Dka vs hhs

1. CME ETD 2023
DKA VS HHS
PRESENTER: NAVIN RAVI

2. Let’s start from a real
case study.

3. Case study
Mr. A, 23 years old Malay Male brought by family members to ED at 4.30pm due to less responsive
since yesterday evening.
Further history from family members:
- Patient previously NKMI
- Was unwell for past 5/7
- Having fever x5/7, non-productive cough x5/7 and vomiting x3/7, unsure amount and episodes,
last episode yesterday
- Noted to be less responsive since yesterday evening, not answering questions, appears drowsy
- Visited GP in the morning, treated as acute tonsillitis and discharged with T.Augmentin 625mg BD,
T.Ponstan 500mg TDS, T.Papase II/II TDS and Lozenges I/I PRN.
- Claimed patient was able to ambulate when going to clinic, but after came back from clinic became
more drowsy and not responding to questions.

4. Otherwise,
- Denied diarrhoea/abdominal pain
- Denied SOB/chest pain
- Denied UTI sx
- Denied recent history of jungle trekking/water activities/ fogging activities in the
neighbourhood
- Denied taking any illicit drug
- Denied any fitting episode
- Denied any history head trauma

5. Physical examination
GCS: E4V2M5 (11/15), pupils bilateral 2 mm/ 2 mm reactive, pink, lethargic looking, CRT less than
2 seconds, good pulse volume, warm peripheries, dry lips, tongue coated, patient is obese
(estimated weight of 120kg)
•BP: 185/101 mmHg
•PR: 135 bpm
•RR: 22
•Temp: 38.6 OC
•SPO2 : 91% under RA
•DXT: HI
•Blood ketone: 6.3

6. Systemic examination
•Throat: Injected, Tonsils enlarged Grade II, No exudate seen, Uvula central
•Lungs: Clear, equal air entry
•CVS: DRNM
•P/A: Soft, not tender
•Neurology:
Bilateral UL and LL tone normal
Bilateral UL and LL power at least 4
Bilateral UL and LL reflexes normal
Bilateral Babinski downgoing
Bilateral clonus absent

7. Bedside scan:
•No free fluid
•IVC kissing
•Good heart contractility
•No pericardial effusion or pleural effusion
(Poor view due to thick chest/abdominal wall)

8. ECG: sinus tachycardia, HR136

9. POCT
•VBG:
•Covid 19 RTK: Negative
pH 7.29
pO2 59
pCO2 30
HCO3 14.4
BE -10.4
Lac 5.9

10. Diagnosis
1. Severe DKA TRO HHS
2. TRO CAP
3. Cover for meningoencephalitis

11. Investigations
•FBC,RP, LFT, CaMgPo4, CE, Coag, Blood C+S
•UFEME
•CXR
•CT Brain urgent

12. Management
•Uptriage Redzone
•Put on NpO2 3L/min
•Put on cardiac monitoring
•Start fluid resuscitation 10cc/kg: IVD Sterofundin 1L over 1H
•Insert CBD, strict I/O charting
•Start IVI insulin fixed rate 0.1 units/kg/hour = 12 cc/H
•T.Paracetamol 1g stat
•IV Omeprazole 40 mg stat
•IV Rocephine 2g stat
•DXT monitoring hourly
•GCS charting
Estimated weight 120kg
Adjusted weight 90kg

13. Time Progress Plan
6/5/23
5.50pm
- Completed IVD Sterofundin 1L
- Urine output since insertion: 100cc
- GCS E3V2M5, pupils 2/2 reactive, BP 114/82mmHg,
PR 145bpm, SPO2 96% under NPO2 3L/min
- DXT: Hi
- Bedside scan: IVC still kissing
• Run another
20cc/kg: 1.8L NS
over I hour
• Cont. IVI insulin
fixed scale 12cc/H
• Keep NPO2 3L/min
• For CT brain as
planned
• DXT monitoring
hourly
1L
Sterofundin

