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In the Name of God, Most Gracious, Most Merciful

DIABETIC EMERGENCIES
- HYPOGLYCEMIA - HYPEROSMOLAR HYPERGLYCEMIC STATE
Dr. Mohammed Sadiq Azam Dr. D. Sudeepta Rao II yr. Postgraduates: MD (Gen Med) Deccan College of Medical Sciences

HYPOGLYCEMIA

- Dr. Mohammed Sadiq Azam

HYPOGLYCEMIA - OUTLINE
Definition Glucose Homeostasis Clinical Features Mechanisms Diagnosis Clinical Classification Hypoglycemia in DM Impact & Frequency Risk factors

Hypoglycemia asso. autonomic failure

HYPOGLYCEMIA - OUTLINE
Drugs asso. with hypoglycemia

Hyperinsulinemic hypoglycemia D/D


Endogenous hyperinsulinemia D/D, and, a word on insulinoma Hypoglycemia in Infancy & Childhood Diagnostic approach to an adult with hypoglycemia

Management Emergency management & prevention

DEFINITION
Glucose levels <55mg/dl (<3.0mmol/l) with symptoms that are relieved promptly after the glucose level is raised document hypoglycemia. Hypoglycemia is most convincingly documented by, Whipples triad, i.e:
Symptoms consistent with hypoglycemia

Low plasma glucose concentration (measured with a precise method)


Relief of symptoms when plasma glucose concentration is increased.

GLUCOSE HOMEOSTASIS Key roles


RESPONSE GLYCEMIC THRESHOLD (mg/dl) 80-85 65-70 65-70 65-70 50-55 < 50 PHYSIOLOGIC EFFECTS ROLE IN GLUCOSE REGULATION 1st line of defense (Primary glucose regulatory factor) 2nd line of defense (Primary glucose counterreg. factor) 3rd line of defense (critical when glucagon ) Defense against prolonged hypoglycemia, not critical Prompt behavioral defense(food ingestion) Compromises behavioral defense against hypoglycemia

Insulin Glucagon Epinephrine Cortisol & GH Symptoms Cognition

Ra ( Rd) Ra Ra Rc Ra Rc Recognition of hypoglycemia -----

Ra = Rate of glucose appearance, Rd = Rate of glu disappearance, Rc = Rate of glu clearance

ARTERIAL GLUCOSE

INSULIN GLUCAGON

LIVER
KIDNEY
GLUCONEOGENIC PRECURSORS GLUCOSE PRODUCTION

PANCREAS BRAIN

PITUITARY

SYM ADR OUTFLOW

MUSCLE

FAT
ARTERIAL GLUCOSE

GH
ACTH

ADR MEDULLA

E
GLU CLEARANCE INGESTION

ADR CORTEX CORTISOL Post Gn SymN NE Ach

SYMPTOMS

CLINICAL FEATURES - Symptoms


Neurogenic symptoms:
Sweaty Hungry Tingly Shaky (Tremulous) Poundy (Palpitations)

Nervy (Anxious/Nervous)
These symptoms are the result of the perception of physiologic changes caused by the ANS discharge (Adr & Chol) triggered by hypoglycemia.

CLINICAL FEATURES - Symptoms


Neuroglycopenic symptoms:
Warm Weak Confused/Difficulty thinking Tired/Drowsy Faint Dizzy

Difficulty speaking
Blurred vision

These symptoms are the result of direct CNS glucose deprivation.

CLINICAL FEATURES - Signs


Pallor Diaphoresis PR

BP
TIA occasionally (Permanent damage is rare)
The magnitude of the responses to hypoglycemia is an inverse function of the nadir plasma glucose concentration rather than the rate of decrease in plasma glucose. (Ref: Williams T. of Endo 10/e)

MECHANISMS OF HYPOGLYCEMIA
Hypoglycemia implies that the rate of glucose efflux from circulation > rate of glucose influx into circulation.
Efflux Utilisation Exercise Pregnancy Sepsis Losses Pregnancy Renal Glycosuria

Influx Endogenous glucose production in the absence of exogenous glucose delivery Most Common cause

MECHANISMS OF HYPOGLYCEMIA
Defects causing Hypoglycemia
REGULATORY ENZYMATIC SUBSTRATE

Secretion of Insulin OR Secretion of glucose counter regulatory hormones

Primary OR May result from hepatic disease

Failure to mobilize or utilize gluconeogenic substrates

DIAGNOSIS
1. Whipples triad 2. Venous plasma glucose after an overnight fast:
> 70mg/dl (>3.9 mmol/) : Normal

50 - 70 mg/dl (2.8-3.9 mmol/l) : s/o Hypoglycemia


< 50 mg/dl (<2.8 mmol/l) : => Postabsorptive hypoglycemia

3. Postprandial (=Reactive) hypoglycemia:


Diagnosis requires documentation of Whipples triad after a mixed meal (low venous plasma concentration post oral glucose load is not sufficient for diagnosis).

