Obesity + DM (Lea) Flashcards

(132 cards)

1
Q

What is obesity?

A

Obesity is a disorder of energy balance
Defined as 20% or more above ideal weight
Measured by Body Mass Index (BMI)
“A complex, multifactorial disease”
Weight (kg)/ (m)2 = BMI

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2
Q

BMI Classification

A
  • Underweight <18.5
  • Normal 18.5-24.9
  • Overweight 25-29.9
  • Obese I 30-34.9
  • Obese II 35-39.9
  • Obese III (Morbid) > 40
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3
Q

Children and body weight class

A

Weight class Percentile
Overweight 85-94th
Obese 95-98th
Severely Obese 99th

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4
Q

Ideal Body Weight

A

Men IBW (kg) = height (cm)- 100
Women IBW (kg) = height (cm)-105

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5
Q

Android vs. Gynecoid

A

Android: associated with increase risk of ischemic heart disease, hypertension, dyslipidemia and death
Gynecoid: associated with joint disease and varicose veins
Apples (android) or pears (gynecoid)

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6
Q

Metabolic Syndrome

A

Cardiovascular risk is 50-60% higher than in the general population
Requires at least three of the following:
Large waist >40” men >35” women
Triglycerides > 150 mg/dl
High Density Lipoprotein <40 m < 50 w
BP > 135/80
Fasting BS > 100mg/dl

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7
Q

Respiratory Effects of Obesity

A

Causes a restrictive ventilatory defect
Lungs are compressed lung volumes and compliance is reduced
Increase in pulmonary blood flow also reduces compliance
Lung inflation is inhibited by chest fat that compresses the ribcage and prevents outward expansion
Abdominal fat shifts the diaphragm towards the head

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8
Q

FRC is inversely proportional to ____

A

BMI

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9
Q

GA causes the FRC to decrease by ___

A

50% in the obese patient compared to 20% in non obese

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10
Q

Increase O2 consumption and decrease FRC leads to ______.

A

rapid desaturation

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11
Q

Restrictive Lung pattern causes

A

Decreased Lung Compliance
Increased O2 consumption and CO2 production
Increased weight in the chest increased work of breathing results in a rapid shallow breathing pattern
A high CO2 in an obese patient signals impeding respiratory failure

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12
Q

Obesity and Lung Volumes

A

Decreased FRC
Decreased vital capacity and TLC
Decreased Expiratory reserve volume
Normal residual volume

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13
Q

Optimal tidal volume for the obese patient

A

6-8 ml/kg of Ideal Body Weight
Lungs do NOT grow in proportion to body mass
Increase RR to maintain PaCO2

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14
Q

Strategies to optimize anesthesia for obese patients

A
  • Increased O2 consumption and Decreased FRC = rapid desaturation
  • Pre Oxygenated with 100% until end tidal O2 > 90 %
  • Head Elevated Laryngoscopy Position (HELP) Aligns the oral pharyngeal and laryngeal axes
    A horizontal line drawn for the sternal notch to the external auditory meatus
  • Reverse Trendelenburg relieves the pressure on the chest and improves the FRC
  • Utilize on induction and extubation
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15
Q

How do we prevent Atelectasis?

A

Keep FiO2 < 80% Prevent absorption atelectasis
Recruitment maneuver (Valsalva) 40 cmH2O for 10 sec, may decrease BP and HR
PEEP 5-15 cmH2O

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16
Q

Postop Hypoxemia is highest risk for ___
How can we prevent it?

A

Highest risk in OSA patients
Minimize risk by:
CPAP or BiPAP after extubation esp if used at home
Elevate HOB 30 degrees
Early ambulation
Control surgical pain (non-opioid and regional to minimize resp depression)

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17
Q

Morbid obesity and aspiration…what’s the deal?

A

Obesity alone does not mandate RSI
RSI should be made on other individual risk factors of GERD and DM

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18
Q

Cardiovascular effects of Obesity

A

Two Key Changes
Expansion of intravascular volume
High cardiac output

HR is usually unchanged, SV and CO increase

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19
Q

Common EKG Changes seen with obesity

A
  • Low voltage EKG (increased distance b/t heart and leads)
  • Left axis deviation (stomach pushes heart to the left)
  • Right axis deviation (RV hypertrophy from OSA and volume overload)
  • QT prolongation (Inc. risk of sudden death)
  • Dysrhythmias (fatty infiltration of conduction system)
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20
Q

general definition of volume of distribution

A

The volume of distribution is a proportionality factor that relates the amount of drug in the body to the concentration of drug measured in a biological fluid. That’s it … a proportionality factor … nothing more.