14. Time Progress Plan
6/5/23
6.25pm
Given 1L Sterofundin, Ongoing 1.8L Normal
saline
Blood investigations came back:
FBC Hb 18.1/HCT 65/PLT351 /WBC 14.53
Urea 16.8/ Creat 289/ Na 139(176) /K 4.4/ Ch
94/Ca 2.61/ PO4 1.73/ Mg 1.5
INR 1.1 /PT 14.8/ APPT 29.7
Alb 38/ Glo 59/ ALT 32/ AST 40/ ALP 178/ CK
165/ LDH 268
RBS 93.3
Serum osmolality: 371.3
CXR: Right perihilar haziness
Case D/w Dr Nazrul (EP oncall):
• To treat as DKA mixed with
HHS, cover for
meningoencephalitis
• To complete 30cc/kg fluid
bolus as planned
• Then to start fluid
replacement 1L/1H, then
1L/2H, then 1L/4H and then
1L/6H with IVD 6pint/24H
with K+ supplement
• Cont. IVI insulin fixed scale
12cc/H
• To proceed CT brain as
planned
• No need for intubation for
now, KIV for intubation if
worsening acidosis/GCS
• To repeat VBG & RP post
bolus and 2 hourly

15. Time Progress Plan
6/5/23
8.15pm
Total fluid in 2.8L, ongoing IV 1L NS/1H
Urine output 700cc
Noted BP hypotensive 88-91/53-70mmHg
Started on IVI Noradrenaline 6.8cc/H
(0.2mcg/kg/min)
BP pick up to 118/74, PR 141, SPO2 96% under
NPO2
Done CT brain: No ICB/infarct seen
Required sedation IV Midazolam 4mg
Revised Imp:
1. Severe DKA mixed with HHS
2. Septic shock secondary to CAP
3. Cover for meningoencephalitis
4. AKI
• Cont. fluid replacement
1L/2H with 1g KCL in each
pint, then 1L/4H and then
1L/6H
• IVD 6pint/24H with 1g KCL
in each pint
• Fast correct KCL 1g in 100cc
NS/1H
• Cont. IVI insulin fixed scale
12cc/H
• Titrate IVI Noradrenaline
• S/C Fondaparinux 2.5mg
stat
• DXT monitoring hourly
• Strict I/O hourly
• Repeat RP and VBG 2 hourly
• KIV for intubation if
worsening acidosis/ GCS
• Referred to medical team at
8.45pm

16. Time Progress Plan
6/5/23
9.00pm
• Noted GCS E1V2M5 (8/15) with acidotic breathing
• Was put on HFMO2 15L/min
BP 125/74 (on IVI Noradrenaline 10.2cc/H- 0.3mcg/kg/min)
PR 115
SPO2 98% under HFMO2
• Given IV Flumazenil total 1mg
6/5/23
9.30pm
Attended by Dr Nazrul (EP oncall), to proceed with
intubation
Pre-medications: IV Midazolam 3mg stat
IV Fentanyl 100mcg stat
IV Rocuronium 50mg stat
Intubated with single attempt using video laryngoscope with
ETT size 8, anchored at 22cm

17. Time Progress Plan
6/5/23
10.00pm
• Post intubation:
BP 129/90 mmHg (on IVI Noradrenaline 13.5cc/H)
0.4mcg/kg/min
PR 131
SPO2 98% under ventilator
DXT HI
Blood ketone 0.4 6.3

18. Time Progress Plan
Imp:
1. Severe DKA with HHS
2. Septic shock secondary to CAP
3. Cover for meningoencephalitis
4. AKI
• Ventilation (SIMV, PEEP 8, TV 540, Rate
24, PS 15, FiO2 1.0)
• Change fluid to half saline and cont.
fluid regime 1L HS/4H then 1L HS/6H
• IVD maintenance 6pint HS/24H with 1g
KCl in each pint
• Fast correct another 1g KCL in 100cc
NS/IH
• Reduce IVI insulin fixed scale to 6cc/H
• Start sedation with IV Midazolam 30mg
and IV Fentanyl 300mcg infusion run
8cc/H
• Insert Ryle tube
• Strict I/O charting
• Repeat blood investigation at 11.30pm
- ABG, RBS, BUSE
• DXT monitoring hourly
• VBG and BUSE 2 hourly
• ECG, CXR post intubation
• Titrate IVI Noradrenaline
• Insert CVL

