HYPEROSMOLAR HYPERGLYCAEMIA
HONK (<10% present with coma)
HHS: Hyperosmolar hyperglycaemic state
HHNS: Hyperosmolar hyperglycaemic Nonketotic State
USUALLY SEEN IN:
Undiagnosed or poorly controlled TYPE 2 DM
FEATURES:
SEVERE hyperglycaemia: Glucose > 30
Calculated osmolality > 315mOsm/L
pH > 7.3 (may be more acidaemic)
HCO3- >15
Small ketones (may be large)
Anion gap < 12 (however 50% have raised AG Met Acidosis)
Alteration in mental state: common
MORTALITY = MUCH HIGHER THAN DKA (15-30% vs 5%)
Main difference with DKA = metabolism of lipids during insulin deficiency
DKA:
More lipolysis  more ketones formed  main cause of acidosis
HHNS:
Acidosis more likely due to
Lactate: hypoperfusion
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Starvation ketosis
} in various combinations
Renal failure
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NB: MIXED ACID BASE patterns may be seen
SHARED FEATURES:
 Hyperglycaemia
 Hyperosmolarity
 Severe volume depletion
 Electrolyte disturbance
 Acidosis (only sometimes)
PATHOPHYSIOLOGY
Relative insulin resistance in T2DM  hyperglycaemia + hepatic gluconeogenesis
Osmotic diuresis  volume depletion (if no free access to H20 eg N.home Pt)
Eventually: dehydration  ARF  unable to excrete glucose
MECHANISM BEHIND LACK OF KETONES = POORLY UNDERSTOOD
TRIGGERS: Often INSIDIOUS ONSET
Concomitant illness: ESPEC PNEUMONIA & UTI (30-50% of cases)
Non-compliance
Anything that predisposes to:
Hyperglycaemia
Dehydration
Eg: Drugs
Li+, B-blockers, Glucocorticoids, Ca2+ blockers, Mannitol, Phenytoin, many others
Conditions:
DM, Pancreatitis, GIT bleed, PE, Heat illness, Iscaemic gut, AMI, Infection, Burns,
CRF, Dialysis, CVA, Rhabdo
In view of frequency of precipitating causes & underlying associated medical
problems: A WIDE RANGE OF ANCILLARY TESTS SHOULD BE
CONSIDERED:
Bld Cultures
MSU
Lipase
CK/Trop
TFT
Coags
CxR
ECG
+/- CT, LP, Tox studies
ELECTROLYTE ISSUES:
HYPOKALAEMIA: MAIN IMMEDIATE RISK
Drops further with volume replacement  REQUIRES REPLACEMENT
MAKE SURE YOU CORRECT IF ACIDAEMIC
Initial K+ < 3.3 = treat (as will drop as soon as fluid started), otherwise wait til
U.O. starts, IV up to 10-20mEq/hr
STILL NEED TO CORRECT SODIUM FOR ELEVATED GLUCOSE
OFTEN HAVE MIXED ACIDOSIS/ALKALOSIS
MAY HAVE “NORMAL” pH BUT WITH SEVERE METABOLIC
DERANGEMENT (ie acidosis/alkalosis cancel each other out)
OSMALRITY
> 300 = ABNORMAL
> 320 = ABNORMAL MENTAL STATE
TREATMENT:
1) VOLUME REPLACEMENT
a. Alone can  glucose by 80%
b. Av. H20 defecit = 20-25% of TBW
c. ½ in 1st 12 hours, rest over 24hrs
d. Caution: renal/cardiac failure
e. Risk of cerebral oedema with >50ml/kg in 1st 4 hrs
2)
3)
4)
5)
TREAT CAUSE/TRIGGER
TREAT ELECTROLYTE ABNORMALITIES
GRADUAL REDUCTION OF GLUCOSE
INSULIN – LAST TREATMENT
a. Given early  drags H20 into cells  risk of further intravascular
depletion & CVS collapse
b. Subcut unreliable  give IV 0.1U/kg/hr