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21
Q

volume of distribution in obese pts (lipophilic vs hydrophilic)

A
  • The Vd of lipophilic drugs is increased due to a larger fat mass
  • The Vd of hydrophilic drugs is increased due to a larger muscle mass and blood volume and increases some because of large plasma volume
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22
Q

Vd in obese patients and rate of absorption

A
  • Increased blood volume; requires a larger loading dose to achieve a given plasma concentration
  • Increased CO; faster drug delivery to the vessel rich group
  • Altered plasma protein binding; alters the free fraction available
  • Lipid solubility of the drug; large fat mass increases the Vd of lipophilic drugs
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23
Q

Drug Dosing in the Obese patient

A

IBW may under dose due to large Vd
TBW may over dose because fat is less vascular and greater percentage will go to vessel rich group
Lean Body Weight solves the issue

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24
Q

Lean Body Weight

A

LBW is IBW plus extra for increased muscle mass
LBW = IBW X 1.3

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25
Dose a Propofol bolus based on ___
AdjBW
26
Dose a Propofol maintenance infusion based on ___
AdjBW
27
Dose Etomidate based on ____
AdjBW
28
Dose Thiopental based on ___
AdjBW
29
Dose Benzodiazepine boluses based on ___
TBW
30
Dose benzodiazepine infusions based on ____
AdjBW
31
Dose dexmedetomidine based on ___
TBW
32
Dose synthetic opioids (fentanyl, remifentanil) based on ____
TBW
33
Dose morphine based on ___
IBW
34
Dose hydromorphone based on ____
IBW
35
Dose steroidal NMBAs based on ____
IBW
36
Dose Succinylcholine based on ____
TBW
37
Nitrous Oxide (what's the MAC and Blood-Gas Partition Coefficient)
MAC = 104% Blood-Gas Coefficient = 0.47
38
Desflurane (what's the MAC and Blood-Gas Partition Coefficient)
MAC = 6% Blood-Gas Coefficient = 0.45
39
Sevoflurane (what's the MAC and Blood-Gas Partition Coefficient)
MAC = 2% Blood-Gas Coefficient = 0.65
40
Enflurane (what's the MAC and Blood-Gas Partition Coefficient)
MAC = 1.7% Blood-Gas Coefficient = 1.8
41
Isoflurane (what's the MAC and Blood-Gas Partition Coefficient)
MAC = 1.4% Blood-Gas Coefficient = 1.4
42
Halothane (what's the MAC and Blood-Gas Partition Coefficient)
MAC = 0.75% Blood-Gas Coefficient = 2.3
43
PEARLS for Volatile Agents in Obese Pts
Volatile agents are lipophilic. Agents with low blood gas solubility coefficients should be used. MAC is unchanged by obesity
44
Propofol dosing
Loading dose based on LBW and maintenance based on TBW
44
Succ dosing
Intubating dose based on TBW.  This is due to increased blood volume (increased Vd) and increased pseudo cholinesterase activity (increased clearence) 
45
Non depolarizing neuromuscular drugs dosing
Roc and Vec are dosed on LBW Cisatracurium and atracurium and probably TBW
46
Remi dosing
ALWAYS LBW
47
Midazolam dosing
Midazolam administered on **TBW** but will cause prolonged elimination and duration
48
Epidural Local Anesthetics
Engorgement of epidural veins and increase in epidural fat content will cause a greater spread of local anesthetics in the epidural space Reduce the dose to 75%
49
OSA pathophysiology
Review: Pharyngeal muscles maintain airway patency Tensor Palatine—opens the nasopharynx Genioglossus---opens the oropharynx Hyoid Muscle---opens the hypopharynx Fat accumulation in the pharynx causes the internal diameter to narrow, decreases airflow and increase airway collapse
50
OSA
Defined as cessation of airflow for at least 10 seconds with five or more unsuccessful efforts to breathe and a greater than 4% reduction in SaO2 Hypoapnea is defined as 50% reduction in airflow for 10 seconds, 15 or more times per hour, and is linked to snoring and decreased SaO2
51
OSA and obesity
OSA is directly linked to obesity Increases with BMI > 30 kg/m2, abdominal fat distribution and large neck circumference - men > 17in - women > 16in OSA is an independent risk factor for development of HTN, CV disease, morbidity and death
52
Apnea/hypoapnea Index (AHI)