19. Time Progress Plan
Cont.
• Input: 6300 cc (1000cc sterofundin+ 4800cc NS+ 500cc HS)
• Output: 798 cc
• Positive balance: 5502 cc
Given IV 1g KCl in 100cc NS x 2

20. Time Progress Plan
6/5/23
10.00pm
Seen by Medical team
Imp:
1. Septic shock secondary to bacterial pharyngitis
2. HHS/DKA secondary to 1
3. AKI secondary to 1
4. TRO metabolic syndrome
5. TRO OSA
• To increase IVI insulin
fixed scale to 8 cc/hour
• IVD 1 L HS over 4 hours
• IVD maintenance 7 pints
HS/24H with 0.5g KCL
• IV Ceftriaxone 2 g OD
• S/C Clexane 60 mg OD
• IV Omeprazole 4omg OD
• T. Paracetamol 1g PRN
6/5/23
10.50pm
Seen by Anaest team: plan for admission to ICU Patient was subsequently
admitted to ICU around
12.00 am

22. Admitted to ICU @ 12.20am
• Actual weight 150kg, estimated height 170cm
• Ventilated with PSIMV PEEP 10, PC 10, PS 14, FiO2 0.6, rate 12, I:E 1:2
• Sedated with IVI midafentanyl 8ml/h
• IVI noradrenaline 0.24mcg/kg/min
• IVI insulin 8u/H fixed scale
• ABG : pH7.29/ pCO2 42/ pO2 75/ HCO3 20.2/ BE -6.2/ lac 4.0/ DXT >27.8/ PF ratio 125
• Hydration improve, skin turgor fair, good pulse volume, CRT< 2sec
• Urine output upon admission 0.75cc/kg/h
• Lung bibasal crepitations, no pedal edema
• IVD maintenance 6pint sterofundin/ 24hour with 1g KCL each pint

23. • IVI noradrenaline trend slowly increasing since 5am
• At 6.10am, IVI noradrenaline increased to 1.0mcg/kg/min, started IVI adrenaline
0.5mcg/kg/min, tachycardia HR 150bpm
• Good pulse volume, regular pulse, CVS DRNM, CRT < 2sec
• ECG stat: ST elevation at lead III; ST depression at aVL; T inversion at lead I, aVL, V3-V6
• ABG : pH 7.27/ pCO2 40/ pO2 65/ HCO3 18.4/ BE -8.0/ lac 3.4/ K+ 2.6/ Na 162/ PF ratio 108
• IV MgSO4 10mmol stat x1
• IV KCL 1g fast correct x 2

25. • Develop VF x 2 around 6.49am, shock (200J) x 2, and started CPR pulse VT x1, synchronized cardioversion (150J) x1
• Total adrenaline 1mg x 2, CPR x 6min
• ROSC at 6.55am
• Develop VF again at 7.15am, shock (200J) x 1 and started CPR
• CPR x 45min
• IV adrenaline 1 mg x 17
• IV Ca gluconate 10mmol x 1
• IV KH2PO4 10mmol x1
• IV amiodarone 300mg x1
• IV NaHCO3 100ml x 1
• No ROSC, death pronounce at 8.05am 7/5/2023
• Cause of Death : HHS with multiorgan failure

28. CXR 6/5/23, 6pm
CXR post intubation
6/5/23, 1030pm

30. Pitfalls/Learning points
1. Fluid deficit correction
• Duration of correction 48 - 72hours
• Fluid status is dynamic, treatment should be adjusted accordingly
• Fluid deficit (150kg) : 23.1L, total corrected from ED till 6am : 7.2L (over 14hours)
• Possibility of false good CRT/BP/ pulse volume due to rapid fluid shift
• CXR: ARDS feature, PF ratio < 150, lung bibasal crepitations
2. Electrolyte correction
• K+/ Mg/ PO4/ Ca
• Total K+ corrected 6g @ ED, 3g @ ICU
• KH2PO4 10 mmol x 1
• Pt developed VF likely due to hypokalemia, differential myocardial infarct
• PO4 correction as PO4 will be depleted in HHS patient , further drop if supported with Noradrenaline
• Severe PO4 deficiency can worsen respiratory failure, precipitate cardiac arrhythmias and cause rhabdomyolysis

