Hyperosmolar hyperglycemicHyperosmolar hyperglycemic
non ketotic comanon ketotic coma
1
Presented By: Irum Siddiquie
2
Hyperosmolar hyperglycaemic state (HHS) occurs in
people with type 2 diabetes. Very high blood
glucose levels (often over 50 mmol/L (900 mg/dl).
HHS is characterised by
severe hyperglycaemia with marked serum
hyperosmolarity, without evidence of significant
ketosis. HHS is a potentially life-
threatening emergency.
PATHOPHYSIOLOGY
3
4
Ketosis does not occur due to the
presence of basal insulin secretion
sufficient to prevent ketogenesis, but
insufficient to reduce blood glucose.
Why basal insulin secretion
continues in type 2 diabetes?
5
The infrequency of ketoacidosis and milder
presentation in type 2 diabetes is presumably
because of higher portal insulin levels in these
patients than in type 1 diabetics which
prevents un-restricted hepatic fatty acid
oxidation and keep the formation of
ketonebodies in check.
6
In the decompenstated state,these
patients may develop hyperosmolar non
ketotic coma due to severe dehydration
resulting from sustained osmotic diuresis
(particularly in patients who donot drink
enough water to compensate for urinary
losses from chronic hyperglycemia).
7
HHS usually presents in older patients with
type 2 DM and carries a higher mortality than
DKA, estimated at approximately 10-20%.
8
This is because of absent of
ketoacidosis and its
symptoms( nausea,vomiting,respir
atory difficulties) delay in
seeking of medical attention until
severe dehydration and coma
occurs.
9
Precipitating factors
10
Common in elderly diabetics.
Noncompliance with treatment
Inability to drink sufficient water to keep up with urinary
losses
Infections
Stroke
Steroids and immunosuppressant agents
Diuretics
Sometimes therapeutic procedures such as peritoneal or
hemodialysis,tube feeding of high protein formulas,and high
carbohydrates infusion.
What Are the Early Symptoms of Diabetic Coma?
Early symptoms that may lead to diabetic coma if
not treated include:
Increased thirst
Increased urination
Weakness
Drowsiness
Altered mental state
Headache
Restlessness
Inability to speak
Paralysis
11
Difference b/w DKA and HHS
12
Non-ketotic Hyperglycemic Coma
13
Diagnosis of HHS
14
•Elavated blood glucose ( >50 mmol/l (900 mg/dl))
•Elevated plasma osmolality
Normal serum osmolarity is 290 ± 5 mOsm per L. A rough approximation of
the measured value can be obtained as follows:
•Profound dehydration, up to an average of 9L
•Serum pH greater than 7.30
•Bicarbonate concentration greater than 15 mEq/L
•Small ketonuria and absent-to-low ketonemia
•Some alteration in consciousness
Important investigations
15
The following are important but should not delay the institution of
intravenous fluids and insulin replacement:
•Venous blood: for urea and electrolytes , glucose,bicarbonate.
•Arterial blood gases: to assess severity of acidosis.
(the severity of ketoacidosis can be assessed rapidly by measuring the venous
plasma bicarbonate;less than 12mmol/l indicates severe acidosis.the hydrogen
ion gives a more precise measure and requires arterial blood.
•Urinanlysis for ketones: (a meter is available to quantify ketones in plasma,
and a test strip can be used as a semiquantitative guide to plasma
concentration of acetoacetate and acetone.)
•ECG
•Anion gap : Normal range: 8 to 16 meq/L 
= [Na+] - [Cl-] - [HCO3-]
or alternative formula:
AG = [Na+] + [K+] - [Cl-] - [HCO3-]. 
•Infection screen: full blood count
blood and urine culture
c-reactive proteins, CXR.
(altough leucocytosis invariably occurs ,this represents a
stress response and does not necessarily indicates infection.
16
Detection and treatment of an underlying illness are critical.
Standard care for dehydration and altered mental status is
appropriate, including airway management, intravenous (IV) access,
crystalloid administration.
Although many patients with HHS respond to fluids alone, IV
insulin in dosages similar to those used in DKA can facilitate
correction of hyperglycemia.
Insulin used without concomitant vigorous fluid replacement
increases the risk of shock.
Management
• Aim:
1. Restoration of circulatory volume and
tissue perfusion.
2. Replacement of fluid loses and correction
of total fluid deficits.
3. Correction of hyperglycemia and serum
hyperosmolarity.
4. Replacement of electrolyte losses.
17
Approach to Treatment….