Polysomnography is the definitive test for OSA, and allows for the calculation of the AHI AHI = # of episodes of apnea/hypoapnea divided by hours of sleep Mild 5-15 Moderate 15-30 Severe > 30
53
STOP - BANG
Snoring Tiredness Observed Apnea Pressure (HTN) BMI > 35 kg/m2 Age >50 Neck circumference > 40 cm (15.74in) Gender (male) *High risk > 3 Low risk <3*
54
Obesity Hypoventilation Syndrome
- OHS is a long term result of OSA - Medulla fails to respond to hypercarbia - OHS classically includes apnea during sleep without respiratory effort - Pickwickian syndrome is the old term - Signs; obesity, daytime hyper somnolence, hypoxemia, hypercarbia, resp. acidosis, comp metabolic alkalosis, polycythemia and pulmonary HTN
55
Types of bariatric surgery
Gastric bypass surgery Roux-en-Y (open or laparoscopic) Biliopancreatic diversion bypass Gastric banding (open or laparoscopic) Gastric sleeve surgery
56
Types of malabsorption procedures
1. Biliopancreatic diversion bypass 2. Jejuno-ileal bypass 3. Duodenal Switch  Gastric reduction and removal of portion of small intestine limits nutrient absorption.  Vitamin K, B12, iron and folate depletion
57
Restriction surgerys
1. Gastric Band 2. Gastric Sleeve Limits the quantity of food that can be consumed. Least invasive. Gastric hormone secretion reduced. Small intestine intact
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Combo malabsorption + restricton
Roux-en Y gastric bypass Combination of malabsorption and restriction Yields the best weight loss and comorbidity reduction Risk nutrient deficiency
59
Anastomotic Leak
2% incidence Patients should not receive ketorolac Most common signs: - Tachycardia (72%) - Fever (63%) - Abdominal Pain (54%) - Other signs shoulder pain, pelvic pain, substernal pressure, dyspnea, hypotension, oliguria, increased thirst, restlessness, hiccups
60
Carcinoid Syndrome
- Associated with secretions of vasoactive substances from enterochromaffin cells usually in the GI tract - When liver function is normal carcinoid hormones are cleared, with liver dysfunction sign and symptoms occur - Symptoms can occur if tumors are located in the lungs and bypass the liver and enter the circulation
61
Carcinoid Hormones
1. HISTAMINE 2. KININS AND KALLIKRENS 3. SEROTONIN
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Histamine systemic effects
Bronchoconstriction Vasodilatation Hypotension Flushing of head and neck
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Kinins and Kallikrens systemic effects
Bronchoconstriction Vasodilatation Hypotension Flushing of head and neck Inc. histamine release from mast cells
64
Serotonin systemic effects
Bronchoconstriction Vasodilatation Hypotension Supra ventricular tachydysrhythmias Inc. GI motility, diarrhea, abdominal pain
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Drugs to avoid with carcinoid syndrome
- Histamine releasing drugs: MS meperidine, atracurium, thiopental, and succinylcholine - Succinylcholine induced fasciculation causes hormone release from tumor cells - Exogenous catecholamines can precipitate hormone release - Sympathomimetic agents ephedrine and ketamine
66
drugs to give with carcinoid syndrome
- Somatostatin (octreotide or lanreotide) inhibit release of vasoactive substances from carcinoid tumors - Antihistamines (H1 and H2) diphenhydramine and ranitidine or cimetidine - 5HT3 antagonist (ondansentron) - Steroids - Phenylephrine or vasopressin for hypotension
67
carcinoid crisis
Life threatening response in patients with carcinoid syndrome  S/S include: - Inc. HR - hypertension or hypotension - intense flushing (#1) - abdominal pain - diarrhea (#2)
68
Pancreas
Endocrine & Exocrine Organ Anatomy 15 cm in length  Weighs 60-140 grams Anatomic relationship Duodenum Ampulla of Vater Common bile duct Superior mesenteric artery Portal vein Spleen Transverse colon Left lobe of the liver
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pancreas photo
70
Pancreatic Cells
Composed of two tissue types: 1st. Acinar Cells - Make up 98% of the glands weight and secrete digestive fluids into duodenum (exocrine function) 2nd. Islets of Langerhans - Make up 2% of glands weight and compose of alpha, beta, delta, and pancreatic peptide (PP) cells (endocrine function)
