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DKA vs. HHNKS

Diabetic Ketoacidosis compared with Hyperosmolar Hyperglycemic Nonketotic Syndrome
by

Noor Sawalha

on 25 June 2013

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Transcript of DKA vs. HHNKS

Acute Complications of DM A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism.

Biochemically:
1) ketones >5 mEq/L
2) blood glucose >250 mg/dL (usually much higher)
3) pH <7.3
4) bicarbonate =<18 mEq/L (< 5 mEq/L severe DKA)
5) Ketonemia and ketonuria are characteristic

--> Venous = Arterial {pH, HCO3, K}! DKA Mainly in DM-1 , but not uncommon in DM-2.
Causes:
1) concomitant infection (40%)
2) missed insulin treatments (25%)
3) newly diagnosed diabetes (15%)

Klebsiella pneumoniae (the leading cause of bacterial infections precipitating DKA).

** in DM-2:
1) Intercurrent illness (eg, MI, pneumonia, prostatitis, UTI).
2) Meds (eg, corticosteroids, pentamidine, clozapine). Etiology Insulin deficiency --> Hyperglycemia --> Osmotic Diuresis --> Dehydration
1) Hepatic gluconeogenesis, glycogenolysis
2) increase in counter-regulatory hormones.

Hepatic metabolism (lipolysis)--> inc free fatty acids (alternative energy source)--> inc ketones, ketoacids --> Ketoniemia --> Acidosis (compensatory Kussmaul breathing)

Ketones include acetone (fruity breath), beta-hydroxybutyrate (N&V-->D), and acetoacetate. Pathophysiology *V\S:
Tachycardia, Tachypnea, Hypotension, Hpo-\hyperthermia.

*Signs of Dehydration:
Dry skin & mucous membranes
Decreased skin turgor

* Others:
Labored breathing (kussmaul)
Acetone breath odor
Decreased reflexes
Abdominal tenderness
Confusion, coma Physical Exam Blood glucose (>250mg\dl)
q1-2 h until patient is stable, then q 6 h
S.electrolyte
q1-2 h until stable, then q4-6 h
K (high\nl -->low), Na (low)
Initial (BUN)
Initial (ABG), followed w bicarbonate when needed.
Urine Dipstick Testing --> +ve for Glu & ketones (BhB). missed insulin injections.
Symptoms of precipitating factors {Polydipsia + Polyuria}
Weakness
Nausea & vomiting
Abdominal pain
Anorexia.
Altered in LOC (hyperosmolarity + dehydration + acidosis -->increased osmolarity in brain) History Treatment of DKA Hyperosmolar hyperglycemic state (HHS) Infections (pneumonia \UTI)
Stress reaction (counter regulatory hormones) to any acute illness ( stroke, silent MI, PE)
RF, CHF
Drugs
Noncompliance with oral hypoglycemics or insulin therapy
Elder abuse & neglect Etiology Pathophysiology General appearance & hygiene
Signs of dehydration ( tachycardia, hypotension, turgor ..not ortho!)
Mentation
underlying cause (fever\hypothermia ..) Physical Exam Treatment HHNKS DKA Glucose >600
No Ketones
Normal pH
Type 2 (usually)
Older patients
No change in breath Glucose >300
Urine ketones
pH 6.8-7.3
Type 1 (usually)
Younger patients
Fruity breath DKA vs. HHNKS HYPOGLYCEMIA **Clinical situation characterized by a reduction in plasma glucose concentration to a level that may induce symptoms or signs such as altered mental status and/or sympathetic nervous system stimulation.

**highly variable level, threshold <50 mg/dL SYMPTOMS
OF HYPOGLYCEMIA *If patient is conscious:
rapidly absorbed sugar

*If unconscious:
Dextrose IV (50ml of 50%DW) w N\S flush
Glucagon 1mg IM for adults


** monitor Glu q1hr, if stable q4hr
** may need 10% dextro drip to prevent recurrence Noor Al.huda Sawalha The most characteristic disturbance is total body potassium loss.
Due to:
1) Acidosis: in exchange with H--> K shifts (intracellular-->extracellular space) --> lost in urine via osmotic diuresis.
2) no Insulin to shift it into cells.

*Yet, K {low, high, normal}!

**High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia.
Na is lost in the urine during the osmotic diuresis.

***Typical overall loss: K 200-500 mEq/L, Na 300-700 mEq/L, Cl 350-500 mEq/L S.Electrolytes (pnemonia, UTI, MI) Search for signs of infection is MANDATORY in all patients! Work up Fingerstick! 2011 JBDS guideline recommends the use of venous blood rather than arterial blood in blood gas analyzers. Above 100 mg\dl Glu:
every 100 mg\dl Glu lowers Na by 1.6 mEq\L Anion Gap
elevated ([Na + K] - [Cl + HCO3] >13 mEq/L). Work up Work up (cnt'd) Pitfalls:

