This document discusses diabetic emergencies including hypoglycemia, diabetic ketoacidosis (DKA), and hyperglycemic hyperosmolar state (HHS). It provides details on the diagnostic criteria, symptoms, and general approach to managing patients with DKA. Key points include: DKA is caused by insulin deficiency leading to hyperglycemia and ketonemia; diagnostic criteria includes blood glucose over 11 mmol/L, ketones over 3 mmol/L, and venous pH below 7.3; symptoms include nausea, vomiting, and altered mental status; management involves assessing airway, breathing, circulation, and providing IV fluids and insulin.

1. DIABETIC
EMERGENCIES
PRESENTER: HIDAYAH CHE SOH
SUPERVISOR :DR RUZAINA

2. Content
◦ Hypoglycaemia
◦ Diabetic Ketoacidosis (DKA)
◦ Hyperglycaemic Hyperosmolar State (HHS)

3. HYPOGLYCEMIA
Hypoglyc
emia
Low plasma glucose level
(<3.9mmol/L)
Reversed by CHO
intake
Presence of autonomic or
neuroglycopenic symptoms

4. GENERAL APPROACH TO
HYPOGLYCAEMIC PATIENT

5. ◦ Risk factors for hypoglycaemia
◦ Risk factors for hypoglycaemia include:
◦ Insulin-dependent diabetes
◦ Previous history of hypoglycaemic episodes or reduced hypoglycaemia
awareness
◦ Impaired renal function
◦ Cognitive dysfunction/dementia
◦ Alcohol misuse
◦ Profound starvation
◦ Increased exercise
◦ Food malabsorption issues (e.g. coeliac disease, bariatric surgery,
gastroenteritis)

6. Autonomic
Trembling
Palpitations
Hunger
Tingling
Nausea
Anxiety
Sweating

7. Neuroglycop
enic
Confusion, headache
Weakness/ stroke like symptoms
Seizures/ coma
Difficulty speaking
Vision changes
Drowsiness
Difficulty
concentrating

8. ◦ Airway
◦ Clinical assessment
◦ Can thepatienttalk?
◦ Yes: ifthepatientcan talk,theirairwayispatentandyoucan moveon totheassessmentofbreathing.
◦ No:
◦ Lookforsignsof airwaycompromise: theseinclude cyanosis,see-sawbreathing,use ofaccessorymuscles,diminishedbreathsounds
andaddedsounds.
◦ Openthemouthandinspect: lookforanythingobstructingtheairwaysuchassecretionsoraforeignobject.
◦ Interventions
◦ Regardlessoftheunderlyingcauseofairwayobstruction,seek immediateexpertsupport fromananaesthetistandtheemergency
medicalteam(oftenreferredtoasthe‘crashteam’).Inthemeantime,you canperformsomebasicairwaymanoeuvrestohelpmaintain
theairwaywhilstawaitingseniorinput.
◦ Head-tiltchin-lift manoeuvre
◦ Openthepatient’sairway usingahead-tiltchin-lift manoeuvre:
◦ 1.Place one handon thepatient’sforeheadandtheotherunderthechin.
◦ 2.Tilttheforeheadbackwhilstliftingthechin forwardstoextendtheneck.
◦ 3.Inspecttheairwayforobviousobstruction.Ifanobstructionisvisiblewithintheairway,usea fingersweep or suction toremove
it.
◦

9. ◦ Breathing
◦ Clinical assessment
◦ Observations
◦ Review the patient’s respiratory rate:
◦ A normalrespiratory rate is between 12-20 breaths perminute.
◦ Patients with severe hypoglycaemia may develop a slow, irregular pattern of breathing.
◦ Review the patient’s oxygen saturation (SpO2):
◦ A normalSpO2 range is 94-98%in healthy individuals and 88-92%in patients with COPD who areat high-risk of CO2 retention.
◦ Hypoxaemia mayoccur due to aspiration or bradypnoea in the context of severe hypoglycaemia.
◦ Auscultation
◦ Auscultate the chest to screen for evidence of other respiratory pathology (e.g. coarse crackles maybe present if the patient has developed
aspiration pneumonia secondary to a reduced level of consciousness).
◦ Investigations and procedures
◦ Arterial bloodgas
◦ Take an ABG if indicated (e.g. low SpO2) to quantify the degree of hypoxia.
◦ Chest X-ray
◦ A chest X-ray maybe indicated if abnormalities arenoted on auscultation (e.g. reduced airentry, coarse crackles) to screen for evidence of
aspiration pneumonia. A chest X-ray should notdelay the emergency management of hypoglycaemia.