71
Islets of Langerhans
1. PP cells secrete pancreatic polypeptide which inhibits exocrine secretions 2. Delta cells secrete somatostatin which restrains the rate in which nutrients are absorbed (10%) 3. Alpha cells secrete glucagon which raises blood sugar (25%) 4. Beta cells secrete insulin and amylin. Insulin regulates fat and carbohydrate metabolism and causes the cell to take up glucose (70%)
72
Pancreatic polypeptide (PP)
Inhibits pancreatic exocrine secretion, gallbladder contraction, gastric acid secretion, and gastric motility
73
Somatostatin
- Growth-hormone-inhibiting-hormone - Released by the delta cells - Inhibits insulin and glucagon - Inhibits splenic blood flow, gastric motility and gallbladder contraction
74
Glucagon
- A catabolic hormone that promotes energy release from adipose and the liver  - A physiologic antagonist to insulin  - Released between meals (BG < 90 mg/dL), glucagon concentration increases to maintain fuel production - Exogenous glucagon administration - Increases myocardial contraction, HR, and AV conduction - Useful in BB overdose, CHF, Low CO after MI, relaxing sphincter during ERCP, and hypoglcemia - Side effect N/V
75
Insulin
- An anabolic hormone that promotes energy storage - Elimination ½ life of 7 minutes - Increases glucose permeability in skeletal muscle, liver, and fat - Converts carbohydrates to glycogen in the liver and skeletal muscle - Converts excess carbohydrates to fat  - Promote cellular uptake of amino acids, potassium, magnesium and phosphate
76
Normal insulin secretion
1 unit per hour into portal circulation After a meal insulin increases 5-10 fold Total is 40u per day
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factors that influence insulin release
78
Type 1 DM
5 – 10% of people with diabetes have Type 1 And absolute deficiency in insulin Entirely dependent on exogenous insulin Insulin dependent diabetics Autoimmune destruction of the beta cells of the pancreatic islets
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Type 2 DM
90% of people with diabetes have Type 2 Impaired insulin secretion peripheral insulin resistance and excess hepatic glucose production Relative to BG, an insulin deficiency exists May be complicated by nonketotic hyperosmolar, hyperglycemic state Treatment includes hypoglycemic agent, exercise and diet therapy Insulin-treated diabetics
80
Chronic complications from DM
Microvascular: - Retinopathy - Neuropathy - Nephropathy Macrovascular: - Coronary artery disease - Peripheral vascular disease - Cerebrovascular disease Other: - Infections - Cataracts - Stiff Joint Syndrome - Glaucoma - Poor wound healing
81
Rapid-acting Insulin*
Onset: 5 to 15 minutes Peak: 45-75 minutes Duration: 2 to 4 hours Lispro (Humalog) Aspart (Novolog) Glulisine (Apidra)
82
Short-acting insulin*
Onset: 30 min Peak: 2 - 4 hours DOA: 6 - 8 hours Regular (Human Regular) (Novulin Regular)
83
Intermediate-acting insulin
Onset: 2 hours Peak: 4-12 hours DOA: 18-28 hours NPH (Humulin NPH) (Novolin NPH)
84
Long acting insulin
Glargine (Lantus) Onset: 1.5 hour Peak: NONE DOA: 20-24 hours Detemir: Onset: 2 hours Peak: 5-9 hr DOA: 6 - 24 hours
85
Long acting insulin
Glargine (Lantus) Onset: 1.5 hour Peak: NONE DOA: 20-24 hours Detemir: Onset: 2 hours Peak: 5-9 hr DOA: 6 - 24 hours
86
Ultra-long acting insulin
Degludec Onset: 2 hours Peak: none DOA: 40+ hours
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Risks of insulin therapy
Hypoglycemia Allergic Reaction Lipodystrophy Insulin Resistance Drug Interactions
88
hypoglycemia
High risk if exogenous insulin given during fasting Under GA sign and symptoms are masked SNS stimulation increases HR, BP and the presence of diaphoresis  Possible cause of delayed emergence Brain requires glucose: confusion, seizures coma, brain damage and death Treat with D50 50-100ml or glucagon
89
allergic reaction
More common when animal derived products were used Chronic NPH use (or fish allergy) may sensitize to protamine Use caution with large doses
90
risks w/ insulin