31. 3. Higher risk of cardiac event due to
• Morbid obesity
• HHS
• Hyperviscosity , Hb 18.1/ Hct 68
• S/C Fondaparinux 2.5mg x1 @ ED, S/C Clexane 60mg OD x1 @ 6am
4. Timing of starting and withhold of insulin
• Persistent low K+ < 3.0, can omit insulin for 1-2 hours, with aggressive K+ correction (max K+ correction 3g/hour via central line)
• To start IVI insulin when blood glucose persistent high despite adequate fluid resuscitation
5. High risk of rhabdomyolysis in HHS patient
• CK level
• Urine colour and output monitoring

32. 6. Calculate! Make it a habit in practice
• Proper calculation will reveal the adequacy/ inadequacy of treatment and resuscitation
• Sodium ↓ over 14 h -> 8 mmol/L (adequate)
• Serum osmolarity ↓ over 14h -> 0.71 mOsm/kg/h (inadequate)
• Serum glucose ↓ over 14 h -> 4.85mmol/L/h (adequate)
• Free water deficit -> 23.1L -> corrected 7.2L over 14 hours
Aim for gradual reduction in serum osmolality at the rate of 3-8 mosm/kg/hr.
Aim for reduction in blood glucose of 4-6 mmol/L/hr
Rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours.

33. DKA vs HHS

34. DKA HHS
• DXT >11mmol/L
• Capillary ketones >3mmol/L or
Urine ketones ≥2+
• Venous pH <7.3 and/or
HCO3 <15mmol/L
•Severe dehydration
•Marked hyperglycaemia (plasma glucose >30
mmol/L)
•Serum osmolality >320 mosmol/kg
•There is no significant ketonaemia (<3
mmol/L) or acidosis (pH>7.3, HCO3->15
mmol/L).
Effective serum osmolality = 2 (Na2+) [mmol/L] + glucose [mmol/L]

35. APPROACH TO PATIENT

36. COMMON PRECIPITATING FACTORS “5I”
Infection
(UTI/Pneumonia/skin/
abdominal)
Infarction
(Myocardial/Stroke/
Bowel infarction)
Infant on board
(Pregnancy)
Indiscretion
(Dietary non-
adherence)
Insulin deficiency
(Insulin non-compliant)

37. DKA

38. PATHOPHYSIOLOGY

39. CLINICAL PARAMETERS OF SEVERE DKA
•Venous bicarbonate <5 mmol/L
•Venous pH <7.1
•Plasma ketones >6 mmol/L
•Hypokaemia on admission <3.5mmol/L
•GCS <12
•O2 saturation <92% on air
•SBP <90mmHg
•Pulse rate >100bpm
•Anion gap >16 (Anion gap = [Na++ K+ ] – [Cl- + HCO3- ])

40. PRINCIPLES OF MANAGEMENT
•Correction of
dehydration
•Correction of
electrolyte
imbalance
Insulin
therapy
•Treatment of
precipitating
factor
•Prevention of
complications

43. AIMS OF TREATMENT
•Rate of fall of ketones of at least 0.5 mmol/L/hr, OR
•Bicarbonate rise of 3 mmol/L/hr, AND
•Plasma glucose fall of at least 3 mmol/L/hr, AND
•Maintain serum potassium within normal range.

44. CORRECTION OF DEHYDRATION
•Fluid deficits in DKA may be up to 10% of total body weight. Restoration
of circulating volume is a priority.
•SBP on admission <90 mmHg (likely due to low circulating volume,
but consider other causes such as heart failure or sepsis).
• Start administration of fluid as shown below:

45. SBP on admission is ≥90 mmHg, start administration of fluid as
shown below:

46. The rate of hydration should be guided by:
•Haemodynamic status
•State of hydration
•Serum electrolyte levels
•Urinary output
More cautious fluid replacement in:
•Young people <18 y/o
•Elderly
•Pregnant
•Existing heart or renal failure
In the above instances, consider HDU/ICU admission & insertion and monitoring via central line

47. CORRECTION OF ELECTROLYTE IMBALANCE
Potassium replacement:
Aim to maintain serum potassium between 4-5 mmol/L.
Withhold K + replacement if there is no urine output.
1 g KCl = 13.3 mmol K +
Maximum potassium replacement per hour is 40 mmol/h.