(Ref: Williams T. of Endo 10/e, Harrisons Principles of Int Med 17/e, 339:2308)

CLINICAL CLASSIFICATION
1. Postabsorptive (=Fasting) Hypoglycemia 2. Postprandial (=Reactive) Hypoglycemia
Significance: Reproducible hypoglycemia in the postabsorptive state, implies the presence of disease and requires diagnostic explanation and treatment. It may become apparent during the latter part of any interdigestive period (NOT necessarily in the fasting state) esp. post-exercise. Postprandial (=reactive) hypoglycemia does not usually imply a serious underlying disorder.

CLINICAL CLASSIFICATION
I) POSTABSORPTIVE (=FASTING) HYPOGLYCEMIA: 1. DRUGS:
Esp. Insulin, SU, alcohol Pentamidine, quinine

Rarely salicylates, sulphonamides


Others

2. CRITICAL ILLNESSES:

Hepatic failure
Cardiac failure Renal failure Sepsis Inanition contd

CLINICAL CLASSIFICATION
I) POSTABSORPTIVE (=FASTING) HYPOGLYCEMIA: 3. HORMONAL DEFICIENCIES:
Cortisol or GH or both Glucagon or Epinephrine

4. NON CELL TUMORS


5. ENDOGENOUS HYPERINSULINISM
Pancreatic cell disorders

cell secretagogue (eg: SU)


Autoimmune hypoglycemia (IA, IRA, ? cell Ab) ? Ectopic insulin secretion

6. HYPOGLYCEMIA OF INFANCY & CHILDHOOD

CLINICAL CLASSIFICATION
II) POSTPRANDIAL (=REACTIVE) HYPOGLYCEMIA: 1. Congenital deficiencies of enzymes of carbohydrate metabolism:
Heriditary Fructose intolerance Galactosemia

2. Alimentary Glycosuria:
Post gastrectomy

3. Idiopathic (=Functional) postprandial hypoglycemia

HYPOGLYCEMIA IN DM
IMPACT & FREQUENCY: Limiting factor in the glycemic management of DM 1. Causes recurrent morbidity in MOST cases of T1DM and MANY with T2DM and is sometimes fatal. 2. Precludes maintenance of euglycemia over a lifetime of diabetes and thus full realization of the benefits of glycemic control. 3. Causes a vicious cycle of recurrent hypoglycemia by producing hypoglycemia associated autonomic failure the clinical syndromes of defective glucose counterregulation and of hypoglycemia unawareness.

HYPOGLYCEMIA IN DM The Burden


T1DM-

Fact of life
Average of 2 episodes of symptomatic hypoglycemia per week and at least one episode of sever, at least temporarily disabling hypoglycemia each year. Estimated 2-4% of people with T1DM die due to hypoglycemia. Less frequent than T1DM.

T2DM-

Metformin, TZDs, AGIs, GLP-1 analogues, DDP-4 inhibitors should not cause hypoglycemia, however the risk increases when combined with insulin/SU.
As insulin resistance increases and patients require insulin the risk of hypoglycemia in T2DM approaches that in T1DM.

RISK FACTORS THE PREMISE


The conventional risk factors for hypoglycemia in diabetes are based on the premise that relative or absolute insulin excess is the sole determinant of risk. - Harrisons Principles of Int Med 17/e, 339:2306

Iatrogenic hypoglycemia in T1DM is the result of the interplay of therapeutic insulin excess and compromised glucose counterregulation.
-Williams T. of Endo 10/e

CONVENTIONAL RISK FACTORS


Absolute/Relative Insulin Excess occurs when:
Insulin (or secretogogue) doses are excessive, ill-timed or of the wrong type The influx of exogenous glucose is reduced (e.g., overnight fast or following missed meals/snacks) Insulin-independent glucose utilization is increased (e.g., exercise) Sensitivity to insulin is increased (e.g., improved glycemic control, in the middle of the night, late of the exercise, or with increased fitness or weight loss) Endogenous glucose production is reduced (e.g., alcohol ingestion) Insulin clearance is reduced (e.g., renal failure)

COMPROMISED GLUCOSE COUNTERREGULATION


Absolute insulin deficiency (C-peptide negativity):
cell destruction: No decrease insulin in response to fall in glucose Unknown: No increase glucagon in response to fall in glucose

H/O severe hypoglycemia/aggressive treatment per se:


Lower glucose goals, low HbA1c Attenuated autonomic activation & symptoms in response to fall in glucose.

