This document defines diabetes mellitus and provides details on the classification, signs and symptoms, epidemiology, etiology, diagnosis, and treatment of both type 1 and type 2 diabetes. Key points include:
- Diabetes is defined by hyperglycemia and can be diagnosed based on fasting plasma glucose levels, random plasma glucose levels, or oral glucose tolerance tests.
- Type 1 diabetes is characterized by an autoimmune destruction of pancreatic beta cells leading to insulin deficiency, while type 2 diabetes involves insulin resistance and relative insulin deficiency.
- Common signs and symptoms include polyuria, polydipsia, weight loss, blurred vision, and fatigue. Long-term complications affect the eyes, kidneys, nerves, and
MODY is the name given to a collection of different types of inherited forms of diabetes that usually develop in adolescence or early adulthood.
MODY stands for “Maturity-onset diabetes of the young” and was given that name in the past because it acted more like the adult type of diabetes (Type 2 Diabetes) but was found in young people.
MODY limits the body’s ability to produce insulin, but is different than the juvenile type of diabetes (Type 1 Diabetes).
When our bodies don’t produce enough insulin, it can increase blood glucose levels. High blood glucose levels lead to diabetes.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
MODY is the name given to a collection of different types of inherited forms of diabetes that usually develop in adolescence or early adulthood.
MODY stands for “Maturity-onset diabetes of the young” and was given that name in the past because it acted more like the adult type of diabetes (Type 2 Diabetes) but was found in young people.
MODY limits the body’s ability to produce insulin, but is different than the juvenile type of diabetes (Type 1 Diabetes).
When our bodies don’t produce enough insulin, it can increase blood glucose levels. High blood glucose levels lead to diabetes.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
Definition of diabetes - introduction - classification of diabetes - etiology of diabetes type 1 and type 2- risk factors for diabetes - diagnosis of diabetes - clinical manifestations of diabetes type 1 and type 2- investigations for diabetes - treatment of diabetes - non-pharmacological treatment and pharmacological treatment - pharmacotherapy of type 1 and type 2 - acute complications of diabetes and treatment
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
The Diabetic coma is one the most dangerous and again emergent case experienced during dental care delivery. Actually it mistreated and aggravated-diabetic cases resulting coma, that is categorized into Hypoglycemic coma, Diabetic ketoacidosis and Hyperosmolar coma.
Gastro esophageal Reflux Disease (GERD) and its managementDr. Ankit Gaur
In this presentation I have tried to explain in brief about gastro esophageal Reflux Disease (GERD), its etiology, risk factors, diagnosis, and its management via pharmacotherapy.
Definition of diabetes - introduction - classification of diabetes - etiology of diabetes type 1 and type 2- risk factors for diabetes - diagnosis of diabetes - clinical manifestations of diabetes type 1 and type 2- investigations for diabetes - treatment of diabetes - non-pharmacological treatment and pharmacological treatment - pharmacotherapy of type 1 and type 2 - acute complications of diabetes and treatment
CHRONIC DYSPEPSIA
Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed
Internal Medicine
College of Medicine - University of Kirkuk
The Diabetic coma is one the most dangerous and again emergent case experienced during dental care delivery. Actually it mistreated and aggravated-diabetic cases resulting coma, that is categorized into Hypoglycemic coma, Diabetic ketoacidosis and Hyperosmolar coma.
Gastro esophageal Reflux Disease (GERD) and its managementDr. Ankit Gaur
In this presentation I have tried to explain in brief about gastro esophageal Reflux Disease (GERD), its etiology, risk factors, diagnosis, and its management via pharmacotherapy.
Non-pharmacological Management of Diabetes Mellitus.pptxSamson Ojedokun
Diabetes mellitus DM, is a metabolic disorder of biomolecules characterized by chronic hyperglycemia due to defects in insulin synthesis or utilization or both
DM requires lifelong therapy. A multidisciplinary approach is needed to control glycemia, as well as to limit the development of its devastating complications and manage such complications when they do occur.