48. IV bicarbonate:
•The use of IV HCO3 - is not indicated to correct acidosis in DKA due to:
- Rise of partial pressure of carbon dioxide (pCO2 ) in cerebrospinal fluid (CSF) which may
lead to a paradoxical increase in CSF acidosis
- Delay in the fall of plasma lactate and ketone level
- Risk of cerebral oedema especially in younger age group
•IV HCO3 - may be considered if pH is persistently <6.9 despite adequate
hydration and insulin treatment

49. INSULIN THERAPY
•Start a fixed rate IV insulin infusion (FRIII): 0.1 unit/kg/hr based on estimate of
weight.
•50 units short-acting human insulin or rapid-acting insulin analogue made up to 50 ml
with 0.9% saline solution.
•Delay insulin infusion if the initial potassium <3.5mmol/L until serum potassium is
corrected.

50. MONITORING
•Measure blood ketones and capillary glucose hourly (note: if meter reads
“blood glucose Hi” venous blood should be sent to the laboratory hourly or
measured using venous blood in a blood gas analyser until the point of care
testing meter is within its QA range)
•Vital signs and input-output charting hourly
•Venous HCO3 - and K+ at 60 minutes, 2 hours and 2-hourly thereafter
•6-hourly BUSE and blood/urine ketones

51. •Review the response to FRIII hourly by calculating the rate of change of ketone level fall (or rise
in bicarbonate or fall in glucose)
•If blood ketone measurement is available and blood ketones are not falling by at least 0.5
mmol/L/hr, increase the insulin infusion rate by 1.0 unit/hr increments hourly until the ketones
are falling at target rates (also check infusion**)
•If blood ketone measurement is not available, use venous bicarbonate. If the bicarbonate is not
rising by at least 3.0 mmol/L/hr, increase the insulin infusion rate by 1 unit/hr increments
hourly until the bicarbonate is rising at this rate**
•Alternatively use plasma glucose. If the glucose is not falling by at least 3.0 mmol/L/hr, increase
the insulin infusion rate by 1.0 unit/hr increments hourly until glucose falls at this rate. Glucose
level is not an accurate indicator of resolution of acidosis in ketoacidosis, so the acidosis
resolution should be verified by venous gas analysis

52. •If ketones and glucose are not falling as expected always check the insulin infusion pump is
working and connected and that the correct insulin residual volume is present (to check for
pump malfunction)
•If the potassium is outside the reference range (4.0 – 5.5 mmol/L), assess the appropriateness of
the potassium replacement and check it hourly.
•If the glucose falls below 14.0 mmol/L, commence 10% glucose(D10%) given at 125 ml/ hour
alongside the 0.9% sodium chloride solution. In addition consider reducing the rate of
intravenous insulin infusion to 0.05 units/kg/hr.
•Continue the FRIII until the ketone measurement is less than 0.6 mmol/L and/or venous pH over
7.3
•Do not rely on urinary ketone clearance to indicate resolution of DKA, because these will still be
present when the DKA has resolved

53. RESOLUTION
Resolution is defined as:
•pH >7.3
•Plasma ketone <0.6mmol/L
Do not rely on bicarbonate alone to assess the resolution of DKA at this point due to the
possible hyperchloraemia secondary to high volumes of 0.9% sodium chloride solution. The
hyperchloraemic metabolic acidosis will lower the bicarbonate and thus lead to difficulty is
assessing whether the ketosis has resolved. The hyperchloraemic acidosis may cause renal
vasoconstriction and be a cause of oliguria.

