Dka Vs Hhs Edit 1

NADI HOSPITAL CME
TOPIC: DIABETIC KETOACIDOSIS VS

HYPERSOMOLAR HYPERGYLCEMIC STATE
GROUP MEMBERS:
RAZEEN ALI - 20180014
MOHAMMED AWAIS KHAN 20160546
ROHIT MURARI 20180304
SHIRHA KRISHNA 20170399
RANSHIKA DEEPASHNA DEVI 20180010
ERON LAL 20180159
DIABETIC KETOACIDOSIS
• Diabetic ketoacidosis (DKA) is an acute, major, life-threatening
complication of diabetes characterized hypergylcemia, ketoacidosis,
and ketonuria.
• The presence of ketone bodies is a consistent finding in DKA.
• DKA occurs predominantly in Type 1 diabetic patients but can also
occur in Type 2 diabetes.
Criteria of DKA
According to the American Diabetes Association, the criteria for DKA is as follows:
• Plasma glucose (mg/dL)
>250 in DKA.
• Arterial pH
7.25 to 7.3 in mild DKA
7.00 to <7.24 in moderate DKA
<7.00 in severe DKA.
• Serum bicarbonate (mEq/L)
15-18 in mild DKA
10-15 in moderate DKA
<10 in severe DKA.
• Urine and serum ketones (nitroprusside reaction method)
+ in DKA.
• Effective serum osmolality (mOsm/kg)
variable in DKA.
Anion gap (mEq/L)
>10 in mild DKA
>12 in moderate and severe DKA.
• Mental status
alert in mild DKA
alert/drowsy in moderate DKA
stupor/coma in severe DKA
Etiology
The most common cause for diabetic ketoacidosis (DKA) are:
•underlying or concomitant infection
•missed or disrupted insulin treatments
•newly diagnosed, previously unknown diabetes
Causes of DKA in type 1 diabetes mellitus include the following:

•Poor compliance with insulin through the omission of insulin injections, due to lack of
patient/guardian education or as a result of psychological stress, particularly in
adolescents
•Missed, omitted or forgotten insulin doses due to illness
•vomiting or excess alcohol intake
•Bacterial infection and intercurrent illness (eg, urinary tract infection [UTI])
•Klebsiella pneumoniae (the leading cause of bacterial infections precipitating DKA)
•Medical, surgical, or emotional stress
Causes of DKA in type 2 diabetes mellitus include the following:
•
Pathophysiology
Clinical Features
The most common early symptoms of DKA are:
• insidious increase in polydipsia and polyuria.
• Malaise, generalized weakness, and fatigability
• Nausea and vomiting; may be associated with diffuse abdominal pain, decreased
appetite, and anorexia
• Rapid weight loss in patients newly diagnosed with type 1 diabetes
• History of failure to comply with insulin therapy or missed insulin injections due
to vomiting or psychological reasons or history of mechanical failure of insulin
infusion pump
• Altered consciousness (eg, mild disorientation, confusion); frank coma is
uncommon but may occur when the condition is neglected or with severe
dehydration/acidosis
Diagnosis
For the diagnosis of DKA, an initial history and rapid physical examination should focus
on:
• Airway, Breathing and Circulation (ABC ) status
• Mental status (GCS)
• Possible precipitating events (e.g. Infection, myocardial infarction and drug non-
compliance)
• Volume status
• Pathology: Venous blood gases, glucose, U&E’s, Creatinine, chloride, bicarbonate, FBC.
• Test urine for ketones. MSU/ CSU
• Ensure continuous cardiac monitoring and baseline ECG.
• Investigate for precipitant e.g. occult sepsis including abdomen, skin, feet, throat. If
sepsis clinically, likely consider blood cultures and chest X-ray and give IV antibiotics.
Early surgical consult if source controlled requires surgical procedure e.g. abscess, foot
sepsis, cholecystitis.
Management
1. Fluid
• If hypernatremia develops or is anticipated consider changing to 0.45%
sodium chloride after the first 2-3L of normal saline.
• Once glucose falls to 15mmol/l commence 5% dextrose 1L over 8 hours
• In addition continue hydration line with normal saline until rehydration
complete.
• If conscious state normal, and patient not in renal failure do not insert
IDC (increases risk of infection) but continue to monitor fluid balance
• Aim for urine output < 0.5ml/kgl/hr
2. Insulin Infusion
• Do not give bolus dose of IV insulin
• Rapid correction of hyperglycemia & hyperosmolarity may
shift water rapidly to the hyperosmolar intracellular space
and induce cerebral oedema.
• Ideal decline in capillary blood glucose is 3mmol/hr
• Insulin infusion should commence at 0.1U/kg/hr
• Actrapid 100 units in 100ml Sodium Chloride =1 unit/ml
• Insulin sticks to plastic requiring thorough priming of line,
discarding first 10-20mls before connecting to patient.
Glucose Insulin units/hr = ml/h
>25.1 mmol/l 5
20- 25 mmol/l 4
15.1- 20 mmol/l 3
10.1- 15 mmol/l 2
5-10 mmol/l 1
< 5 mmol/l Stop for 1 hour then recommence at 0.3ml/hr
• If initial potassium <4mmol/l cease infusion for short time until potassium replacement is
commenced.
• If blood glucose falls rapidly the danger is hypoglycemia( especially if initial glucose is 15-
25mmol/l) cease infusion for 1 hour and restart at lower rate.
• Aim to halve blood glucose within 8-16 hours.
• If glucose drops more rapidly, reduce insulin infusion rate by 50%.
• Hypoglycemia results in a rebound ketosis derived by counter- regulatory hormones and
necessitates a longer duration of treatment
• If glucose is dropping <3mmol/l per hour increase infusion rate and review with repeat
glucose in one hour.
• Ideal increase any plasma by bicarbonate is by 3mmol/hr.
• Insulin infusion should be continued until ketosis resolves (ketones less than 0.3/mmol/l,
pH >7.3, HCO3 >18mmol/l and patient eating and drinking regardless of serum glucose.
3. Potassium
• Do not wait to replace until serum K falls below normal.
• Check serum K , renal function and urine output
• Vomiting may affect absorption of oral potassium
Serum K mmol/l KCL infusion via infusion pump