10. ◦ Circulation
◦ Clinicalassessment
◦ Pulseandblood pressure
◦ Assessthepatient’s pulseandbloodpressure:
◦ Tachycardiamaybepresentinthe contextof hypoglycaemia.
◦ Bradycardiaisa latesignand often precedescardiacarrest.
◦ Hypovolaemiamaybepresentsecondarytoreducedfluid intake orsepsis.
◦ Inspection
◦ Inspect the patient fromthe endofthe bed:they mayappeardrowsy,confusedand/orclammy/pale.
◦ Capillaryrefilltime
◦ Capillaryrefilltimemay beprolongedifthe patientishypovolaemic.
◦ Fluidbalanceassessment
◦ Calculatethe patient’sfluidbalance:
◦ Calculatethe patient’scurrentfluid balanceusingtheirfluidbalancechart(e.g. oralfluids,intravenousfluids,urineoutput,
drainoutput, stooloutput, vomiting)toinformresuscitationefforts.
◦ Reducedurineoutput (oliguria)istypicallydefinedaslessthan 0.5ml/kg/hour inan adult.

11. ◦ Disability
◦ Clinicalassessment
◦ Consciousness
◦ In thecontext ofhypoglycaemia,a patient’s consciousnesslevelmay bereduced.
◦ Assessthepatient’s levelof consciousnessusingthe AVPU scale:
◦ Alert:the patientisfully alert,althoughnot necessarilyorientated.
◦ Verbal:thepatient makes somekind ofresponsewhenyoutalkto them (e.g. words,grunt).
◦ Pain:the patientrespondstoa painfulstimulus(e.g. supraorbitalpressure).
◦ Unresponsive:the patientdoesnotshowevidenceofany eye,voiceormotor responsestopain.
◦ If amoredetailedassessmentofthe patient’s levelofconsciousnessisrequired,usethe GlasgowComaScale(GCS).
◦ Pupils
◦ Assessthepatient’s pupils:
◦ Inspectthesizeandsymmetryofthe patient’spupils
◦ Assessdirectand consensualpupillaryresponses
◦ Patientswithseverehypoglycaemiaand associatedmetabolicencephalopathymaydevelopbilateral miosis.3

16. DIABETIC KETOACIDOSIS
(DKA)

17. DIABETIC KETOACIDOSIS
◦ The most serious acute complications of diabetes
◦ Caused by combination of absolute or relative insulin deficiency, which
increase in counter regulatory hormone  lead to increase
gluconeogenesis, lipolysis and hepatic fatty acid oxidation result in
hyperglycemia and ketonemia

18. precipitating cause
◦ DKA is occasionally the initial manifestation of diabetes, but it usually occurs in the context of known diabetes plus a
trigger. This is especially true of patients with type-II DM, who don't generally require exogenous insulin but may
develop DKA in the context of physiologic stress. Most triggers of DKA are benign (e.g., nonadherence, viral
gastroenteritis). However, DKA can be caused by any source of physiologic stress. Occasionally, DKA is the
presentation of a serious underlying problem, especially sepsis. Common triggers of DKA include:
◦ Absolute insulin deficiency:
◦ Insulin nonadherence.
◦ Inadequate dosing of basal insulin.
◦ Insulin pump failure.
◦ New diagnosis of diabetes.
◦ Infection (e.g., gastroenteritis, pneumonia, urinary tract infection, diabetic foot infection).
◦ Pancreatitis.
◦ Pregnancy.
◦ Trauma, surgery.
◦ Substance abuse or alcoholism.
◦ Medications:
◦ Steroid.
◦ Sympathomimetics.
◦ SGLT-2 inhibitors.
◦ Atypical antipsychotics.
◦ HIV protease inhibitors.
◦ Checkpoint inhibitors (e.g., pembrolizumab, nivolumab).
◦ Pentamidine
◦ Anti-calcineurin immunosuppressives

20. Diagnostic criteria of DKA
◦ All three must be met :
a) CBG >11 mmol/L
b) Capillary ketones >3 mmol/L or urine ketones 2+ or more
c) Venous pH <7.3 and/or HCO3 <15 mmol/L

