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 pre-
Inappropiate
coma, and requiring Gliclazide
Tx,18%
intravenous glucose) were 33% Gliclazide
observed in 43 patients. GIT upset Missed meal
20%
Alcohol
GIT upset
Alcohol Missed Inappropiate Tx
• Important to check for sepsis, 22% meal 36%
renal failure, heart failure,
accidental overdose

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 C-

peptide 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

• 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:

• 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
• 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
• 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
• 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 6 th 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–
 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–

 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 Correction
Electrolyte
Stability Of hyperglycaemia Find precipitant Avoid complications
homeostasis
&hyperosmolarity

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…
see notes – click end show

• Elders – cardiac and renal disease.

• Thromboembolic events, cerebral edema,
adult respiratory distress syndrome, and
rhabdomyolysis may occur.
• Low dose subcut heparin - thrombosis

th
 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: Kitabchi et al
Prof Wallis Diabetes Care V 29 : 12
Prof Pons December 2006
Prof Mattu Hyperglycemic crises in adult patients with
Prof Cydulka diabetes
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