Increases cost of living and reduces life expectancy
Introduction to Diabetes & anti diabetic drug screening methodsAnurag Raghuvanshi
Diabetes is one of the most common life long disese now days & there are various works done in pharma. how dugs are developed & the animals used in this methodolgy is well brief in these slides.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
2. DEFINITION
• A metabolic syndrome characterized by
hyperglycemia
• ADA definition of DM:
1. FPG(FBS) ≥126 mg/dl,
2. NPG(RBS) ≥200 mg/dl, or
3. OGTT ≥200 mg/dl in the 2-hr sample
• Upper limit of normal FBS=100 mg/dl
• FBS= 100 to 126 mg/dl IFG
• OGTT=110 mg/dl and 200 mg/dl IFG
3. Type 1 Type 2
Age of
Onset
Usually <30 yr,
particularly childhood
and adolescence, but any
age
Usually >40 yr,
but any age
Genetic
predisposition
Moderate;
environmental
factors required for
expression: 35%-50%
concordance in
monozygotic twins;
several candidate
genes proposed
Strong; 60%-90%
concordance in
monozygotic twins;
many candidate
genes proposed;
some genes
identified in MODY
HLA
Associations
Linkage to DQA and
DQB, influenced by
DRB (3 and 4) (DR2
protective)
None
known
4. Type 1 Type 2
Other
Associations
Autoimmune; Graves'
disease, Hashimoto's
thyroiditis, vitiligo,
Addison's disease,
pernicious anemia
Heterogenous group,
ongoing subclassification
based on identification of
specific pathogenic
processes and genetic
defects
Precipitating and
Risk Factors
Largely unknown;
microbial, chemical,
dietary, other
Age, obesity (central),
sedentary lifestyle,
previous gestational
diabetes
Findings at
diagnosis
85%-90% of patients
have one and usually
more autoantibodies
to ICA512/IA-2/IA-2β,
GAD65, insulin (IAA)
Possibly complications
(microvascular and
macrovascular)
caused by significant
preceding
asymptomatic period
5. Type 1 Type 2
Endogenous
Insulin Levels Low or absent
Usually present
(relative deficiency),
early
hyperinsulinemia
Insulin
Resistance
Only with
hyperglycemia
Mostly present
Prolonged Fast Hyperglycemia, DKA Euglycemia
Stress, withdrawal
of insulin
DKA HNKS,
occasionally
DKA
6. EPIDEMIOLOGY
• Prevalence: U.S. population vs. Pima Indians
DM= 5% to 7% vs. 35%
• Incidence: 2% in 20 to 44 yr olds vs. 18% in 65
to 74 yr olds
• 8% of all legal blindness
• Leading cause of ESRD in the US
• CVS- disease: 2x the risk in non- DM patients
8. CLINICAL PRESENTATION- P/E
• Normal in early stages
• Diabetic retinopathy:
a. Non-proliferative (background diabetic
retinopathy):
1. Initially: micro-aneurysms, capillary
dilation, waxy or hard exudates, dot
and flame hemorrhages, AV shunts
9. CLINICAL PRESENTATION- P/E
2. Advanced stage: micro-infarcts with
cotton wool exudates, macular edema
b. Proliferative retinopathy: formation of
new vessels, vitreal hemorrhages,
fibrous scarring, and retinal
detachment
• Cataracts and glaucoma
10. CLINICAL PRESENTATION- P/E…
• Peripheral neuropathy:
a. Mononeuropathies- CN- III, IV, and VI
Diplopia, abnormalities of visual
fields
-intercostal nerves, and femoral nerves
b. Sensation
c. Motor- DTR, weakness and atrophy of
interossei muscles
11. CLINICAL PRESENTATION- P/E…
• Autonomic neuropathy:
a. GI disturbances: esophageal motility
abnormalities, gastroparesis, diarrhea
(usually nocturnal)