21. ◦ three ways to evaluate for ketoacidosis
◦ (#1) anion gap
◦ Anion Gap = (Na – Cl – Bicarbonate)
◦ Using this formula, an elevated anion gap is above 10-12 mEq/L.
◦ Please don't correct for albumin, glucose, or potassium. Don't make this unnecessarily complicated.
◦ Anion gap may be elevated due to a variety of causes . Therefore, an elevated anion gap does not
necessarily imply DKA! This is especially true among patients with chronic renal failure, who may
have a chronically elevated anion gap.
◦ (#2) urinary dipstick for ketones
◦ The urinary ketone dipstick tests for acetoacetate.
◦ This test has a high sensitivity for DKA (98-99%), with urinary ketones are generally being ≧2+.False
negatives may occur in patients with highly acidic urine.
◦ The specificity of a positive measurement of urinary ketones is low, so a positive urinary
measurement of ketones doesn't establish a diagnosis of DKA. For example, starvation
ketoacidosis is a more common cause of urinary ketones in most contexts.
◦ (#3) blood beta-hydroxybutyrate level
◦ Beta-hydroxybutyrate level is the gold standard for defining the presence and extent of ketoacidosis
in DKA.
◦ Rough interpretation:
◦ 0-0.6 mM: Normal
◦ 0.6-1 mM: Mild ketosis, may consider adjustment of insulin regimen. Among patients who initially presented with
DKA, a reduction of the beta-hydroxybutyrate level below <1 mM indicates resolution of the DKA
◦ 1-3 mM: Moderate ketosis, medical intervention is warranted. There is a risk of progression to DKA.
◦ >3 mM: Consistent with DKA.
◦ >6 mM: Severe DKA.

23. Criteria For Severe Ketoacidosis
- need for ICU referral/ critical care
◦ Venous HCO3 <5 mmol/L
◦ Blood ketones >6 mmol/L
◦ Venous pH <7.1
◦ Anion Gap > 16 [Anion Gap = (Na+ + K+) – (Cl- + HCO3-)]
◦ GCS <12
◦ SPO2 <92% on air (ABG required)
◦ Systolic BP <90 mmHg
◦ Pulse >100 or <60 bpm

24. Symptoms and sign of DKA
◦ Nausea vomiting
◦ Abdominal pain
◦ Confusion, drowsiness, reduced level of
consciousness, LOC
◦ Dehydration
◦ Tachycardia
◦ Tachypnea
◦ Kussmaul respiration ; acetone-smell breath
◦ Prior to above presentations, pt usually has
classical symptoms of DM

25. GENERAL APPROACH TO PATIENT
WITH DKA
◦ AIRWAY
◦ Can the patient talk?
◦ Yes: if the patient can talk, their airway is patent and you can move on to the
assessment of breathing.
◦ No:
◦ Look for signs of airway compromise: these include cyanosis, see-saw
breathing, use of accessory muscles, diminished breath sounds and added
sounds.
◦ Open the mouth and inspect: look for anything obstructing the airway such
as secretions or a foreign object.

26. ◦ BREATHING
◦ Review the patient’s respiratory rate, A normal respiratory rate is
between 12-20 breaths per minute.
◦ Patients with DKA may develop deep, laboured breathing (known as
Kussmaul breathing) in a response to metabolic acidosis (i.e. respiratory
compensation).
◦ Review the patient’s oxygen saturation (SpO2):
◦ A normal SpO2 range is 94-98% in healthy individuals and 88-92% in
patients with COPD who are at high-risk of CO2 retention.
◦ Hypoxaemia may occur due to aspiration or bradypnoea in the context
of severe DKA.
◦ Auscultate the chest to screen for evidence of respiratory pathology (e.g.
unilateral coarse crackles may be present if the patient has pneumonia
which may have been the precipitant for DKA).

27. Arterial blood gas
◦ An arterial blood gas (ABG) can provide lots of useful information to
management including:
◦ PaO2: may be reduced in the context of pneumonia (e.g. DKA precipitated
by a respiratory infection).
◦ PaCO2: may be low in the context of DKA due to respiratory
compensation as a result of metabolic acidosis.
◦ pH: low in the context of DKA due to the presence of acidic ketones.
◦ HCO3-: low in the context of DKA due to metabolic acidosis.
Chest X-ray
◦ A chest X-ray may be indicated if abnormalities are noted on auscultation
(e.g. reduced air entry, coarse crackles) to screen for evidence of
pneumonia. A chest X-ray should not delay the emergency management
DKA.