1) Dilutional hyponatremia d\t high glucose.
2) Factitious low glucose d\t high triglyceride.
3) Factitious elevated creatinine d\t high levels of ketones. Blood & Urine Cx
CXR
EKG
Initial isotonic NS \ LR
The recommended schedule for restoring fluids is as follows:
1-3 L 1st hr
1 L 2nd hr
1 L the following 2 hrs
1 L q 4 hrs, depending on the degree of dehydration and central venous pressure readings
if Glu <180 mg/dL use 5-10% dextrose + half isotonic sodium chloride solution.
After stabilization, switch to half-normal saline at 200-1000 mL/hr. IVFs * 1 hr after IVFs
* use only short-acting
* IV,IM>SC ICU Management 24-48hrs 20 U IM stat
followed by 6 U\hr IM Regular insulin infusion rate 6U\hr
(24 U in 60 ml NS)
When Glu<180 : rate (2-3U\hr) The optimal rate of glucose decline is 100 mg/dL/h. Do not allow the blood glucose level to fall below 200 mg/dL 1rst 4-5 hrs Insulin Electrolytes if K >6 mEq/L--> do not give KCl if K 4.5-6 mEq/L--> give 10 mEq\hr KCl if K 3- 4.5mEq/L--> give 20 mEq\hr KCl *Monitor hourly, if K>5 mEq --> stop infusion *In severe hypokalemia, not starting insulin therapy is advisable unless KCL is under way; (to avoid potential arrhythmia)
*Potassium replacement should be started with initial fluid replacement if potassium levels are normal or low. Acid-Base Balance Bicarbonate typically is not replaced as acidosis will improve with the above treatments alone. if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis.
If NaHCO3 is indicated, 100-150 mL of 1.4% concentration is infused initially.
repeated every 1\2 hour if necessary. Treatment of Concurrent Infection administration of proper antibiotics is guided by the results of culture and sensitivity studies *Hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis. Plasma glucose >= 600 mg/dL
Effective serum osmolality >=320 mOsm/kg
Profound dehydration, up to an average of 9L
pH >7.30
HCO3 >15 mEq/L
Small ketonuria & absent-to-low ketonemia
Some alteration in consciousness Diagnostic features may include the following: * most commonly in DM-2, reported in DM-1 (DK more common)

* Mortality > DKA HHS Atypical antipsychotics (clozapine)
Alcohol and cocaine
Antiarrhythmics (eg, encainide and propranolol)
Antiepileptics (eg, phenytoin)
Antihypertensives (eg, CCB)
Antipsychotics (eg, chlorpromazine,and olanzapine)
L-asparaginase Beta blockers
Corticosteroids
Diuretics (eg, chlorthalidone, ethacrynic acid, and thiazides)
Histamine-receptor blockers (eg, cimetidine)
Immunosuppressive agents
TPN & fluids w dextro Drugs effective
Insulin counterregulatory
hormones Stress Dehydration & reduced fluid intake Hyperglycemia & hyperosmolarity --> osmotic diuresis & shift into IV space --> dehydration & E loss (K, Na) * Why no ketoacidosis?!
unkown, Insulin sufficient enough to inhibit ketogenesis but not hyperglycemia! Hx of DM-2
initial presentation 30-40%
over weeks
no abd pain History Focal and Global neurologic changes:
Drowsiness and lethargy
Delirium
Coma -20%
Focal or generalized seizures
Visual changes or disturbances
Hemiparesis
Sensory deficits Plasma glucose >= 600 mg/dL (repeat q1hr)
Effective serum osmolality >=320 mOsm/kg
Profound dehydration, up to an average of 9L
pH >7.30
HCO3 >15 mEq/L
Small ketonuria & absent-to-low ketonemia
Some alteration in consciousness Diagnostic features may include the following: Work Up CBC --> eleveated Hb, Hct
CXR
Urine & Blood Cx NL range 280-290 mOsm/kg Osm = (2 × Na) + (glucose/18) + (BUN/2.8) Osmolality IVFs Admit & monitor
secure Airway Electrolytes & V-B-Gas q 2-4 hr 500-mL bolus 0.9% N\S
1-2 L isotonic saline 1st 2 hrs (higher\lower, up to 2L\1st hr) When BP & UO NL --> switch to 1\2 N\S .. when Osm< 320 --> switch back to N\S
When Glu<300 g\dl --> Dextrose 5% in .9%N\S
use pressor support in ICU
monitor UO or PCWP *Cerebral edema if rapid correction of Glu or Na Dextrose (50 mL of % dextrose in water [D50]). Coma Insulin Start after kidneys show evidence of being perfused. continuous insulin infusion of 0.1 U/kg/h
Monitor q1hr --> 3hr stable--> q2hr
Target Glu (250-300) mg/dL
Glu >350 mg/dL, increase infusion rate by 1 U/h
Glu 301-350 mg/dL, increase infusion rate by 0.5 U/h
Glu 250-300 mg/dL, do not change infusion rate.
Glu <250 mg/dL, decrease infusion rate by 0.5 U/h
Do not discontinue the insulin drip When Glu 200-300 , improved mentation for 1 day --> Tight glycemic control { Glu 80-120, HbA1c 7%} K started at =< 5 mEq/L.
Hypokalemia at the onset of rehydration requires up to 60 mEq/L to correct the K concentration.
Monitor K q 4hrs

PO4, Mg,& Ca are not replaced routinely. Electrolyte Replacement 1)documentation of low blood sugar
2)presence of symptoms
3)reversal of these symptoms when the blood sugar level is restored to normal Whipple triad Hx of insulin usage\ oral hypoglycemic
Medical history: DM, RF, LF, Alcoholism, other endocrine diseases, or recent surgery.
(CNS) symptoms: headache, confusion, and personality changes. Management
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