b. GU disturbances: neurogenic bladder
(hesitancy, weak stream, and
dribbling), impotence
12. CLINICAL PRESENTATION- P/E…
c. Orthostatic hypotension: postural
syncope, dizziness, light-
headedness
• Nephropathy: pedal edema, pallor,
weakness, uremic appearance
• DFU: 15% of DM pts (incidence
2%/yr), leading cause of
hospitalization
13. CLINICAL PRESENTATION- P/E…
• Neuropathic arthropathy (Charcot's
joints)
• Necrobiosis lipoidica diabeticorum:
- plaque like reddened areas
- central area that fades to white-
yellow
- on anterior surfaces of the legs;
- very thin; can ulcerate readily
14. ETIOLOGY
• Type 1 DM
• Hereditary factors:
1. ICA (in 90% of pts in the 1st yr of dx)
2. Higher incidence of HLA types DR3, DR4
3. 50% concordance in identical twins
4. Environmental factors: viral infection
(possibly coxsackie virus, mumps virus)
15. ETIOLOGY…
• Type 2 DM
• Hereditary factors: 90% concordance in identical
twins
• Environmental factor: obesity
• DIABETES 2° TO OTHER FACTORS:
• Hormonal excess: Cushing's syndrome,
acromegaly, glucagonoma, pheochromocytoma
• Drugs: glucocorticoids, diuretics, oral
contraceptives
16. ETIOLOGY…
• DIABETES 2° TO OTHER FACTORS:
• Insulin receptor unavailability (with or
without circulating Ab)
• Pancreatic disease: pancreatitis,
pancreatectomy, hemochromatosis
• Genetic syndromes: hyperlipidemias,
myotonic dystrophy, lipoatrophy
• Gestational diabetes
17. The Clinical Pattern of DM in Ethiopians
Diabetes Care. 1984 Jan-Feb;7(1):6-11, Lester FT.
• Among 849 Ethiopians with DM
• 171 -type I, 462 type II nonobese, 210 type II
obese, and 4 drug-induced
• Undernutrition (BMI less than 18 kg/m2)-
12.9%
• DKA- 7.8%
• 73%- ≤10 yr of DM, 11% - ≥15 yr, and none
>32 yr
18. The Clinical Pattern of DM in
Ethiopians
• During 7 yr, 66 (7.8%) are known to have died
(CRF 30.3%, and DKA 3%)
• ~4% with 6-10 yr DM- clinically significant
complication
• “Diabetic triopathy" at 16-20 yr - 27.7% had
nephropathy, 27.7% neuropathy, and 33.3%
retinopathy
• Cataracts- 1.4% of new DM patients, 40.7% in
>20 y DM
20. LABORATORY TESTS
1. Fasting glucose ≥126 mg/dl
2. Nonfasting plasma glucose ≥200 mg/dl
• DM- nephropathy- microalbuminuria -
2 to 3 elevated levels within 3- to 6-
months
• Yearly fasting serum lipid panel, serum
creatinine, and electrolytes
21. NONPHARMACOLOGIC THERAPY
• Diet - Calories
- 15 cal/lb of ideal body weight;
- 20 cal/lb for an active person and
- 25 cal/lb for heavy physical labor
- 50% to 60% carbohydrates, <30%
fat, 15% to 20% protein
22. NONPHARMACOLOGIC THERAPY…
• Glycemic index
• Fibers: delay glucose absorption and
attenuate the postprandial serum glucose
peak
• Lower the elevated triglyceride level often
present in uncontrolled diabetics(20 to 35
g/day of soluble and insoluble fiber)
23. NONPHARMACOLOGIC THERAPY…
• Sodium restriction: -2400 to 3000 mg/d
- <2400 mg/d- If hypertensive
- <2000 mg/d- nephropathy and htn
• Exercise
• Weight loss
• Screening for nephropathy, neuropathy,
and retinopathy
24. OHA’s
• OHA’s (metformin, sulfonylureas, repaglinide
& acarbose , miglitol, pioglitazone &
rosiglitazone )
• Sitagliptin- inhibits the enzyme DPP-4
(inactivates and degrades GLP-1 & GIP)
↑insulin synthesis and release and decrease