28. ◦ INTERVENTION
Administer oxygen to all critically unwell patients during
your initial assessment. This typically involves the use of a non-
rebreathe mask with an oxygen flow rate of 15L. If the patient has COPD
and a history of CO2 retention you should switch to a venturi mask as
soon as possible and titrate oxygen appropriately.
◦ If the patient is conscious, sit them upright as this can also help with
oxygenation.
◦ Antibiotics- If an infection is suspected, IV antibiotics should be
administered as soon as possible.

29. ◦ CIRCULATION
◦ Pulse and blood pressure-Assess the patient’s pulse and blood pressure:
◦ Tachycardia is common in the context of DKA due to hypovolaemia and
catecholamine release.
◦ Bradycardia is a late sign and often precedes cardiac arrest.
◦ Hypovolaemia is common in the context of DKA due to reduced oral intake
and vomiting.
◦ Inspect the patient from the end of the bed: they may appear drowsy,
confused and/or clammy/pale.
◦ Capillary refill time- may be prolonged if the patient is hypovolaemic.
◦ Fluid balance assessment- Calculate the patient’s fluid balance:
◦ Calculate the patient’s current fluid balance using their fluid balance chart (e.g.
oral fluids, intravenous fluids, urine output, drain output, stool output,
to inform resuscitation efforts.
◦ Reduced urine output (oliguria) is typically defined as less than 0.5ml/kg/hour
an adult.

30. DISABILITY
◦ Consciousness-In the context of DKA, a patient’s consciousness level may
be reduced.
◦ Assess the patient’s level of consciousness using the AVPU scale:
Alert: the patient is fully alert, although not necessarily orientated.
Verbal: the patient makes some kind of response when you talk to them
(e.g. words, grunt).
Pain: the patient responds to a painful stimulus (e.g. supraorbital pressure).
Unresponsive: the patient does not show evidence of any eye, voice or
motor responses to pain.
◦ If a more detailed assessment of the patient’s level of consciousness is
required, use the Glasgow Coma Scale (GCS).
◦ Pupils-Assess the patient’s pupils:
Inspect the size and symmetry of the patient’s pupils
Assess direct and consensual pupillary responses

31. Principles of Management
◦ Restoration of hydration
◦ Suppression of ketoacidosis
◦ Restoration of biochemical normality
◦ Careful and frequent monitoring to avoid complications due to therapy
◦ Hypokalemia, cerebral edema, pulmonary oedema

33. 1st Hour: Immediate Management
◦ Commence 0.9% NS drip using large bore cannula.
◦ Commence a fixed rate IVI insulin (0.1 unit/kg/hr based on estimate of
weight).
◦ Assess patient
◦ BP • Pulse • Temp • RR • SPO2 • GCS
◦ Hydration status • Full clinical exam

34. Investigations :
- CBG and venous BG
- ABG, Blood or urinary ketones
- BUSE, FBC, Blood cultures
- ECG, CXR
Outline monitoring regimen:
- Hourly CBG, Vital signs and input-output charting hourly ,Venous
HCO3 and K+ at 60 mins, 4H and 6hrly thereafter, 6hrly BUSE and
urine ketone, Continuous SPO2, Continuous cardiac monitoring
Look for precipitating causes and treat accordingly Start broad-
spectrum antibiotics if infection suspected

35. Initial Fluid & K+ Replacement
SBP <90 mm Hg (usually due to under volume)
◦ Give 500 mL of 0.9% NS over 10–15 mins. If SBP remains <90 mmHg,
repeat.
◦ Most patients require between 500-1000 mL given rapidly. Consider
colloids e.g. Gelafundin if BP fails to pick up.
◦ Once SBP >90 mmHg, give 1L of 0.9% NS / next 60 mins. Addition of K+
is likely to be required in the 2nd litre of fluid, especially if baseline K+
<5 mmol/L and to maintain K+ between 4-5 mmol/L.
SBP on admission ≥ 90 mmHg
◦ Give 1L of 0.9% NS for first 60 mins