HYPOGLYCEMIA ASSOCIATED AUTONOMIC FAILURE


Defective glucose counterregulation Hypoglycemia unawareness
Defective glucose counterregulation compromises physiologic defense, and hypoglycemia unawareness compromises behavioral defense.

DEFECTIVE GLUCOSE COUNTERREGULATION


Failure of ALL 3 lines of defense. Result of antecedent iatrogenic hypoglycemia

Glycemic threshold is shifted to lower plasma glucose concentrations.


25x or more risk of sever iatrogenic hypoglycemia during aggressive glycemic therapy .
No Insulin Glucose No Glucagon No Epinephrine Glucose

HYPOGLYCEMIA UNAWARENESS
Caused by the attenuated sympathoadrenal response (largely the sympathetic neural response) to hypoglycemia. Characterised by the loss of warning adrenergic & cholinergic symptoms that previously allowed the patient to recognise

developing hypoglycemia ad therefore abort the episode by


ingesting carbohydrates. 6x increased risk of severe iatrogenic hypoglycemia during aggressive treatment .

HYPOGLYCEMIA ASSOCIATED AUTONOMIC FAILURE


Insulin deficient diabetes (Imperfect insulin replacement)

(No insulin, No Glucagon) Antecedent hypoglycemia


Sleep Reduced sympathoadrenal responses to hypoglycemia

Antecedent exercise

Reduced sympathetic neural responses


Hypoglycemia unawareness

Reduced epinephrine responses


Defective glucose counterregulation

Recurrent hypoglycemia

ADDITIONAL RISK FACTORS T1DM


1. Insulin deficiency that indicates that insulin levels will not decrease and glucagon levels will not increase as plasma glucose falls 2. A h/o severe hypoglycemia or of hypoglycemia unawareness,

implying recent antecedent hypoglycemia, that indicates that


the sympathoadrenal response will be attenuated; and 3. Lower HbA1c levels or lower glycemic goals that, all other factors being equal, increase the probability of recent antecedent hypoglycemia.

HYPOGLYCEMIA IN T2DM
THERAPY Diet Sulphonyl urea Insulin Diet Metformin 379 922 689 297 251 N HBA1C 8.0 7.1 7.1 8.2 7.4 % ANY HYPO 3.0 45.0 76.0 2.8 17.6 % MAJOR HYPO 0.2 3.3 11.2 0.4 2.4

Ref: UKPDS, Diabetes 1995-44-1249-1258

DRUGS CAUSING HYPOGLYCEMIA


ESTABLISHED DRUGS:
DISORDER
DM Infection

DRUG
Insulin, SU, other secretogogues, metformin, alcohol Pentamidine, Quinine, Sulphonamides

Arrhythmias
Pain

Quinidine, dispyramide, cibenzoline


Acetylsalicylic acid

DRUGS CAUSING HYPOGLYCEMIA


PUTATIVE DRUGS: Fluroquinolones esp. Gatifloxacin Acetaminophen ACEI, BB (nonsel>sel), Frusemide

MAOI, Haloperidol, CPZ, Fluoxetine


Diphenhydramine, Clofibrate, Phenytoin, Pencillamine

Enflurane, Halothane, Ranitidine, Colchicine

HYPERINSULINEMIC HYPOGLYCEMIA D/D


INSULIN C-PEPTIDE PROINSULIN SU INSULIN ANTIBODY DIAGNOSIS Exogenous insulin

Insulinoma, Congenital hyperinsulinism


Suphonylurea

+/-

(Free )

(Free )

+
-

Insulin autoimmune
Insulin Receptor autoimmune (Insulin receptor Antibody +)

ENDOGENOUS HYPERINSULINEMIA
Hypoglycemia related to endogenous hyperinsulinemia can be caused by A primary pancreatic islet () cell disorder, typically a cell tumour (insulinoma), sometimes multiple insulinomas, or, esp. in infants/young children, a functional cell disorder with cell hyperplasia or without an anatomic correlate. A cell secretogogue, often a SU, theoritically a cell stimulating antibody. An antibody to insulin Ectopic insulin secretion (rare).

