICINE

2. DKA
Hyperosmolar Hyperglycaemic State(HSS)
Hypoglycaemia
DM – Chronic systemic disease characterized by insulin deficiency
or peripheral resistance resulting in hyperglycaemia and
non enzymatic glycosylation of proteins.
 Diagnosis – WHO Criteria
1. FBS - 7mmol/L and above
2. OGTT - 11.1mmol/L and above
3. HbA1c – 6.5% (48mmol/mol) and above

3. DKA
Occurs in IDDM(Type 1)
Type 1 occur in young people
Due to autoimmune destruction of beta cells of
the islets of langerherns
Triggered by an infection(coxsackie B virus) in
genetically susceptible individuals
Individuals with specific point mutation in HLA genes
(DR3,DR4,DQ)
Type 4 HS reaction

4. Triad of DKA
1. Hyperglycaemia
2. Acidosis
3. Ketonaemia
PATHOGENESIS
 Occurs when insulin deficiency is accompanied by
increased stress hormones(Glucagon,cortisol,GH,
catecholamines)
 Increased hepatic gluconeogenesis and glycogenolysis
resulting in severe hyperglycaemia
 Increased lipolysis leads to Increased serum FFAs
 FFA metabolizes to alternate energy sources via
ketogenesis
3 TYPES OF KETONE BODIES
 Acetone
 Acetoacetate
 3-beta-hydroxybutyrate – predominant in DKA
Ketonaemia leads to metabolic acidosis due to anion deficit

5. DIAGNOSIS OF DKA
1. BM > 11.1mmol/L
2. pH < 7.3 or HCO3- <15mmol/L
3. Ketonaemia > 3mmol
CLINICAL FEATURES
 Polyuria,polydipsia
 Malaise
 Generalized weakness and fatigabilty
 Signs of infection – fever,cough, dysuria,SOB
 Abdo pain,vomitting,anorexia
 Altered consciousness – disorientation,confusion,coma

6. EXAMINATION FINDINGS
Dehydration
Sweet acetone breath
Kussmaul respiration – deep sighing breath
Hyporeflexia
Signs of hypovolaemic shock
INVESTIGATIONS
Urine dip – glucose,ketone
Bedside BM – increased
Blood ketone measurement – elevated
FBC – incr. WBC,
Plasma osmolality > 290mosm/L
CXR – r/o infection
CT Head – High index of suspicion for patients in coma
to check for cerebral oedema esp. in children – not routine!

7. Venous Blood Gas
pH <7.3
K+ Normal or elevated
Na+ decreased
Cl- decreased
HCO3- decreased
ANION GAP
((Na+) + (K+)) - ((HCO3-) + (Cl-))
Normal – 8-16mmol/L
Large anion gap acidosis is seen in DKA
ECG – To r/o silent MI
Telemetry

8. TREATMENT
Correct dehydration - IVF
Correct hyperglycaemia – give insulin
Correct acid-base imbalance
Correct electrolyte disturbances
Treat any concurrent infection if present
1. Fluid Resuscitation
• 0.9% N. Saline 1L – 1hr
• 0.9% N. Saline 1L – 2hr
• 0.9% N. Saline 1L – 2hr
• 0.9% N. Saline 1L – 4hr
• 0.9% N. Saline 1L – 4hr
• 0.9% N. Saline 1L – 6hr
Caution in paediatric patients – 10-20ml/kg
 Elderly
 CCF
 CKD
 Pregnancy

9. 2. Commence sliding scale at 0.1ml/kg/hr
Only give bolus insulin 0.1units/kg if any delay in setting
up sliding scale
3. Correction of electrolyte imbalance
 Potassium replacement
• K+ 4.5 -5.5 = give 10mmol/L
•K+ 3- 4.5 = give 20mmol/L
•K+ < 3 =40mmol/L
- correct other electrolytes as indicated by blood biochemistry
4.Blood pH will return to normal as ketonaemia resolves
- a major marker of response to treatment
5. Treat any infection if present
6. Low molecular Weight Heparin is give as prophylaxis for VTE,
MI and ischaemic stroke

10. COMPLICATIONS
1. Cerebral oedema
- mostly due to fluid overload
- common in children
- mannitol/hypertonic saline
2. Pulmonary oedema
- common in patients with heart failure
- rare in young adults
3. Myocardial Injury
- can occur in severe DKA
- elevated cardiac enzymes do not necessarily
signify MI

11. HYPEROSMOLAR HYPERGLYCAEMIC STATE
Formerly HONC
Occurs in NIDDM, has higher mortality than DKA
Challenging to manage due to complications from fluid overload
- central pontine myelinosis
- cerebral oedema
Commoner in the elderly with other co-mobidities
Has been reported in young adults as the age of onset of NIDDM is decreasing
TRIAD OF HHS
1. Marked hyperglycaemia > 30mmol/L, without ketonaemia(ket. <3mmol)
2. Osmolality > 320mosm/kg
3. Hypovolaemia,
Other findings are
- HCO3 - >15mmol/L
- ketonuria
- altered consciousness

12. PATHOGENESIS
Almost same with DKA
Stress hormone incr. demands for glucose
Lipolysis is not high due to small available insulin receptors
CAUSES
1. Any condition that predisposes to dehydration and stress
2. Disease conditions – CVA, MI, PE
3. Drugs – antiepileptics, antihypertensives,antiarrythmics
4. Non compliance to oral hypoglycaemics
5. Elderly abuse and neglet

13. CLINICAL FEATURES
1. Signs of dehydration
2. Altered consciousness
3. Signs of infection
4. CNS disturbances
5. Visual symptoms
6. Signs of shock
7. Tachypnoea
8. Hyperthermia/hypothermia
INVESTIGATIONS
- Urinalysis –glucose, ketones
- BGM > 30mmol
- Serum osmolality > 320
Osmolality = 2Na + glucose +urea
Normal = 280- 290
- VBG – Ph >7.3,HCO3 >15mmol/L

14. FBC
-Raised Hb
-Raised WBC
U/E –correct electrolytes as indicated
CXR
- pneumonia
- pleural effusion
Blood cultures if raised or low temp.

15. TREATMENT
1. Normalise osmolity
0.9% Normal saline as indicated
2. Replace electrolyte deficits
KCL commonly 10mmol/L
3. Correction of hyperglycaemia
Only give insulin(sliding scale) after commencing
fluid and ketonaemia present
4. Treat infection if present
Give antibiotics
5. LMWH for VTE prophylaxis
6.Foot protection and assessment for ulcer