36. K+ REPLACEMENT
- Given in maintainance drip via separated IVL
- Maintaince IVD 500ml NS 3hrly to 4hrly (depend on hydration status and
urine output)
• K+ replacement in every 500ml NS :-
◦ ≥ 5.5 – nil
◦ 4.6-5.4 – 0.5g KCl
◦ 4.1 – 4.5 – 1g KCl
◦ 3.5-4.0 – 1.5g KCL
◦ <3.5 – medical/endocrine consult, cardiac monitoring
- Maintain serum K+ level at 4-5mmol/L

37. ◦ Intravenous bicarbonate:
The use of intravenous bicarbonate is not indicated to correct acidosis in DKA
due to:
◦ Rise in pCO2 in CSF which may lead to a paradoxical increase in CSF acidosis.
◦ Delay in the fall of blood lactate and ketone level
◦ Risk of cerebral oedema especially in younger age groups. (esp <5years old)

38. Aims of treatment
◦ Rate of ↓ of ketones of at least 0.5 mmol/L/hr
◦ HCO3 ↑ 3 mmol/L/hr
◦ CBG ↓ 3 mmol/L/hr
◦ Maintain Se K+ in normal range
◦ Avoid hypoglycaemia
• Once CBG ↓ below 14 mmol/L
- Switch to D5% at 125 mL/hr and reduce IVI insulin rate to 0.05
units/kg/hr
- Or switch to D10% at 125 mL/hr with no change in IVI insulin rate.

41. MONITORING

42. RESOLUTION

44. INTUBATING DKA PATIENT
◦ avoid intubation - Whenever possible, avoid intubation.
◦ Intubating a patient due to altered mental status is usually a mistake. The mental
status should improve over several hours, so careful observation is generally the best
approach.
◦ Indications for intubation may include:
◦ Frank inability to protect airway (e.g. gurgling, inability to control secretions).
◦ Intubation needed to facilitate surgical procedure (e.g. patient has DKA plus perforated
viscus).
◦ Respiratory arrest or impending arrest (e.g. patient in extremis).
◦ If intubation is necessary (e.g. for a surgical procedure), it may be wise to delay it for a
few hours to allow vigorous treatment of DKA first.
risks involved with intubation
◦ Hemodynamic collapse: If hypovolemia isn't corrected prior to intubation
◦ Vomiting/aspiration: These folks often have gastroparesis and illeus.
◦ Decompensation of acidosis: Most patients have severe metabolic acidosis with a
compensatory respiratory alkalosis. Paralysis takes away their respiratory
compensation, potentially leading to profound acidosis.

45. mitigating the risks
◦ Hemodynamic collapse:
◦ Volume resuscitate prior to intubation.
◦ If necessary start a vasopressor infusion to establish MAP >75-80mm before the procedure.
◦ Use hemodynamically stable induction drugs (e.g. ketamine).
◦ Avoid regurgitation
◦ Visualize the stomach with ultrasound, if it's distended consider NG drainage prior to intubation.
◦ If the patient is intermittently vomiting, encourage them to vomit immediately before anesthetic induction (while
they can still protect their airway).
◦ Consider giving some bicarbonate prior to intubation if the bicarbonate level is <10 mEq/L.
◦ For example, slowly push 2-3 ampules (100-150 mEq) of bicarbonate over 10-15 minutes, at least ~10 minutes
prior to intubation.
◦ Bicarbonate contains dissolved CO2, which the patient must blow off. In order to benefit from the bicarbonate,
the patient should have enough time to blow off additional CO2 prior to intubation.
◦ Consider using mechanically controlled apneic ventilation (with BiPAP or a ventilator) during
induction of anesthesia if you're adept at this. If you're not, then it's probably best to perform
RSI to minimize risk of regurgitation (without any breaths interposed between paralytic and
intubation).
◦ Use a relatively large ETT to minimize airway resistance (ideally nothing smaller than a 7.5-mm
◦ Use rocuronium, so that after intubation the patient will be paralyzed and sync perfectly with the
ventilator.
◦ As soon as the ETT is secured, increase tidal volume & respiratory rate to hyperventilate the
(thus restoring respiratory compensation).
◦ Set the tidal volume at 8 cc/kg.
◦ Crank the respiratory rate as high as possible without causing autoPEEP (will often end up around ~24-28
breaths/minute).
◦ Shoot for a very high minute ventilation (e.g. 12-18 liters/minute).