ENDOGENOUS HYPERINSULINEMIA
Fundamental pathophysiologic feature of endogenous hyperinsulinemia caused due to a primary cell disorder or an insulin secretogogue is failure of insulin secretion to fall to very low levels during hypoglycemia.

Critical diagnostic findings:


Plasma insulin 3 uU/ml Plasma C-Peptide concentration 0.6 ng/ml

Plasma proinsulin concentration 5.0 pmol/l, when the plasma


glucose concentration is < 55 mg/dl with symptoms of hypoglycemia.

INSULINOMA
Uncommon, 1/250,000; > 90% benign, treatable cause of

potentially fatal hypoglycemia.


Median age of presentation 50 yrs (sporadic cases), third decade in MEN 1. Symptoms:
Various combinations of diplopia, blurred vision, sweating, palpitations or weakness: 85% Confusion or abnormal behaviour: 80% Unconsciousness or amnesia: 53% Grand mal seizures: 12%

HYPOGLYCEMIA IN INFANCY/CHILDHOOD
1. Transient Intolerance of fasting:
Preterm/ SGA infants. Hypopitutrism, adrenal hypoplasia, congenital adrenal hyperplasia Ketotic hypoglycemia of childhood.

2. Hyperinsulinism:
IDM

Maternal drugs (SU,B2, adr. Agonist)


Congenital hyperinsulinism, insulinoma Misc Rh incompatibility, Beckwith Wiedemann syndrome, exchange transfusion.

HYPOGLYCEMIA IN INFANCY/CHILDHOOD
3. Enzyme defects:
CARBOHYDRATE METABOLISM :

Glycogen storage disease Types I / II/ VI


Glycogen synthase deficiency Fructose 1,6 bis phosphatase deficiency Fructose 1-phosphate aldolase deficiency Gal 1-phosphate uridyl transferase deficiency

HYPOGLYCEMIA IN INFANCY/CHILDHOOD
3. Enzyme defects:

PROTEIN METABOLISM :
Branched chain ketoacid dehydrogenase complex deficiency

FAT METABOLISM :
FA oxidation defects induding deficiencies in the carnitine cycle oxidation spiral defects ETC defects Ketogenesis sequence defects

NEONATAL HYPOGLYCEMIA
Diagnostic Criteria (Cornblath et al):
< 2.5 mmol/l (<45mg/dl) in infants with clinical

manifestations compatible with hypoglycemia, and,


<2.0 mmol/l (<30mg/dl) in infants at risk for hypoglycemia Now outdated, current guidelines suggest higher cutoff values around 50 mg/dl to prevent neonatal mortality &

morbidity.

DIAGNOSTIC APPROACH

DIAGNOSTIC APPROACH - ALGORITHM


Suspected/Documented Hypoglycemia Diabetes
Treated with: Insulin Sulphonylurea Other secretogogue Adjust regimen Document improvement and monitor
Clinical clues Drugs Organ failure Sepsis Hormone deficiencies Non--cell tumor Previous gastric Sx

No diabetes
Apparently healthy

Provide adequate glucose, treat underlying cause

Suspected/Documented Hypoglycemia < 55 mg/dl

No diabetes

Apparently healthy Fasting glucose

History Strong Insulin, Whipples triad Extended fast Weak

55 mg/dl

< 55 mg/dl

Glucose

55 mg/dl

C-peptide

C-peptide

Mixed meal
Exogenous insulin + Reactive hypoglycemia Whipples triad

Insulinoma

Autoimmune

SU
Likely Factitious

-Hypoglycemia excluded

TREATMENT
Oral treatment with glucose tablets or glucose containing fluids, candy or food is appropriate if the patient is able & willing to take these. Initial dose = 20 g of glucose

Unable to take oral foods parenteral therapy


IV glucose 25 g bolus followed by infusion guided by serial plasma glucose measurements.

Inj.Glucagon 0.1 mg sc/im can be used esp in T1DM. (it has no role in alcohol induced hypoglycemia)

Eat ASAP restore glycogen stores.

