Diabetic Emergencies
Sa’ad Lahri
Registrar
Dept Of Emergency Medicine
Outline
• Hypoglycaemia
• Diabetic Ketoacidosis (DKA)
• Hyperglycemic Hyperosmolar state
(HHS)
• Lactic Acidosis
Hypoglycaemia
• Case Study
• 55 y old diabetic brought to ER with history of “L
CVA” by EMS crew.
• Management en - route: “calmed and
reassured”
• Glucose in ER = 1,1 mmol/l
• Nurses records: “seen by Dr X and 50mls 50%
dextrose given IV. Patient now talking and
moving all limbs freely”
• Definition: blood glucose level <2.5 mmol/l
Postgrad Med J 2007; 83:79-86
Principles of Disease
• Protection against hypoglycaemia :
• Cessation of insulin release and
mobilisation of counter regulatory
hormones – increase in glucose
production and decrease glucose use.
Rosen’s Emergency Medicine 6th Ed
Causes of hypoglycaemia
Hypoglycaemic admissions among diabetic patients in Soweto, South Africa
• A total of 51 episodes of
biochemically confirmed
hypoglycaemia (blood glucose
< 2.2 mmol/l with coma or precoma, and requiring
intravenous glucose) were
observed in 43 patients.
Inappropiate
Tx,18%
Gliclazide
33%
GIT upset
20%
Gliclazide
Missed meal
Alcohol
GIT upset
• Important to check for sepsis,
renal failure, heart failure,
accidental overdose
Alcohol
22%
Missed
meal 36%
Inappropiate Tx
Diabet Med. 1993 Mar;10(2):181-3
Metformin and hypoglycaemia?
• Metformin – decreases hepatic production
of glucose and increases insulin
sensitivity.
• Symptoms of OD : nausea, vomiting,
abdominal pain and lactic acidosis.
• Lactic acidosis can be fatal
Emergency Medicine Secrets 4th Ed
Hypoglycaemia due to OD
• OD – delayed hypoglycaemia
• Observation period – 12-16hrs
• Sulphonylurea – Octreotide
Emergency Medicine: Just the facts 2nd Ed
Diagnostic Strategies
• Cardinal test: blood glucose (before therapy)
• Finger prick : beware insufficient sample
• Other tests should address aetiology (eg sepsis)
• Factitious hypoglycaemia: low levels of Cpeptide helpful
Rosen’s Emergency Medicine 6th Ed
Clinical Symptoms and signs
• Autonomic: (sweating, anxiety, nausea,
palpitations and hunger) (3.3 – 3.6 mmol/l)
• Neuroglycopenia: confusion, drowsiness, altered
behaviour and focal deficits. (<2.6 mmol/l)
Postgrad Med J 2007; 83:79-86
• ABCD “EFG”
• Doctor “she is extending” (glucose 1mmol/l)
Management
• Alert with mild symptoms – sugar
containing food
• Unable to take po – IV 50 mls 50 %
dextrose.
• 30% gel (hypostop) buccal mucosa
Postgrad Med J 2007; 83:79-86
• Irritant to veins – venous sclerosis rebound hypoglycaemia. Problem children
Rosen’s Emergency Medicine 6th Ed
Dextrose 10% or 50%?
Emerg Med J 2005; 22:512-515
• Dextrose 10% or 50% in the treatment of hypoglycaemia
out of hospital? A randomised controlled trial:
• Main outcome measures: To compare for each
dextrose concentration the time to achieve a Glasgow
Coma Scale (GCS) score of 15, and the dose required to
obtain a blood glucose level of 4.5 mmol/l.
• Results:
• No statistically significant differences in median time to
recovery
• Dextrose 10 % lower post treatment glucose levels
• Thiamine if alcohol abuse
• No IV – 1mg Glucagon IM.
• Onset of action 10 -20 mins and peak
response 30-60 mins.
• Ineffective if glycogen absent – alcohol
induced hypoglycaemia.
Rosen’s Emergency Medicine 6th Ed
“Appropiate Disposition”
• Admit/observe – suicidal ; excessive amounts of
oral hypoglycaemics or long – acting insulin.
Persistent altered mental status.
Emergency Medicine Secrets 4th ED
• Hypoglycaemia uncomplicated by other disease
– discharged if caused found and corrected.