glucagon production
• ↓HbA1c of 0.5% vs. 1.5% for metformin
25. INSULIN
• Injectable/Inhaled insulin
• ~50% to 60%- long-acting insulin- 1-2x/d,
• 40% to 50%- short/rapid acting (aspart,
lispro> regular)
• Bedtime insulin glargine -↓risk of nocturnal
hypoglycemia and less weight gain
• Insulin detemir - long-acting insulin analog
• not associated with weight gain
26. THERAPY
• Pramlintide (Symlin), synthetic analog of
human amylin
• Exenatide (Byetta), synthetic peptide ,
stimulates release of insulin
• CSII, or insulin pump- DM presenting in
childhood/adolescence /pregnancy
• ASA- 81 mg/d
• Strict lipid control (LDL<70 mg/dl)
27. CHRONIC COMPLICATIONS
• Diabetic retinopathy is - ~15% at 15
yr, increases 1%/yr after diagnosis
• Neuropathy in type 2 DM- ~70% to
80%
• Nephropathy- 35% to 45% in type 1
DM and 20% in type 2 DM
28. PREVENTION
• DCCT- intensive treatment- ↓risk of
retinopathy, nephropathy, and neuropathy
by 35% to 90%
• Annual ophthalmologic examination
• Podiatric care
• HbA1C- twice yearly
• Microalbumin - yearly
• Creatinine and serum-lipid panel - yearly
29. DKA
• Severe dehydration and alterations in sensorium
resulting from severe insulin deficiency
• Mortality: ~ 2-4 % in adults; ↑as age > 50 (5% to
10%)
• ~ 0.2-0.4% in children; mostly 2⁰ to cerebral
edema
• Children <10 yr, DKA 70% of DM related
deaths
• Cerebral edema occurs in 1% of episodes of DKA
in children; mortality rate of 40% to 90%.
33. Pathophysiology...
• Insulin action in normal host
–Decrease blood glucose via decreasing
hepatic glucose production
–Decrease ketone production via
decrease in lipolysis and glucagon
secretion
–Peripheral tissue utilization of glucose
34. Pathophysiology...
• The antilipolytic action of insulin occurs
at much lower concentrations of insulin
than does it’s glucose lowering effects
–Any dose of insulin that corrects sugars
should correct ketoacid production
–No ketoacid production in Type II as these
diabetics have small amounts of
endogenous insulin
35. Pathophysiology...
• Presence of ketones GI symptoms
stop drinking and get sick faster
–1-2 days in DKA VS 1 week in HHS
• 3 Ketones
–Acetoacetate captured on urine dip and
levels increase as DKA resolves
–Beta-hydroxy-butyrate main ketone
(75%) in DKA, often not measured directly
–Acetone “fruity breath” in 5% pt’s
36. CLINICAL PRESENTATION
• Evidence of dehydration
• Clouding of mental status
• Kussmaul's respiration
• Fruity breath odor
• Lipemia retinalis in some patients
• Possible evidence of precipitating factors
• Abdominal or CVA tenderness in some
patients
38. Feature DKA HNKS
Age of patient Usually <40 yr Usually >60 yr
Duration of symptoms Usually <2 days Usually >5 days
Serum glucose Usually <800 mg/dl Usually >800 mg/dl
Serum Na+ Likely normal or low Likely normal or high
Serum HCO3 Low Normal
Ketone bodies At least 4 + in 1:1 dilution <2 + in 1:1 dilution
pH Low Normal
Serum osmolality Usually <350 mOsm/kg Usually >350 mOsm/kg
Cerebral edema Occasionally clinical
symptoms
Rarely (never?) clinical
Prognosis 3%-10% mortality 10%-20% mortality
Subsequent course Insulin therapy required
in almost all cases
Insulin therapy not
required in most cases
39. LABORATORY TESTS
• Pco2 <40 mm Hg
• 1. Serum HCO⁻₃ <18 mEq/L.