PREVENTION
Identifying & addressing the cause Encouraging SMBG by patient Education & empowerment of patient Flexible insulin or OAD regimens

Rational, individual glycemic goals


Ongoing professional guidance & support

Integrated approach between patient, family & health


care professionals

HYPEROSMOLAR HYPERGLYCEMIC STATE

- Dr. D. Sudeepta Rao

Hyperosmolar Hyperglycemic State


Dr Sudeepta Rao, PG 2nd yr Gen Med DCMS

Introduction
Hyperosmolar hyperglycemic state (HHS) and diabetic ketoacidosis (DKA) represent two distinct metabolic derangements manifested by insulin deficiency and severe hyperglycemia DKA is defined as the presence of all three of the following: (i) hyperglycemia (glucose >250 mg/dL), (ii) ketosis, and (iii) acidemia (pH <7.3) . HHS is characterized by severe hyperglycemia and hyperosmolarity. HHS and DKA are not mutually exclusive but rather two conditions that both result from some degree of insulin deficiency. They can and often do occur simultaneously

Incidence of DKA 1980-2003

Mortality rate of DKA 1980-2001

Introduction
Age adjusted mortality rates in the U.S. have dropped by 22% between 1980 and 2001 Contrary to DKA mortality, the mortality rate of HHS has remained high, ~ 15%, compared to less than 5% in patients with DKA Severe dehydration, older age, and the presence of comorbid conditions in patients with HHS, account for the higher mortality in these patients .

Definitions
DKA consists of the biochemical triad of hyperglycemia, ketonemia and metabolic high anion gap acidosis The term hyperglycemic hyperosmolar nonketotic coma has been replaced with the term hyperglycemic hyperosmolar state (HHS) 1)the hyperglycemic hyperosmolar state may consist of moderate to variable degrees of clinical ketosis detected by nitroprusside method and 2) alterations in consciousness may often be present without coma .

Pathophysiology
The underlying defects in DKA and HHS are 1) reduced net effective action of circulating insulin as a result of decreased insulin secretion (DKA) or ineffective action of insulin in HHS 2) elevated levels of counterregulatory hormones: glucagon, catecholamines , cortisol, and growth hormone, resulting in increased hepatic glucose production and impaired glucose utilization in peripheral tissues 3) dehydration and electrolytes abnormalities mainly due to osmotic diuresis caused by glycosuria 4) If insulin deficiency is severe enough, ketosis and ultimately acidosis develop .

Pathophysiology
In HHS: 1) there is enough insulin to prevent lipolysis and ketogenesis but not adequate to cause glucose utilization (as it takes 1/10 as much insulin to suppress lipolysis as it does to stimulate glucose utilization) 2) possible smaller increases in counterregulatory hormones

Hyperglycemia

Dehydration & Hyperosmolarity:


Hyperglycemia

Glycosuria

Osmotic Diuresis

Increased GFR

Dehydration

Hypovolemia

Hyper Osmolarity

Decreased GFR & Renal Glucose Loss

Hyperglycemia

Ketogenesis and Acidosis:

Precipitating Causes:

History and Physical Examination:


DKA usually evolves over a shorter period (usually less than 24 hours) than HHS, which tends to evolve over a few days. The common clinical pictures in DKA and HHS due to hyperglycemia include polyuria, polyphagia, polydipsia, weight loss, weakness and physical signs of dehydration such as dry buccal mucosa, sunken eye balls, poor skin turgor, tachycardia, hypotension and shock in severe cases. Kussmaul respiration, acetone breath, nausea, vomiting and abdominal pain may also occur primarily in DKA. Mental status in DKA may vary from full alertness to profound lethargy or coma but less frequent than HHS.

Initial Evaluation of the Patient:

Assessment of the degree of dehydration


Decreased tissue turgor suggests 5% dehydration. An orthostatic change in pulse alone suggests that there has been loss of approximately 10% of extracellular fluid volume (~2 L), orthostatic change in pulse and blood pressure (>15/10 mm Hg) suggests a 15% to 20% fluid deficit (3 to 4 L). Supine hypotension, when present, suggests either severe dehydration and a decrease in extracellular fluid volume of more than 20% or underlying sepsis. Assessment of degree of dehydration may be difficult in the elderly and those with underlying autonomic neuropathy, who may have orthostatic hypotension at baseline.

Relationship between serum osmolality and level of consciousness:

Admission Clinical And Biochemical Profile And Response To Therapy Of Comatose Vs. Non comatose Patients:

Laboratory Evaluation:
*

* Blood urea nitrogen Serum chloride Carbon dioxide, also known as CO2 Creatinine Blood glucose Serum potassium Serum sodium

Admission biochemical data in patients with HHS and DKA

Serum Sodium
The serum sodium level may be low or normal. It may even be elevated in patients who are severely dehydrated even though total body sodium is depleted. True sodium concentration (millimolar )can be obtained by multiplying excess glucose above 100 mg/dl by 1.6 /100 *. If the corrected sodium level is extremely low , hypertriglyceridemia (secondary to uncontrolled diabetes ) should be suspected.
*

Serum Potassium
Serum potassium levels at presentation may be high, normal, or low even though total body potassium may be depleted.