• Give meal before discharge – ability to tolerate
oral feeds and replenish glycogen stores.
Rosen’s Emergency Medicine 6th Ed
What about Non – diabetic
Patients?
• Classify as Postprandial or fasting.
• Postprandial: alimentary hyperinsulinism –
gastrectomy, fructose intolerance.
• Fasting: imbalance production and use.
• Underproduction: hormone deficiencies,
liver disease.
• Overuse: hyperinsulinism ; drugs,
insulinoma, tumours.
Rosen’s Emergency Medicine 6th Ed
Case Study 2
• Referral letter from Primary Care:
• 19 y old male presents with hx of nausea,
vomiting and abdominal pain.
• Notice him to be dehydrated with acidotic
breathing
• Glucose … HI!
• Urine 3+ ketones
• Diagnosis … Diabetic ketoacidosis
DKA
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Triad of:
hyperglycaemia, ketosis and acidaemia.
Diagnostic criteria (ADA)
Blood glucose >14
Ph <7.30
Serum Bicarb <18mmol/l
Anion Gap >10
Ketonaemia
Postgrad Med J 2004; 80: 253-61
Precipitants
QJ Med 2004;97:773 -780
• Infections and inadequate insulin doses.
• Most frequent dx infections: pneumonia
and UTI. Check for meningism &PID
• Others include Myocardial infarction, CVA,
pulmonary embolism
Postgrad Med J 2004; 80: 253-61
History and Physical Exam
• DKA usually short time (<24hrs)
• Classic clinical picture: polyuria,
polydipsia, weight loss, vomiting,
abdominal pain, dehydration, weakness,
mental stage change and coma.
Diabetes Care 2006;29: 2739 - 2747
Physical findings:
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Poor skin turgor
Kussmaul respirations
Tachycardia
Hypotension
Shock
Coma
Severe hypothermia poor prognostic sign.
Abdominal pain may be present – 50-75% resolves
correction of hyperglycaemia and acidosis.
• Abdominal pain? – dehydration of muscle tissue,delayed
gastric emptying and ileus Postgrad Med J 2004; 80: 253-61
Diabetes Care 2006;29: 2739 - 2747
Endocrinol Metab Clin N Am 35 (2006) 725–751
Laboratory Tests and Evaluation
• ABG not necessary – can use venous
blood
• Lab: Na, K , Urea, Creatinine
• Serum ketones
• Culture of blood and urine if clinically
indicated.
• ECG and CXR
• Preg test if female
Postgrad Med J 2004; 80: 253-61
Discussion of tests
• Leucocytosis common finding – stress and
dehydration.
• Leukocytosis above 25000 suggests
ongoing infection. Band neutrophils high
sensitivity and specificity.
• Na : usually low osmotic flux of water.
• If high profound water loss.
• K: may be up due to extracellular shift
Endocrinol Metab Clin N Am 35 (2006) 725–751
Management Aims
Correct
Acidosis
Hyperglycaemia
Electrolytes
Precipitant
Fluids
Insulin
Potassium
Education
EMJ 2003, 20 :210-213
Fluid Therapy
• Controversy is rife!!!
• Which fluid?
• How much?
• At what rate?
Which Fluid?
• Current guidelines ADA – Initial Fluid 0.9%
Saline
• Other’s prefer Hartmann’s.
• 0.9% Saline – hyperchloraemiac
metabolic acidosis
• Hartmann’s – 29mmol/l lactate. In DKA
high lactate to pyruvate ratio.
• Hartmann’s – generate glucose from
lactate
BMJ 2007;334:1284-5
• Hartmann’s – 5mmol/l K. DKA patient may
be hyperkalaemic
• 0.9% saline acidotic Ph 4.5
• Hartmann’s Ph 6,0
• Need a trial !
BMJ 2007;334:1284-5
Fluid replacement
• Aim to expand extracellular volume and
restore renal perfusion.
• Rate of 15-20ml/kg hour or 1-1.5l 1st hour.
• Subsequent choice depends on state of
hydration, serum electrolytes and urine
output.
• O.45% NaCl at 4-14ml/kg/hr if hyperNa or
euNa 0.9% if hypoNa
• Glucose <14 mmol/l 5% glucose
containing solutions at 100-125mls/hr.