2. Serum K⁺ may be low, normal, or high
3. Serum Na⁺ is usually decreased
(hyperglycemia, dehydration, and
lipemia)
4. Calculate AG: AG = Na+ - (Cl- + HCO-3)
40. LABORATORY TESTS…
• CBC with differential, urinalysis,
urine and blood cultures to rule out
infectious precipitating factor
• Serum Ca⁺, Mg⁺, and P0₄⁻
• BUN and creatinine
• Amylase, liver enzymes if abdominal
pain
43. NONPHARMACOLOGIC THERAPY
• Monitor mental status, vital signs, and urine
output qh until improved, then monitor q2 to
4h
• Monitor electrolytes, renal function, and
glucose level
44. DKA: Management Goals
• Replacement of fluid deficits
• Resolution of metabolic
ketoacidosis (pH >7.3, AG < 12, BG <12)
• Correction of electrolyte
abnormalitiesHCO3 >18
• Diagnose and treat coexisting
illnesses
• Prevent complications
45. FLUID REPLACEMENT
• “Focus on shock NOT sugar”
– Average deficit is 100ml/kg or 5-7L
– Fluid loss 2⁰ to osmotic diuresis
• Fluid resuscitation alone will lead to
improvements in acidosis and blood sugar
– ~80% reduction of BG in 1st 4 hr of therapy is
from fluids alone
• First step is to attain euvolemia
46. FLUID REPLACEMENT…
• If the patient is “shocky”- IV NS 1-2 L/hr
• Rough guide: correct ½ deficit in 1st 8-12
hrs and the remainder over 12-16hrs:
–IV NS 500 ml/hr X 4hr
–IV NS 250 ml/hr X 4hr
–Change to D5NS or D10 when BS < 14
mmol/L
• If Na is normal or elevated ½ NS
47. DKA: R. Insulin(0.1U/Kg/hr)
• Insulin is used to treat acidemia/ketonemia
– The effects on blood sugar are secondary
– Average time to clearance: 18 hours
– No rush to start insulin, no need to give large
amounts up front
– Find out serum potassium before starting
insulin
– Titrate insulin drip against the anion gap,
serum ketones
48. Serum Potassium Action
< 3.3 Hold Insulin
Give 40 mmol/L KCL if
u/o
3.3-5 Start insulin drip
KCL @ 10-40 mmol/L
>5 Start insulin drip
Hold potassium, re-
check K in 2 hr
49. HKNS
• A state of extreme
hyperglycemia, marked
dehydration, serum
hyperosmolarity, altered mental
status, and absence of
ketoacidosis
50. CLINICAL PRESENTATION
• Evidence of extreme dehydration
• Neurologic defects (reversible
hemiplegia, focal seizures)
• Evidence of precipitating factors
(pneumonia, infected skin ulcer)
• Coma (25% of patients), delirium
51. ETIOLOGY
• Infections, 20% to 25%
• New or previously unrecognized diabetes (30%
to 50%)
• Reduction or omission of diabetic medication
• Stress (MI, CVA)
• Drugs: diuretics (dehydration), phenytoin,
diazoxide (impaired insulin secretion),
glucocorticoids, chemotherapeutic agents,
calcium channel blockers, TPN, substance abuse
(alcohol, cocaine)
53. LABORATORY TESTS
• Serum glucose usually >600 mg/dl,
serum/urine ketones absent or “small.”
• Serum osmolarity usually >320 mOsm/L
• Serum Na: may be low, normal, or high
• Serum K: may be low, normal, or high (body
deficit ~5 to 15 mEq/kg)
• Serum HCO₃: usually >15 mEq/L (average is
17 mEq/L)
54. LABORATORY TESTS…
• Arterial pH: usually >7.3
• BUN: (60 to 90 mg/dl)
• ↓PO₄⁻ (average deficit is 70 to 140 mm)
• ↓Ca (average deficit is 50 to 100 mEq)
• ↓Mg (average deficit is 50 to 100 mEq)
• CBC with differential, urinalysis, blood and
urine cultures should be performed to rule
out infectious etiology
56. MANAGEMENT
• Fluid replacement: 1000 to 1500 ml/hr 0.9% NS
for the initial 1 to 2 L; then 500 ml/hr
• Serum glucose 300 mg/dl 5% DW with 0.45%
NS
• Replace electrolytes and monitor serum levels
frequently (e.g., serum Na and K q2h for 12 hr)
• Continuous ECG monitoring and urinary output
Qhr
• Severe hypoK (<3.3 mEq/L) 40 mEq of K/hr
until K is >3.3 mEq/L.
57. MANAGEMENT
• Correct glucose by at least 50 to 100
mg/dl/hr
• Vigorous IV hydration by 80 mg/dl/hr;
• Regular insulin IV bolus (0.15 U/kg of body
weight)
• Insulin infusion- 0.1 U/kg/hr till BS ~300
mg/dl; then regular SC insulin (sliding scale)
• BS q1-2h in the initial 12 hr