54. HHS

55. • Hyperglycaemic hyperosmolar state (HHS) is a life-threatening emergency and should be
suspected in patients with T2DM who are very ill with significant hyperglycaemia.
• The elderly with multiple co-morbidities are prone to HHS.
• It has a higher mortality than DKA and vascular complications such as MI, stroke or
peripheral arterial thrombosis are common.
• Well-described complications such as seizures, cerebral oedema and osmotic
demyelination syndrome though uncommon can occur due to rapid changes in osmolality
during treatment.
• Whilst the presentation of DKA is rapid (within hours), HHS progresses over many days. As
a result, the dehydration and metabolic disturbances are more profound

56. Pathophysiology of HHS
American Diabetes Association. Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis and Treatment. Diabetes Care 2014; 37: 3124-3131

57. Principles of HHS treatment
1. Use intravenous (IV) 0.9% sodium chloride solution as the principle fluid to restore circulating
volume and reverse dehydration
2. Measure or calculate osmolality every hour for the first 6 hours, then 2 hourly for the next 6
hours to monitor the response to treatment and to avoid sudden osmotic shifts
3. Only switch to 0.45% sodium chloride solution if the osmolality is not declining despite
adequate positive fluid balance.
4. An initial rise in sodium is expected due to the reversal of relative pseudohyponatraemia in
the context of hyperglycaemia and is not itself an indication for hypotonic fluids.
5. The rate of change of serum sodium should not exceed 10 mmol in 24 hours
6. Underlying precipitants of HHS must be identified and treated
Joint British Diabetes Societies for Inpatient Care. The Management of Hyperosmolar Hyperglycemic State (HHS) in Adults. February 2022

58. 6. The fall in osmolality should not be more than 3.0-8.0 mOsm/kg/hr to minimise the risk of
neurological complications
7. The fall in glucose should not be more than 5.0 mmol/L/hr
8. ONLY commence insulin infusion quickly in the following circumstances:
◦ If there is HHS and ketonaemia (blood ketones >1.0 - ≤3.0 mmol/L or urine ketones < 2+) and not
acidotic (venous pH >7.3 and bicarbonate >15.0 mmol/L) then use 0.05 units/kg/hr OR
◦ If there is significant ketonaemia (blood ketones >3.0 mmol/L) or ketonuria (≥ 2+) with a pH <7.3 and
bicarbonate <15 mmol/L (i.e. mixed DKA and HHS) then use the DKA guidelines at 0.1 units/kg/hr
9. IV fluid replacement should aim to achieve a positive balance of 3-6 litres during the first 12
hours and the remaining replacement of estimated fluid loss during the following 12 hours,
although complete normalisation of biochemistry may take up to 72 hours
Joint British Diabetes Societies for Inpatient Care. The Management of Hyperosmolar Hyperglycemic State (HHS) in Adults. February 2022

59. Type of fluid
•The goal of the initial therapy is expansion of the intravascular and extravascular volume and to
restore peripheral perfusion.
•There are almost no data on the benefits or risks of particular fluid replacement regimens in
HHS.
•Rapid changes in osmolality may be harmful. 0.9% sodium chloride solution should be used as
the principle fluid to restore circulating volume and reverse dehydration because it is relatively
hypotonic compared to the serum in someone with HHS
•However, if the osmolality is no longer declining despite adequate fluid replacement with 0.9%
sodium chloride solution AND an adequate rate of fall of plasma glucose is not being achieved,
then 0.45% sodium chloride solution should be substituted.
•There are no data to justify using fluids that are less hypotonic than 0.45% sodium chloride
solution.
Joint British Diabetes Societies for Inpatient Care. The Management of Hyperosmolar Hyperglycemic State (HHS) in Adults. February 2022

60. •Fluid replacement alone (without insulin) will lower glucose concentrations which will lower
measured or calculated serum osmolality by causing a shift of water into the intracellular space.
This inevitably results in a rise in serum sodium (a fall in blood glucose of 5.5 mmol/L will result
in a 2.4 mmol/L rise in sodium). This is not necessarily an indication to give hypotonic solutions
•A rising sodium is only a concern if the osmolality is NOT declining concurrently. If the inevitable
rise in serum sodium is much greater than 2.4 mmol/L for each 5.5mmol/L fall in BG this would
suggest insufficient fluid replacement
•The aim of treatment should be to replace approximately 50% of estimated fluid loss within the
first 12 hours and the remainder in the following 12 hours. However, this will in part be
determined by the initial severity, degree of renal impairment and co-morbidities such as heart
failure, which may limit the speed of correction
•Complete normalisation of electrolytes and osmolality may take up to 72 hours
Joint British Diabetes Societies for Inpatient Care. The Management of Hyperosmolar Hyperglycemic State (HHS) in Adults. February 2022