• Change in osmolality not exceed 3
mmol/kg/hr
CMAJ 2003;168(7) 859 -66
GF Jooste Clinical Guidelines 2007
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Richardson, Meintjies and Burch:
1l N/S stat
1l over 1 1hr
1l over 2 hrs
1l over 4hrs
1 litre 6 hrly
Insulin
• Continous IV infusion
• IV bolus 0.1 u/kg
• Not subcut or IM for shocked. May used mild
DKA or no infusion available.
• If K >3.3 0.1 U/kg per hour.
• Gradual decline 3-4 mmol/l/hr.
• If level not drop 3mmol in first hour infusion may
be doubled.
• When Glucose level reaches 12-14 mmol/l
insulin rate may be decreased by 50% as 5%
dextrose is added
Diabetes Care V 29:12 Dec 2006
GF Jooste Protocol
• Infusion 50 units Actrapid in 200mls
Normal saline at 24mls/hr (6mls/hr)
• Visidex <15:
change to rehydration fluid
• Visidex 10-15: 24 mls/hr
• Visidex 4-10: 12mls/hr
• Visidex <4:
stop Actrapid 2 hrs and
50mls 50% dextrose
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Once the ketoacidosis has been corrected
Glucose <11.0 mmol/l
Serum Bicarb >18 mmol/l
Venous Ph >7.3 and patient able to eat
• Multi dose insulin regimen may be
started
Diabetes Care V 29:12 Dec 2006
Potassium
• Total body potassium depleted.
• May get hyperK because of acidosis.
• Give 20-30mmol K to each litre to maintain K 4 and 5 mmol/l.
• If K < 3.3 mmol/l give K & delay insulin therapy
to avoid arrhythmias
Diabetes Care V 29:12 Dec 2006
Bicarbonate therapy
(could be a presentation on its own)
• Use remains controversial.
• Ph>7.0 insulin blocks lipolysis and
resolves ketoacidosis.
• Disadvantages: Increased risk of
hypokalaemia, decreased tissue oxygen
uptake, cerebral oedema and may even
augment ketone production.
Diabetes Care V 29:12 Dec 2006
Bicarb
• If Ph <7,0 ADA recommends 50mmol
bicarb in 200mls sterile water with 10
mmol of K over 1 hr till ph >7,0.
• No studies PH <6.9. Risk of impaired
myocardial contractility
• 100mmol bicarb in 400mls sterile water
with 20 mmol K at 200mls/hr for 2 hrs until
venous ph >7,0
Endocrinol Metab Clin N Am 35 (2006) 725–751
What about Phosphate and
Magnesium?
• Phosphate: replacement not required for
routine correction. May be harmful –
hypocalcaemia.
• If potential complications of
hypophosphatemia – replacement may be
justified.
• Cydulka and Pennington in Rosen’s 6th Ed
recommend Mg 0.35mEq/kg in fluids, 1st 3
-4 hrs.
Postgrad Med J 2004; 80: 253-61
Treatment related complications
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Hypoglycaemia – poor monitoring
Hypokalaemia – inadequate replacement
Heart Failure – too much fluid
Cerebral oedema – correct water and
sodium deficits slowly. Suspect if
comatose after reversal of acidosis
CMAJ 2003; 168 (7), Rosen’s Emergency Med 6th ed
• Non cardiogenic pulmonary oedema – due
to increased water in lungs and reduced
lung compliance.
• Hyperchloraemic metabolic acidosis: loss
of ketanions necessary for bicarb
regeneration, use of 0.9% saline.
• Acidosis: no adverse effects and corrects
spontaneously
CMAJ 2003; 168 (7)
CASE STUDY 3
• 64 y old type 2 diabetic presents to EU
with hx from family “doc, I had difficulty
waking my mum this morning. She’s
confused”
• Good doc, you check hgt = 48 mmol/l and
notice her to be dehydrated.
• Diagnosis …
Hyperglycaemic hyperosmolar
state
• HHS replaces “hyperosmolar non-ketotic
coma”
• Alterations in sensoria may be present
without coma.
• Mild to moderate ketosis is commonly
present.