- Lipodystrophy: Fat accumulation at injection site - Resistance: When dose exceeds 100u/day antibodies develop to the cell receptor - Drug Interactions: Drugs that counter the hypoglycemic effects of insulin: Epinephrine, glucagon, estrogen, and adrenocorticotropic hormone or enhance the hypoglycemic effect Drug Interactions: - Drugs that counter the hypoglycemic effects of insulin: Epinephrine, glucagon, estrogen, and adrenocorticotropic hormone - Drugs that enhance the hypoglycemic effect: MAO inhibitors, salicylates, and tetracycline
91
Oral Hypoglycemic Med List
Biguanides Sulfonyureas Meglitinides Thiazolidinediones Alpha-Glucosidase Inhibitors Glucagon-like Peptide-1 receptor Agonist Dipeptidyl-Peptidase-4 Inhibitors Amylin Agonist
92
Biguanides
Metformin Inhibits gluconeogenesis and glycogenolysis in the liver and decreases peripheral insulin resistance. Does not cause hypoglycemia Risk of lactic acidosis, increases with renal and liver disease Discontinue 48 hrs. before surgery
93
Biguanides
Metformin Inhibits gluconeogenesis and glycogenolysis in the liver and decreases peripheral insulin resistance. Does not cause hypoglycemia Risk of lactic acidosis, increases with renal and liver disease Discontinue 48 hrs. before surgery
94
Sulfonylureas
Glyburide, Glipizide, Glimepride  Stimulate insulin secretion from pancreatic beta cells Avoid if sulfa allergy Sulfonylureas usually the initial choice for treatment of type II diabetes Hypoglycemia most common side effect Closes K (ATP) channels, inhibits myocardial preconditioning, increases morbidity in high risk patients
95
Meglitinides
Repaglinide, Nateglinide Stimulate insulin secretion from pancreatic beta cells Risk of hypoglycemia
96
Thiazolidinediones
Rosiglitazone and Pioglitazone Decrease peripheral insulin resistance and increase hepatic glucose utilization Does not cause hypoglycemia Contraindicated in liver failure, expand ECF causes edema and increase risk of CHF
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Thiazolidinediones
Rosiglitazone and Pioglitazone Decrease peripheral insulin resistance and increase hepatic glucose utilization Does not cause hypoglycemia Contraindicated in liver failure, expand ECF causes edema and increase risk of CHF
98
Alpha Glucosidase Inhibitors
Acarbose and Migitol Active in the small intestine and result in a delay in glucose absorption. Should be given before a meal. Does not cause hypoglycemia
98
Alpha Glucosidase Inhibitors
Acarbose and Migitol Active in the small intestine and result in a delay in glucose absorption. Should be given before a meal. Does not cause hypoglycemia
99
Glucagon-like Peptide Receptor Agonist
Exenatide, Liraglutide Increases insulin release from beta cells decreases glucagon release from alpha cells and prolongs gastric emptying Risk of hypoglycemia
100
Dipeptidyl-Peptiddase-4 Inhibitors
Meds end in suffix -liptin Increases insulin release Decreases glucagon release Risk of hypoglycemia
101
Amylin Agonist
Pramlintide Inhibits glucagon release from alpha cells and reduces gastric emptying Risk of hypoglycemia when used with insulin, may cause nausea and vomiting
102
DM Tx goals
Fasting and pre-prandial plasma glucose 70-130 mg/dl Peak post prandial  <180 mg/dl Glycosylated Hemoglobin (HbA1c) < 7%
103
DM Deficiency of Insulin Activity
Decreased insulin secretion Decreased response to insulin by target tissue Increase in the counterregulatory hormones that oppose the effects of insulin - Resistin - Adiponectin Primary cause of Type 1 DM - T lymphocytic mediated destruction of beta cells of pancreatic islet
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DM 1 vs. 2 chart*
105
Ketone formation graphic
106
Diabetic Ketoacidosis
Lack of effective insulin - Initial manifestation of DM - Treatment errors - Critical illnesses (MI, trauma, burns….) - Infections Increased serum glucose - Increased hepatic glucose output & Decreased glucose uptake Clinical hallmarks - Metabolic acidosis - Dehydration - Electrolyte abnormalities
107
Diabetic ketoacidosis - pathophys
Pathophysiology Osmotic diuresis and a hyperosmolar state Ketosis and acidosis Low insulin levels = markedly increased glucagon levels - unchecked lipolysis = fatty acids are converted to ketone bodies Acetoacetate and beta hydroxybutyrate cause metabolic acidosis