18
19
The principal goal at the outset of therapy must be restoration of the
intravascular volume to assure adequate perfusion of vital organs.
It remains controversial whether 0.9% or 0.45% NaCl should be the initial
fluid infused intravenously. We prefer to administer 0.9% NaCl until the
vital signs have stabilised and then substitute 0.45% NaCl.
10 to 15 units of regular human insulin should be injected as a bolus,
followed by a continuous infusion of approximately 0.1 U/kg/h. Once the
blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5%
dextrose should be added to the intravenous fluids and the rate of insulin
infusion reduced.
Following recovery many patients presenting with HHNS will not require
long term insulin therapy and can be managed effectively with diet or oral
agents.
http://www.ncbi.nlm.nih.gov/pubmed/2680438
20
The rate of fluid replacement is adjusted on the basis of central venous
pressure, and plasma sodium concentration should be checked frequently.
Complications
Thromboembolic complications are common,and prophylactic subcutaneous
low molecular weight heparin is recommended.
Disseminated intravascular coagulation .(rare)
Cerebral edema due to very rapid reduction in blood glucose, use of
hypotonic fluids and/or bicarbonate.
High mortality
Treat with mannitol ,oxygen.
Acute circulatory failure.
Ongoing Monitoring
21
Summary
Actual intervention
• Administer intravenous fluids and electrolytes
(initial fluids will be administered rapidly).
• Administering rapid acting insulin.
• Maintain flow sheet documenting laboratory and
physiologic parameter.
• Monitor central and peripheral perfusion.
• Monitor fluid balance.
22
Actual interventions
• Provide skin (especially foots) and oral care.
• Monitor heart rate and rhythm.
• Perform active or passive range of motion exercises.
• Institute seizures precautions.
• Prevent hypoglycemia by monitoring trend of lab data
and changing the fluids to dextrose 5% when Blood
Sugar (250-300mg/dl).
• Initiate self-care education to prevent recurring crises
including causes, sign and symptoms, treatment, and
prevention of hyperglycemia. Include strategies for
managing a minor illness.
23
Evaluation
• Plasma glucose < 250mg/dl.
• Other lab results within normal (plasma
osmolality , BUN, electrolyte, PH, plasma and
urine ketoacids, plasma bicarbonate).
• Alert and oriented.
• Adequate hydration.
• Vital signs within patient's normal range.
• Able to tolerate oral liquid feedings.
24
Thank youThank you
25

Honk

  • 1.
    Hyperosmolar hyperglycemicHyperosmolar hyperglycemic nonketotic comanon ketotic coma 1 Presented By: Irum Siddiquie
  • 2.
    2 Hyperosmolar hyperglycaemic state(HHS) occurs in people with type 2 diabetes. Very high blood glucose levels (often over 50 mmol/L (900 mg/dl). HHS is characterised by severe hyperglycaemia with marked serum hyperosmolarity, without evidence of significant ketosis. HHS is a potentially life- threatening emergency.
  • 3.
  • 4.
    4 Ketosis does notoccur due to the presence of basal insulin secretion sufficient to prevent ketogenesis, but insufficient to reduce blood glucose.
  • 5.
    Why basal insulinsecretion continues in type 2 diabetes? 5
  • 6.
    The infrequency ofketoacidosis and milder presentation in type 2 diabetes is presumably because of higher portal insulin levels in these patients than in type 1 diabetics which prevents un-restricted hepatic fatty acid oxidation and keep the formation of ketonebodies in check. 6
  • 7.
    In the decompenstatedstate,these patients may develop hyperosmolar non ketotic coma due to severe dehydration resulting from sustained osmotic diuresis (particularly in patients who donot drink enough water to compensate for urinary losses from chronic hyperglycemia). 7
  • 8.
    HHS usually presentsin older patients with type 2 DM and carries a higher mortality than DKA, estimated at approximately 10-20%. 8
  • 9.
    This is becauseof absent of ketoacidosis and its symptoms( nausea,vomiting,respir atory difficulties) delay in seeking of medical attention until severe dehydration and coma occurs. 9
  • 10.
    Precipitating factors 10 Common inelderly diabetics. Noncompliance with treatment Inability to drink sufficient water to keep up with urinary losses Infections Stroke Steroids and immunosuppressant agents Diuretics Sometimes therapeutic procedures such as peritoneal or hemodialysis,tube feeding of high protein formulas,and high carbohydrates infusion.
  • 11.
    What Are theEarly Symptoms of Diabetic Coma? Early symptoms that may lead to diabetic coma if not treated include: Increased thirst Increased urination Weakness Drowsiness Altered mental state Headache Restlessness Inability to speak Paralysis 11
  • 12.