46. HYPERGLYCAEMIC
HYPEROSMOLAR
STATE
(HHS)

47. Hyperglycaemic Hyperosmolar State
◦ Higher mortality than DKA
◦ The presentation of DKA is rapid (within hours)
◦ HHS progresses over many days  the dehydration and metabolic
disturbances are more extreme

48. Diagnostic Criteria of HHS
◦ Hypovolemia – dehydration
◦ Marked CBG > 33.3 mmol/l
◦ pH > 7.3, HCO3 > 15 mmol/l
◦ Urine or blood ketones nil or minimal
◦ Se osmolality > 320 mosmol/kg
Formula : (2 x serum
[Na]) + [glucose] + [urea]
(all in mmol/L)
Or laboratory measured value

49. Precipitating factors for HHS
a) Infections and sepsis
b) Thrombotic stroke
c) Intracranial haemorrhage
d) Silent myocardial infarction
e) Pulmonary embolism

50. What are the management goals?
Gradually and safely:
1. Normalize the osmolality
2. Replace fluid and electrolyte losses
3. Normalize blood glucose
4. Prevention of complications
Treat the underlying cause
Care in high dependency ward

52. 1st hour ( A&E)
Commence 0.9% saline drip -large bore cannula and
commence - fixed rate IVI insulin (0.05 unit/kg/hr).
Assess patient :
◦ Investigations
◦ Monitoring regime – hourly urine output and fluid input
charting
◦ Look for precipitating causes and treat accordingly
Fluid Replacement:
◦ • NS as quickly as possible in shock, assess hydration, rate
of 10-15ml/kg in 1st few hrs, maximum <50ml/kg 1st 4
hours ( IL/hr)
◦ • dependent on hydration status and urine output. Caution
in elderly.
FRII:
◦ • 0.05 U/kg/hr, ensure adequate hydration first
◦ drop in BGL 3-5mmol/hr
◦ drop in osmolality 3-8 mOsm/kg/hr, increase infusion
(0.1u/kg/hr) if this not achieved
◦ If drop in osmolality >8 mOsm/kg/hr with drop in BGL >
5mmol/hr, reduce infusion
K Replacement:
2nd - 6th hour
◦ Reassess patient, monitor VS
◦ Continue fluid replacement via infusion pump
◦ Assess response to treatment
◦ Additional measures: fluid balance chart; urinary catherisation ;
NBM and NG tube, ABG, ECG monitoring if indicated
◦ DVT prophylaxis
Aims :
◦ Rate of fall Se osmolality 3-8mOsm/kg/ hr
◦ CBG fall 3-5mmol/L/hr
◦ Maintain Se K+ in normal range (4-5mmol/L)
◦ Avoid hypoglycaemia, once BGL ≤ 15 mmol/L, concurrent D5% or
D10% with maintenance NS, maintain BGL 10-15 mmol/L in 1st 24
hrs
Serum Na :
◦ •If Na increasing with drop in osm < 3mOsm/hr, check fluid
balance, if fluid balance adequate, switch to 0.45% saline
◦ Urine output at least 0.5ml /kg/hr
What is the immediate management?

53. 6 - 12 hours
◦ Reassess patient, monitor VS (reduce fluid; K
balance; CBG ≤ 15 mmol/l – D5 infusion)
◦ Reassess CVS status at 12 hrs; further fluid
may be required; Check for fluid overload
◦ Review biochemical and metabolic
parameters: monitor Se osmolality
◦ ;referral to diabetes team
Aims :
◦ Ensure clinical and biochemical parameters
improving
◦ Hourly CBG, 2 -4 hrly Se osmolality
◦ Continue IV fluid replacement
◦ Avoid hypoglycaemia
◦ Assess for complications of tx e.g. fluid
overload, cerebral oedema
◦ Treat precipitating factors as necessary
12 - 24 hours
◦ Reassess patient, monitor VS, review
biochemical and metabolic parameter
Aims :
◦ Gradual decline in BGL, not >5mmol/L/hr
◦ Continue IV fluid & insulin infusion
◦ Gradual decline in Na, with decline in Se
osmolality not >8mOsm /kg/kr
◦ Reassess for complications of treatment
e.g. fluid overload, cerebral oedema
◦ Continue to treat precipitating factors
◦ Change to sc insulin if pt is drinking/eating
normally

55. RESOLUTION OF HHS

57. THANK
YOU

58. Reference
◦ Clinical Practice Guidelines - Management of Type 2 Diabetes Mellitus,
5th edition