108
Diabetic Ketoacidosis S&S
Polyuria Polydipsia Anorexia/Nausea/vomiting Abdominal pain Weakness & myalgias Headache Hypothermia  Kussmaul’s respirations - Metabolic acidosis - pH < 7.0 and/or [HCO3-] < 12 mEq/L Acetone breath Intravascular volume depletion Hypo-reflexia Altered mental status
109
DKA labs initally
**Glucose (300-800 mg/dl)** **Ketones** HCO3- (0-15 mEq/L) pH (6.80-7.30) Na+ (total body depletion) K+ (total body depletion) Creatinine/BUN (slightly elevated BUN, Cr false increase) Hemoconcentration Leukocytosis Hyperuricemia Elevated lactate
110
DKA Caveats
Diagnosis of DKA cannot be made without the presence of ketones Glucose concentration is not a good index of the severity of metabolic derangement Initially give NS to restore intravascular volume regardless of Na+ or K+ values Phosphaturia accompanies all forms of metabolic acidosis
111
DKA Tx
Replete volume Treat hyperglycemia Correct hyperosmolality Reverse ketonemia Reverse acidemia Correct K+ depletion
112
DKA fluid resusitation
Fluid resuscitation NS 2-3 liters over first 2 hours Thereafter -  1/2NS at high flow rates Avoid LR When BS approaches 250 mg/dl add D5W Discontinue IV fluids when diet is tolerated and anion gap acidosis resolved
113
DKA and K+
Profoundly depleted regardless of initial K+ Serum K+  by 0.6 mEq/L for ea 0.1  in pH below 7.40 20-30 mEq/hr is initiated Observe for adequate UOP Hypokalemia - Rehydration - Insulin therapy - Correction of acidosis
114
DKA & insulin replacement
IV bolus of regular insulin at 0.1u/kg Regular insulin IV infusion at 0.1u/kg/hour SC regular insulin 2 hours prior to discontinuation of insulin infusion NaHCO3 - cardiovascular instability or altered mental status with pH < 7.0
115
DKA & insulin replacement
IV bolus of regular insulin at 0.1u/kg Regular insulin IV infusion at 0.1u/kg/hour SC regular insulin 2 hours prior to discontinuation of insulin infusion NaHCO3 - cardiovascular instability or altered mental status with pH < 7.0
116
DKA complications
5% mortality Infection Arterial thrombosis Shock Lactic acidosis Hyperchloremic acidosis Cerebral edema - H/A, papilledema & altered mental status Hypokalemia Hypophosphatemia (potassium phosphate)
117
Hyperglycemic Hyperoslmar State (HHS)
Severe hyperglycemia > 800 mg/dl Severe hyperosmolality > 350 mOsm/L Profound intravascular volume depletion - More severe than DKA - 10-20% of total body wt.  Absence of ketoacidosis Impaired renal function Mental status changes Patient profile: - Elderly - Mild, type II diabetes - Symptomatic polyuria - Loss of ability to ingest or retain fluids as a result of illness, drugs or injury
118
DKA vs. HHS chart
119
Preop considerations
Metabolic Aberrations End – Organ complications Peripheral neuropathies & Stiff joints Renal disease ANS dysfunction – delayed gastric emptying BG – ketones – electrolytes – BUN – creatinine – UA - ECG
120
DM autonomic neuropathy
Painless myocardial ischemia Orthostatic hypotension Lack of heart rate variability (fixed tachycardia) Reduced HR response to atropine and beta blockers Neurogenic bladder Lack of sweating Impotence Gastroparesis
121
DM & airway
Glycosylation of joints– stiff joint syndrome with reduced ROM of AO joints The prayer sigh suggests joint glycosylation and increases the risk of difficult intubation
122
Prayer Sign
A + prayer sign can be elicited on exam w/ the patient unable to approximate the palmar surfaces of the phalangeal joints while pressing their hands together. demonstrates a cervical spine immobility and the potential for difficult intubation
123
flowchart for DM
124
prep and monitoring flow chart
125
choose anesthetic technique
126
Dose Ketamine based on _______
AdjBW
127
Dose Lidocaine bolus and infusion based on _____
AdjBW
128
Dose steroidal neurmoscular blocking agents based on _____
Depends. If you do IBW, you'll get adequate intubating conditions and faster recovery but shorter duration. If you use TBW, you'll get faster onset but longer duration. (well fucking DUH is this answer for real)
129
Dose succinylcholine based on ___
TBW
130
Dose reversal agents like Sugammadex and Neostigmine based on ___
AdjBW