  • 13.
  • 14.
    Diagnosis of HHS 14 •Elavatedblood glucose ( >50 mmol/l (900 mg/dl)) •Elevated plasma osmolality Normal serum osmolarity is 290 ± 5 mOsm per L. A rough approximation of the measured value can be obtained as follows: •Profound dehydration, up to an average of 9L •Serum pH greater than 7.30 •Bicarbonate concentration greater than 15 mEq/L •Small ketonuria and absent-to-low ketonemia •Some alteration in consciousness
  • 15.
    Important investigations 15 The followingare important but should not delay the institution of intravenous fluids and insulin replacement: •Venous blood: for urea and electrolytes , glucose,bicarbonate. •Arterial blood gases: to assess severity of acidosis. (the severity of ketoacidosis can be assessed rapidly by measuring the venous plasma bicarbonate;less than 12mmol/l indicates severe acidosis.the hydrogen ion gives a more precise measure and requires arterial blood. •Urinanlysis for ketones: (a meter is available to quantify ketones in plasma, and a test strip can be used as a semiquantitative guide to plasma concentration of acetoacetate and acetone.) •ECG •Anion gap : Normal range: 8 to 16 meq/L  = [Na+] - [Cl-] - [HCO3-] or alternative formula: AG = [Na+] + [K+] - [Cl-] - [HCO3-].  •Infection screen: full blood count blood and urine culture c-reactive proteins, CXR. (altough leucocytosis invariably occurs ,this represents a stress response and does not necessarily indicates infection.
  • 16.
    16 Detection and treatmentof an underlying illness are critical. Standard care for dehydration and altered mental status is appropriate, including airway management, intravenous (IV) access, crystalloid administration. Although many patients with HHS respond to fluids alone, IV insulin in dosages similar to those used in DKA can facilitate correction of hyperglycemia. Insulin used without concomitant vigorous fluid replacement increases the risk of shock.
  • 17.
    Management • Aim: 1. Restorationof circulatory volume and tissue perfusion. 2. Replacement of fluid loses and correction of total fluid deficits. 3. Correction of hyperglycemia and serum hyperosmolarity. 4. Replacement of electrolyte losses. 17
  • 18.
  • 19.
    19 The principal goalat the outset of therapy must be restoration of the intravascular volume to assure adequate perfusion of vital organs. It remains controversial whether 0.9% or 0.45% NaCl should be the initial fluid infused intravenously. We prefer to administer 0.9% NaCl until the vital signs have stabilised and then substitute 0.45% NaCl. 10 to 15 units of regular human insulin should be injected as a bolus, followed by a continuous infusion of approximately 0.1 U/kg/h. Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Following recovery many patients presenting with HHNS will not require long term insulin therapy and can be managed effectively with diet or oral agents. http://www.ncbi.nlm.nih.gov/pubmed/2680438
  • 20.
    20 The rate offluid replacement is adjusted on the basis of central venous pressure, and plasma sodium concentration should be checked frequently. Complications Thromboembolic complications are common,and prophylactic subcutaneous low molecular weight heparin is recommended. Disseminated intravascular coagulation .(rare) Cerebral edema due to very rapid reduction in blood glucose, use of hypotonic fluids and/or bicarbonate. High mortality Treat with mannitol ,oxygen. Acute circulatory failure.
  • 21.
  • 22.
    Summary Actual intervention • Administerintravenous fluids and electrolytes (initial fluids will be administered rapidly). • Administering rapid acting insulin. • Maintain flow sheet documenting laboratory and physiologic parameter. • Monitor central and peripheral perfusion. • Monitor fluid balance. 22
  • 23.
    Actual interventions • Provideskin (especially foots) and oral care. • Monitor heart rate and rhythm. • Perform active or passive range of motion exercises. • Institute seizures precautions. • Prevent hypoglycemia by monitoring trend of lab data and changing the fluids to dextrose 5% when Blood Sugar (250-300mg/dl). • Initiate self-care education to prevent recurring crises including causes, sign and symptoms, treatment, and prevention of hyperglycemia. Include strategies for managing a minor illness. 23
  • 24.
    Evaluation • Plasma glucose< 250mg/dl. • Other lab results within normal (plasma osmolality , BUN, electrolyte, PH, plasma and urine ketoacids, plasma bicarbonate). • Alert and oriented. • Adequate hydration. • Vital signs within patient's normal range. • Able to tolerate oral liquid feedings. 24
  • 25.