64. Other consideration
•VTE prophylaxis
• Everyone with HHS should receive prophylactic low molecular weight heparin (LMWH) for the full duration of
admission unless contraindicated.
•Other electrolyte imbalances and complications associated with HHS
• Hypophosphataemia and hypomagnesaemia are common in HHS.
•Foot protection
• People with HHS are at high risk of pressure related foot ulceration. An initial foot assessment should be
undertaken on admission and daily during admission. Heel protectors and an appropriate mattress should be
provided for those with immobility, neuropathy, peripheral vascular disease or lower limb deformity.
•HHS can be considered to be resolved when the following criteria are met: when measured or
calculated serum osmolality falls to <300 mOsm/kg, hypovolaemia has been corrected (urine output
≥0.5 ml/kg/hr), cognitive status has returned to the premorbid state and blood glucose <15 mmol/L
•At all times, if the individual is not improving, senior advice should be sought
Joint British Diabetes Societies for Inpatient Care. The Management of Hyperosmolar Hyperglycemic State (HHS) in Adults. February 2022

67. Take home message
 For HHS with no ketosis, the main principle of treatment is fluid resuscitation followed by K+ correction then
only insulin.
 The high DXT and high serum osmolality is due to the shrinkage of intravascular volume, DXT is seemed to be
very high because of the concentrated intravascular fluid. With the fluid administration alone, serum
osmolality will reduce.
 So, when to start insulin in HHS without ketosis? When there is a positive balance but DXT remains plateau,
then can start insulin.
 So, remember run fluid first, insulin later in HHS with no ketosis.
 If ketone raised at initial point (>3.0), then can start insulin at rate of 0.1u/kg/H (use estimated weight NOT
adjusted weight). If ketone level <3.0, insulin rate is 0.05u/kg/H.
 Serum osmolality >360 is considered to be high risk. (Criteria >320 to diagnose HHS)
 Once ketone level is 0 or reduced, can actually off the insulin for 1-2H. Use this period of time, to correct the
K+

68.  K+ need to be monitored closely once start insulin infusion. Make sure to add K+ in the IVD and fast correct if
needed. If peripheral line, 1g KCL per hour. If has CVL, can correct 2-3g/H with cardiac monitoring
 Don’t forget the Phosphate, another important electrolyte. Although at initial time, it found to be within
normal range, as insulin goes in, PO4- level will be reduced. So, monitor PO4- level and correct it.
 Fluid of choice is still 0.9% NaCl as patient still has sodium loss of about 5-15mmol/L/kg. Later can be changed
to Half saline if serum Na+ level keep increasing and serum osmolality decreasing.
 Aim reduction of serum osmolality 3-8mOsm/kg/H and blood sugar 4-6mmol/L/H
 If blood pressure noted to be hypotensive while ongoing of fluid replacement, it is likely to due to intracellular
dehydration. So, need to consider re-start back the fluid resuscitation.
 Hourly DXT, Na+ (corrected Na+) and K+ monitoring. Calculate Serum osmolality Hourly too. VBG is useful tool
to guide if unable to send the blood to lab hourly.
 Strict I/O charting, make sure to chart urine output hourly

69. Thank you!

70. References
•Joint British Diabetes Societies for Inpatient Care. The Management of Hyperosmolar
Hyperglycemic State (HHS) in Adults. February 2022
•American Diabetes Association. Hyperosmolar Hyperglycemic State: A Historic Review of the
Clinical Presentation, Diagnosis and Treatment. Diabetes Care 2014; 37: 3124-3131
•Joint British Diabetes Societies for Inpatient Care. The Management of Diabetic Ketoacidosis
(DKA)in Adults. March 2023
•MOH CPG Management of T2DM (6TH edition). December 2020