• Kitabchi et al …
Postgrad Med J 2004;80:253–261
Postgrad Med J 2004;80:253–261
Predisposing and precipitating
factors
• Infection (eg, pneumonia, urinary tract infection,
and sepsis) is the most common precipitating
illness, occurring in up to 60% of cases
• others - provoke release of counter regulatory
hormones and precipitate HHS include silent
myocardial infarction, cerebrovascular accident,
pulmonary embolism, and mesenteric
thrombosis
Emerg Med Clin N Am 23 (2005) 629–648
Clinical Presentation
• Type 2 diabetics with more insidious onset.
• Polyuria, polydipsia and weight loss over several
week’s duration.
• May have focal neurological signs
• Coma is associated with severe hypertonicity,
with serum osmolarity at 350 mOsm/L or greater,
and usually more significant hypernatremia than
hyperglycemia
• Dehydration
Postgrad Med J 2004;80:253–261
hypoglycaemia
hyponatraemia
sepsis
Diff Diagnosis
Uraemia
Drug od
Emerg Med Clin N Am 23 (2005) 629–648
• Calculate effective osmolarity, which
reflects actual tonicity, the osmotic
pressure of a solution.
• The normal serum osmolarity 275 to 295
mOsm/L. Levels above 320 mOsm/L alteration in cognitive function
Emerg Med Clin N Am 23 (2005) 629–648
Lab investigations
• serum glucose, serum urea ,creatinine,
electrolytes, serum ketones, osmolality,
urinalysis
• complete blood count with differential.
• arterial blood glasses if respiratory
compromise or acidosis is suspected.
• Bacterial cultures of urine and blood
almost always are indicated.
Emerg Med Clin N Am 23 (2005) 629–648
Sodium
• glucose osmotically shifts water into the
extracellular space, sodium is diluted, and
the measured value is decreased falsely.
• Corrected Na mmol/l = plasma Na +
(1.6x{plasma glucose-5.6})/5.6
• Na high – water loss and dehydration
Emerg Med Clin N Am 23 (2005) 629–648
Other studies
• ECG - to look for signs of ischemia and
infarction, and acute changes related to
electrolyte deficiencies.
• CXR – check for pneumonia
Emerg Med Clin N Am 23 (2005) 629–648
Goals of therapy
Haemodynamic
Stability
Electrolyte
homeostasis
Correction
Of hyperglycaemia
&hyperosmolarity
Find precipitant
Avoid complications
Emerg Med Clin N Am 23 (2005) 629–648
Fluids
• Replace one half of the fluid deficit in the first 12 hours
and the remainder in the next 12 to 24 hours
• Initial replacement should be with isotonic crystalloid (eg,
0.9% sodium chloride).
• The ADA guidelines - corrected serum sodium.
• If it is normal or elevated, 0.45% sodium chloride is
infused at 4 to 14 mL/kg per hour depending on
hydration state
• If low, 0.9% sodium chloride is continued at the same
rate
• Beware underlying disease states!
Emerg Med Clin N Am 23 (2005) 629–648
• Potassium – similar to DKA outlined earlier
• Low K greatest risk of complications
including cardiac dysrhythmias, cardiac
arrest, and respiratory muscle weakness.
Emerg Med Clin N Am 23 (2005) 629–648
Insulin
• Secondary role.
• Fluids always precede insulin administration.
• Insulin drives glucose, potassium, and water into
cells, and administration of insulin alone could
lead to circulatory collapse, shock, and even
thromboembolism if fluid has not been replaced
first.
• Dose similar to DKA outlined earlier
Emerg Med Clin N Am 23 (2005) 629–648
Complications
• Reasons for mortality – theories…
• Elders – cardiac and renal disease.
• Thromboembolic events, cerebral edema,
adult respiratory distress syndrome, and
rhabdomyolysis may occur.
• Low dose subcut heparin - thrombosis
see notes – click end show
Rosen’s Emergency Med 6th Ed
Case Study 4
• 75 yold diabetic, hypertensive on oral
hypoglycaemics presents to EU 2 day history of
vomiting, abdominal pain.
• O/E: confused, restless found to be in Cardiac
failure clinically.
• Hgt: 6,0
• Gas: ph 6.96 PC02 5.4 P02 9,0 HCo3 14
BE: -12. lactate 7,0 mmol/l
Diagnosis: ……………….