Unless the initial serum potassium is elevated above 5.5 mEq/L or the patient is in acute renal failure or oliguric, potassium replacement is required when treatment is initiated

Laboratory Evaluation(contd)
level of consciousness correlates more closely with serum osmolality than with pH. Coma in an individual whose serum osmolality is less than 320 mOsm/kg warrants further evaluation for other causes of the coma. Leukocytosis is a common finding in patients with DKA or HHS, but leukocytosis greater than 25,000 /L suggests ongoing infection.

Pitfalls of Laboratory Tests


elevation of serum creatinine, either as a result of dehydration or interference from ketone bodies if a colorimetric method is used. Most of the laboratory tests for ketone bodies use the nitroprusside method, which detects acetoacetate, but not hydroxybutyrate (BOHB ) . Serum ketones may be negative in some situations, such as alcoholic ketoacidosis or DKA associated with hypoxia. Under normal conditions, the ratio of -hydroxybutyrate to acetoacetate is 3:1. This increases to 8:1 in alcoholic ketoacidosis or DKA associated with severe hypoxia drugs that have sulfhydryl groups can interact with the reagent in the nitroprusside reaction, giving a false positive result. Particularly important in this regard is captopril, an angiotensin converting enzyme inhibitor prescribed for the treatment of hypertension and diabetic nephropathy.

Treatment
The goals of therapy in patients with DKA and HHS include 1) Improvement of circulatory volume and tissue perfusion, 2) Gradual reduction of serum glucose and plasma osmolarity, 3) Correction of electrolyte imbalance, and in DKA steady resolution of ketosis, 4) Identification and prompt treatment of comorbid precipitating causes

Fluid Therapy
DKA and HHS are volume-depleted states with water deficit of approximately 6 L in DKA and 9 L in HHS The initial fluid of choice is isotonic saline, which we recommend to be infused at the rate of 1520 ml /kg body weight per hour or 11.5 L during the first hour. The choice of fluid for continued repletion depends on the hydration status, serum electrolyte levels, and urinary output. In patients who are hypernatremic or eunatremic, 0.45% NaCl infused at 414 ml/kg/hour is appropriate and in patients with hyponatremia 0.9% NaCl at a similar rate is preferred.

Fluid Therapy(Contd)
The goal is to replace half of the estimated water deficit over a period of 12- 24 hours. In patients with hypotension, aggressive fluid therapy with isotonic saline should continue until blood pressure is stabilized. The administration of insulin without fluid replacement in such patients may further aggravate hypotension. Patients with DKA and HHS require calories for proper metabolism of ketone bodies.

Fluid Therapy(Contd)
Therefore in DKA, as soon as blood glucose falls below 200 mg/dl, the sodium chloride solution should be replaced with 5% glucose containing saline solution with a reduced rate of insulin administration until acidosis and ketosis are controlled while avoiding too rapid correction of hyperglycemia (which may be associated with cerebral edema especially in children) and also inhibiting hypoglycemia. In HHS, the use of D5 NS should start when blood glucose reaches 300 mg/dl, because overzealous replacement with hypotonic fluids has been associated with the development of cerebral edema

Insulin Therapy
starting with an intravenous loading dose of 0.15 U/kg body weight (usually 10 U in adults) followed by a continuous infusion of insulin at a rate of 0.1 U/kg per hour (usually 5 to 7 U per hour in adults) If the patient is in shock or the initial serum potassium level is less than 3.3 mEq/L, resuscitation with intravenous fluids or potassium replacement or both is instituted before commencing the insulin infusion An insulin infusion of 5 to 7 U per hour should lower serum glucose concentrations by 50 to 75 mg/dL per hour

Insulin Therapy
The insulin infusion rate should be continually reassessed and increased if the rate of decrease in glucose is less than 50 mg/dL per hour, providing that other causes for the lack of response to therapy have been excluded. The rate of insulin should be adjusted to maintain blood glucose between 150-200 mg/dl in DKA and 250-300 mg/dl for HHS until DKA is resolved or mental obtundation and hyperosmolar state are corrected in HHS

Potassium Therapy

Ongoing Monitoring

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