< 3.5 20 mmol/h
3.5- 4.5 10 mmol/h

4.5- 5.5 5 mmol/h
> 5.5 Nil
Potential Complications
• Cerebral oedema( headache, drowsiness, irritability, seizures) suspect
if deterioration in conscious state despite improvement in metabolic
state. Increased incidence in children/ young adults. Requires urgent
ICU consult and mannitol/hypertonic saline therapy
• Acute renal failure
• Acute pulmonary edema
• Cardiac arrhythmia
• Hypoglycemia
• Hypokalemia
HYPEROMOLAR HYPERGLYCEMIC
STATE (HHS)
• Hyperosmolar hyperglycemic state (HHS), also known as
hyperosmotic hyperglycemic nonketotic state isa serious acute
complication of diabetes.
• It is most commonly seen in patients with type 2 DM.
• HHS is characterized by hyperglycemia, hyperosmolarity, and
dehydration without significant ketoacidosis.
Etiology
The 6 I:
1) Insulin
2) Infection
3) Inflammation
4) Infarction
5) Iatrogenic
6) Intoxication
Criteria of Hyperosmolar hyperglycemic
state
Hyperosmolar hyperglycemic state (HHS) can be diagnosed based on
these parameters:
• Serum Glucose > 56 mmol/L
• pH >7.30
• Serum bicarbonate > 15mmol/l
• Urine ketones: Absent to Minimal
• Serum osmolality >320 mOsm/kg
• Calculated osmolality [(Na + K) X2] + urea +glucose
• Neurological abnormalities frequently present
Pathophysiology
Clinical Features
Vital signs related to HHS include the following:
• Tachycardia
• Altered Mental Status
• Hypotension
• Tachypnea
• Weakness
Physical exam findings and signs related to HHS include the following:
• Altered mental status, confusion
• Lethargy
• Ill appearance
• Dry mucous membranes
• Sunken eyes
• Decreased skin turgor
• Poor capillary refill
• Weak thread pulse
• Decreased urine output
• Coma
Investigations
• Capillary Blood Glucose

• Full blood count
• UECr/ LFT
• Arterial Blood Gas
• Urine dipstick
Management
DKA Vs HHS DKA HHS
Serum Glucose <44.4 mmol/L >56 mmol/L
pH <7.3 >7.3
HCO3 <15mEq/l >15mEq/l
Urine/ Serum ketones Elevated Normal to minimal elevations
Anion Gap >12 <12
Serum Osmolarity Elevated/ Normal >320mosm/kg
Diagnostic Feature - Elevated blood glucose - Elevated blood glucose

- Increased anion gap - Increased serum osmolarity
- Increased serum ketones - Altered mental status
Other findings - Acetone breath - Altered mental status

- Kussmaul breathing - Significant dehydration
References

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NADI HOSPITAL CME

TOPIC: DIABETIC KETOACIDOSIS VS

Causes of DKA in type 1 diabetes mellitus include the following:

Serum K mmol/l KCL infusion via infusion pump

3.5- 4.5 10 mmol/h

• Capillary Blood Glucose

Serum Glucose <44.4 mmol/L >56 mmol/L

HCO3 <15mEq/l >15mEq/l

Urine/ Serum ketones Elevated Normal to minimal elevations

Anion Gap >12 <12

Serum Osmolarity Elevated/ Normal >320mosm/kg

Diagnostic Feature - Elevated blood glucose - Elevated blood glucose

Other findings - Acetone breath - Altered mental status

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