Postgrad Med J 2004; 80:253-261
Discussion:
Diabetes and Lactic Acidosis
Definition:
• Severe lactic acidosis is defined as a high
anion gap metabolic acidosis with a blood
lactate concentration 5.0 mmol/l (normal
0.4–1.2 mmol/l).
• The pathological elevation of lactate and
hydrogen ions may result from
overproduction or delayed clearance of
lactate, or a combination of both.
Postgrad Med J 2004; 80:253-261
Type A lactic acidosis
(anaerobic/hypoxic)
• Type A lactic acidosis (anaerobic/hypoxic)
occurs in states of profound tissue hypoxia such
as myocardial infarction, cardiogenic shock, or
profound sepsis.
• Anaerobic metabolism produces excess lactate
that swamps the body’s capability to clear it and
clearance of lactate may also be decreased.
• This situation is not peculiar to diabetes but
people with diabetes (particularly type 2
diabetes) are at increased risk of hypoxic
cardiovascular complications.
Postgrad Med J 2004; 80:253-261
Type B lactic acidosis (aerobic)
• Type B lactic acidosis (aerobic) is rarer and is
associated with a number of systemic diseases
(including diabetes), drugs, toxins, and inborn errors of
metabolism.
• The biguanides metformin and phenformin, used in the
treatment of type 2 diabetes, have both been associated
with the development of type B lactic acidosis.
• Phenformin was withdrawn from the market because of
this complication; the incidence of lactic acidosis is much
lower with metformin, with an estimated incidence of
0.03 episodes per 1000 patient years.
Postgrad Med J 2004; 80:253-261
Metformin
• May be either type A lactic acidosis, where the acidosis
is the result of concurrent complicating illness without the
accumulation of metformin; type B arising from marked
metformin accumulation without concurrent hypoxic
factors; or mixed.
• 90% of absorbed metformin is excreted unchanged by
the kidneys ; so - renal function that determines
metformin clearance.
Postgrad Med J 2004; 80:253-261
Metformin
• The principal contraindication - is renal
impairment: the American Diabetes
Association recommends avoiding
metformin use if serum creatinine
concentration exceeds 125 mmol/l.
• Because of the accumulation of lactate in
hypoxia, metformin is also contraindicated in
conditions such as uncontrolled heart failure that
predispose to lactic acidosis.
Postgrad Med J 2004; 80:253-261
Clinical Presentation
• Hyperpnoea (Kussmaul respiration), nausea,
vomiting,diarrhoea, epigastric pain, anorexia,
lethargy, thirst, and decreased level of
consciousness.
• Hypotension, hypothermia, cardiac
dysrhythmias, and respiratory failure may also
occur in severe metformin-associated lactic
acidosis.
• Blood glucose levels: low, normal, or high in
diabetic subjects.
Postgrad Med J 2004; 80:253-261
Management
• Treatment of lactic acidosis includes appropriate
supportive care (usually on an intensive care unit),
treatment of any concomitant condition and elimination
of any offending drug by renal excretion or dialysis.
• Bicarbonate therapy is still one of the principal
management modalities for lactic acidosis despite
conflicting reports as to its efficacy and even reports of
potential adverse consequences.
• Metformin is a dialysable drug and the use of
bicarbonate in combination with haemodialysis has been
successful.
Postgrad Med J 2004; 80:253-261
summary
• Prognosis in lactic acidosis of all causes is poor with only
between 12%–17% of patients surviving to discharge in
one well conducted study. N Engl J Med 1992;327:1564–9.
• In summary, general management of the underlying
condition, appropriate supportive care, bicarbonate
therapy and haemodialysis are the key approaches to
the management of severe lactic acidosis.
• Further trials needed before we can be clear as to what
represents optimum care.
Postgrad Med J 2004; 80:253-261
Conclusion

“Many Cases of DKA and HHS can be
prevented by better access to medical
care, proper education and effective
communication with the health care
provider during the intercurrent illness”
Acknowledgements:
Prof Wallis
Prof Pons
Prof Mattu
Prof Cydulka
Kitabchi et al
Diabetes Care V 29 : 12
December 2006
Hyperglycemic crises in adult patients with
diabetes